FoundationOne Liquid CDx genomic report (blood drawn 20.08.2026)

FoundationOne Liquid CDx genomic report (blood drawn 20.08.2026) — full report, PDF

Date: 2026-08-30 Institution: Foundation Medicine / Roche, Penzberg, Germany Type: Genomics
Source file (Google Drive, docs_eng/): 2026_new/FoundationOne_Liquid_CDx_20Aug2026.pdf
Note: Full 32-page report: 2026_new/FoundationOne_Liquid_CDx_20Aug2026.pdf.

Links: Source PDF (hosted on this site) the same PDF on Google Drive (backup) [hosted copy] (2026_new/FoundationOne_Liquid_CDx_20Aug2026.pdf)

PATIENT TUMOR TYPE REPORT DATE
03-2026-00152703, UA Stomach GIST 30 Aug 2026
ORDERED TEST # COUNTRY CODE SPECIMEN COLLECTION DATE
ORD-2419716-01 UA 20 August 2026

ABOUT THE TEST FoundationOne®Liquid CDx is a next generation sequencing (NGS) assay that identifies clinically relevant genomic alterations in circulating cell-free DNA.

PATIENT
PHYSICIAN SPECIMEN
DISEASE Stomach GIST ORDERING PHYSICIAN HCP, Mol outsource SPECIMEN ID 00201593 1976/04/25
NAME 03-2026-00152703, UA MEDICAL FACILITY MEDICHNA LABORATORIA CSD SPECIMEN TYPE Blood
DATE OF BIRTH 25 April 1976 ADDITIONAL RECIPIENT None SPECIMEN COLLECTION DATE 20 August 2026
SEX Female MEDICAL FACILITY ID 324370 SPECIMEN RECEIVED 25 August 2026
MEDICAL RECORD # CS5220323 PATHOLOGIST Not Provided

Biomarker Findings Report Highlights
Blood Tumor Mutational Burden - 3 Muts/Mb ● Variants with diagnostic implications that may indicate a
ctDNA Tumor Fraction - High (32%) specific cancer type: KIT exon 11 deletion (Q556_V559>H),
Microsatellite status - MSI-High Not Detected exon 13 (V654A), exon 18 (A829P) (p. 6)

Genomic Findings ● Targeted therapies with NCCN categories of evidence for
For a complete list of the genes assayed, please refer to the Appendix. genomic findings in this patient’s tumor type: Regorafenib (p.
9), Nilotinib (p. 13), Ponatinib (p. 14), Sorafenib (p. 14)
KIT exon 11 deletion (Q556_V559>H), exon 13
(V654A), exon 18 (A829P) ● Targeted therapies with potential resistance based on this
BRCA2 T3085fs*26 patient’s genomic findings: Avapritinib (p. 11), Imatinib (p.
CDKN2A rearrangement intron 2 11), Sunitinib (p. 12)
MTOR A1459D ● High ctDNA Tumor Fraction was detected, indicating a lower
This assay tested >300 cancer-related genes, risk of false negative results (p. 5)
including the following 2 gene(s) routinely assessed ● Clinical trial options based on this patient’s genomic findings:
in this tumor type: KIT, PDGFRA. (p. 15)

BIOMARKER FINDINGS THERAPY AND CLINICAL TRIAL IMPLICATIONS

Blood Tumor Mutational Burden No therapies or clinical trials. See Biomarker Findings section
3 Muts/Mb

ctDNA Tumor Fraction High (32%) High ctDNA Tumor Fraction defined as ≥ 1.0% based on concordance for
defined short variants and fusions. See Biomarker Finding Summary.

Microsatellite status MSI-High not detected. No evidence of microsatellite instability in this
MSI-High Not Detected sample (see Appendix section).

THERAPIES WITH CLINICAL RELEVANCE THERAPIES WITH CLINICAL RELEVANCE
GENOMIC FINDINGS VAF%
(IN PATIENT'S TUMOR TYPE) (IN OTHER TUMOR TYPE)

KIT exon 11 deletion 17.0% Regorafenib 1 Nilotinib 2A

(Q556_V559>H) Ponatinib
Ripretinib 2A

exon 13 (V654A) 8.8% Sorafenib
Avapritinib 2A

exon 18 (A829P) 4.0% Dasatinib
Imatinib
10 Trials see p. 20 Sunitinib

Electronically signed by Tyler Janovitz, MD, PhD | 30 August 2026 Sample Preparation: Foundation Medicine GmbH, Nonnenwald 2, 82377 Penzberg, Germany
Roche Customer Care | www.rochefoundationmedicine.com Sample Analysis: Foundation Medicine GmbH, Nonnenwald 2, 82377 Penzberg, Germany
Comprehensive Report Interpretation | Consult at p2padvice.org Issued By: Foundation Medicine GmbH, Nonnenwald 2, 82377 Penzberg, Germany · DAkkS D-ML-21105-01-00

PAGE 1 of 32

PATIENT TUMOR TYPE REPORT DATE
03-2026-00152703, UA Stomach GIST 30 Aug 2026
ORDERED TEST # COUNTRY CODE SPECIMEN COLLECTION DATE
ORD-2419716-01 UA 20 August 2026

THERAPIES WITH CLINICAL RELEVANCE THERAPIES WITH CLINICAL RELEVANCE
GENOMIC FINDINGS VAF%
(IN PATIENT'S TUMOR TYPE) (IN OTHER TUMOR TYPE)

BRCA2 T3085fs*26 1.5% None None

10 Trials see p. 15

CDKN2A rearrangement intron 2 12.8% None None

6 Trials see p. 18

MTOR A1459D 0.21% None None

4 Trials see p. 23

Extensive evidence showing Limited evidence showing variant(s)
variant(s) in this sample may confer in this sample may confer resistance
resistance to this therapy to this therapy
NCCN category for genomic
findings in patient’s tumor type
NOTE Genomic alterations detected may be associated with activity of certain approved therapies; however, the therapies listed in this report may have varied clinical evidence in the patient’s tumor type. Therapies and the
clinical trials listed in this report may not be complete and/or exhaustive. Neither the therapies nor the trials identified are ranked in order of potential or predicted efficacy for this patient, nor are they ranked in order of level
of evidence for this patient’s tumor type. This report should be regarded and used as a supplementary source of information and not as the single basis for the making of a therapy decision. All treatment decisions remain the
full and final responsibility of the treating physician and physicians should refer to approved prescribing information for all therapies. Therapies contained in this report may have been approved by the US FDA or other
national authorities; however, they might not have been approved in your respective country. In the appropriate clinical context, germline testing of APC, ATM, BAP1, BARD1, BRCA1, BRCA2, BRIP1, CDKN2A, CHEK2, FH, FLCN,
MEN1, MLH1, MSH2, MSH6, MUTYH, NF1, NF2, PALB2, PMS2, POLD1, POLE, PTCH1, PTEN, RAD51C, RAD51D, RB1, RET, SDHA, SDHB, SDHC, SDHD, SMAD4, SMARCA4, SMARCB1, STK11, SUFU, TP53, TSC1, TSC2, VHL, and WT1 is
recommended.

Variant Allele Frequency (VAF) is not applicable for copy number alterations, which include reportable focal amplifications and losses (homozygous deletions).

PAGE 2 of 32

PATIENT TUMOR TYPE ORDERED TEST #
03-2026-00152703, UA Stomach GIST ORD-2419716-01

REPORT DATE 30 Aug 2026
SPECIMEN COLLECTION DATE 20 August 2026

10%
increments

Variant Allele
Frequency Percentage
(VAF%) 0.5%
increments

FoundationOne®Liquid CDx
30 Aug 2026

HISTORIC PATIENT FINDINGS (Biomarker Findings) ORD-2419716-01

Blood Tumor 3 Muts/Mb
Mutational Burden

Microsatellite status MSI-High Not Detected

ctDNA Tumor Fraction 32%

HISTORIC PATIENT FINDINGS (Genomic Findings) VAF%

KIT exon 13 (V654A) 8.8%

exon 18 (A829P) 4.0%

exon 11 deletion 17.0%
(Q556_V559>H)

BRCA2 T3085fs*26 1.5%

CDKN2A rearrangement 12.8%
intron 2

MTOR A1459D 0.21%

IMPORTANT NOTE This comparison table refers only to genes and biomarkers assayed by prior FoundationOne®Liquid CDx or FoundationOne®CDx tests. Up to five previous tests may be shown.

For some genes in FoundationOne Liquid CDx, only select exons are assayed. Therefore, an alteration found by a previous test may not have been confirmed despite overlapping gene lists. Please refer to the Appendix for the
complete list of genes and exons assayed. Variants reported for prior time points reflect reporting practices at the time of the historical test(s). Changes in variant reporting nomenclature, classification, or handling may result
in the appearance of discrepancies across time points. The gene and biomarker list will be updated periodically to reflect new knowledge about cancer biology.

ctDNA Tumor Fraction may include previous Tumor Fraction results which reflect reporting practices at the time of reporting. Changes in biomarker reporting may result in the appearance of discrepancies across time points.

PAGE 3 of 32

PATIENT TUMOR TYPE ORDERED TEST #
03-2026-00152703, UA Stomach GIST ORD-2419716-01

REPORT DATE 30 Aug 2026
SPECIMEN COLLECTION DATE 20 August 2026

As new scientific information becomes available, alterations that had previously been listed as Variants of Unknown Significance (VUS) may become reportable or reportable variants may become VUS.

Tissue Tumor Mutational Burden (TMB) and blood TMB (bTMB) are estimated from the number of synonymous and non-synonymous single-nucleotide variants (SNVs) and insertions and deletions (indels) per area of coding
genome sampled, after the removal of known and likely oncogenic driver events and germline SNPs. Tissue TMB is calculated based on variants with an allele frequency of ≥5%, and bTMB is calculated based on variants with
an allele frequency of ≥0.5%.

Not Tested = not baited, not reported on test, or test preceded addition of biomarker or gene
Not Detected = baited but not detected on test
Detected = present (VAF% is not applicable)
VAF% = variant allele frequency percentage
Cannot Be Determined = Sample is not of sufficient data quality to confidently determine biomarker status

Please note that other aspects of this table may have changed from the previous version to reflect the most up-to-date reporting information.

PAGE 4 of 32

PATIENT TUMOR TYPE ORDERED TEST #
03-2026-00152703, UA Stomach GIST ORD-2419716-01

REPORT DATE 30 Aug 2026 BIOMARKER FINDINGS
SPECIMEN COLLECTION DATE 20 August 2026

BIOMARKER checkpoint inhibitors following single-agent or FINDING SUMMARY
Blood Tumor combination treatments with either CTLA4
inhibitors or chemotherapy, with reported high
Blood tumor mutational burden (bTMB, also
known as mutation load) is a measure of the
Mutational Burden bTMB cutpoints ranging from 6 Muts/Mb-16
Muts/Mb3,8,11-13. In HNSCC, a Phase 3 trial showed
number of somatic protein-coding base
substitution and insertion/deletion mutations from
RESULT that bTMB ≥16 Muts/Mb (approximate circulating tumor DNA in blood. TMB is affected
3 Muts/Mb equivalency ≥8 Muts/Mb as measured by this by a variety of causes, including exposure to
assay) was associated with improved survival from mutagens such as ultraviolet light in melanoma15-16
treatment with a PD-L1 inhibitor alone or in and cigarette smoke in lung cancer17-18, treatment
combination with a CTLA-4 inhibitor1. In CRC, a with temozolomide-based chemotherapy in
POTENTIAL TREATMENT STRATEGIES Phase 2 study showed that bTMB TMB ≥28 Muts/ glioma19-20, mutations in the proofreading domains
Mb (approximate equivalency ≥14 Muts/Mb as of DNA polymerases encoded by the POLE and
— Targeted Therapies —
measured by this assay) was associated with POLD1 genes21-25, and microsatellite instability
On the basis of clinical evidence in solid tumors,
improved OS from a PD-L1 inhibitor alone or in (MSI)21,24-25. High bTMB levels were not detected in
increased blood TMB (bTMB) may be associated
combination with a CTLA-4 inhibitor9-10. this sample. It is unclear whether the bTMB levels
with greater sensitivity to immunotherapeutic
in this sample would be predicted to be associated
agents, including anti-PD-L11-5, anti-PD-12,5-8, anti-
FREQUENCY & PROGNOSIS with sensitivity to PD-1- or PD-L1-targeting
PD-1/CTLA4 therapies2,7 , anti-PD-L1/CTLA4
immune checkpoint inhibitors, alone or in
therapies1,9-13. A Phase 2 multi-solid-tumor trial Among gastrointestinal stromal tumor cases
profiled by F1LCDx, 3.8% of cases had a blood combination with other agents3-4,8,26-27. Depending
showed that bTMB ≥16 Muts/Mb (as measured by
tumor mutational burden (bTMB) of >10 Muts/ on the clinical context, TMB testing of an alternate
this assay) was associated with improved survival
Mb14. Published data investigating the prognostic sample or by another methodology could be
from treatment with a PD-1 inhibitor alone or in
considered.
combination with a CTLA-4 inhibitor7. In NSCLC, implications of TMB in GIST are limited (PubMed,
multiple clinical trials have shown patients with Sep 2025).
higher bTMB derive clinical benefit from immune

BIOMARKER appropriately validated in other countries, if CRC41-42, pancreatic cancer43, Ewing sarcoma and

ctDNA Tumor available. Single observations or changes over time
of circulating-tumor DNA (ctDNA) quantity are not
osteosarcoma44, prostate cancer32,41,45, breast
cancer41,46, leiomyosarcoma47, esophageal cancer48,
Fraction part of any clinical decision-making guidelines but
may be a useful indicator for future cancer
and gastrointestinal cancer49.

RESULT management31-38.
FINDING SUMMARY
High (32%)
The ctDNA tumor fraction provides an estimate of
FREQUENCY & PROGNOSIS the percentage of circulating tumor DNA (ctDNA)
In a large genomic study of 25 solid tumor types, present in a cell-free DNA (cfDNA) sample. The
69% of liquid biopsy samples had ctDNA levels ctDNA tumor fraction algorithm utilized for
POTENTIAL TREATMENT STRATEGIES >1% as measured by an investigational composite FoundationOne Liquid CDx integrates multiple
— Targeted Therapies — tumor fraction algorithm with a median tumor distinct genomic features, including aneuploidy
Specimens with high circulating-tumor DNA fraction of 2.2% across tumor types29. Median and the observed allele frequencies of somatic
(ctDNA) tumor fraction have high ctDNA content ctDNA levels were reported to be highest in small short variants and rearrangements. High ctDNA
and thus higher sensitivity for identifying genomic cell lung cancer, liver, colon, and bladder tumor tumor fraction was detected in this sample. In a
alterations28-29. Such specimens are at a lower risk types and lowest in glioma and appendiceal study of patients with advanced NSCLC, the
of false-negative results28-30. A negative result does cancers29. Higher ctDNA levels were reported for positive predictive agreement and negative
not rule out the presence of a mutation below the patients with metastatic (Stage 4) tumors compared predictive value of liquid biopsy compared with
limits of detection of the assay. Patients for whom with patients with localized disease (Stages 1 to tissue for the detection of targetable driver
no companion diagnostic alterations are detected 3)39. Higher ctDNA levels have been reported to be alterations was 96% and 96%, respectively, when
should be considered for confirmation with a associated with worse prognosis in a variety of ctDNA tumor fraction was high (greater or equal to
tumor tissue test that is FDA approved or advanced solid tumors40, including NSCLC41, 1%)28.

PAGE 5 of 32

PATIENT TUMOR TYPE ORDERED TEST #
03-2026-00152703, UA Stomach GIST ORD-2419716-01

REPORT DATE 30 Aug 2026 GENOMIC FINDINGS
SPECIMEN COLLECTION DATE 20 August 2026

GENE limited clinical71-73 data indicate that KIT A-loop longer recurrence-free survival in univariate

KIT mutations are sensitive to sorafenib, although
preclinical evidence of potential resistance has
analysis; similar results were not observed for
patients with exon 11 insertions, exon 11 point
ALTERATION
been reported specifically for the D816V mutations, exon 9 mutations, or no KIT
exon 11 deletion (Q556_V559>H), exon 13 (V654A), exon 18 mutation69,74-75. Several A-loop alterations at mutation122. Overall, patients with exon 11
(A829P)
residues D816, D820, N822, and A829 have mutations experienced a benefit from adjuvant
exhibited ponatinib sensitivity in preclinical imatinib therapy, which is in agreement with
HGVS VARIANT
evaluations76-81. The use of mTOR inhibitors as an several previous studies120-123; although the
NM_000222.2:c.1668_1676del (p.Q556_V559delinsH),
alternative therapeutic strategy has demonstrated reported effect on OS is favorable, it does not
NM_000222.2:c.1961T>C (p.V654A),
limited success in KIT-mutated, imatinib-resistant always reach statistical significance122-123. However,
NM_000222.2:c.2485G>C (p.A829P)
melanoma, with 1 PR and 3 SD observed for 4 patients who develop imatinib resistance have a
VARIANT CHROMOSOMAL POSITION patients treated with everolimus82-83. However, no poorer prognosis than those who do not, including
chr4:55593601-55593610, chr4:55594258, chr4:55602664 responses were observed for 10 patients with a reduced 5-year survival rate124.
mastocytosis following everolimus monotherapy,
with 8/10 patients harboring the KIT D816V
FINDING SUMMARY
mutation84. The role of KIT amplification as a
POTENTIAL TREATMENT STRATEGIES KIT (also called c-KIT) encodes a receptor tyrosine
biomarker for response to mTOR inhibitors has not
kinase that signals through the PI3K-AKT and
— Targeted Therapies — been investigated (PubMed, Feb 2026).
RAS-MAPK pathways125-126. KIT alterations in exon
On the basis of clinical evidence, primarily in GIST, 11 leading to the disruption of the autoinhibitory
melanoma, AML, and systemic mastocytosis, KIT — Potential Resistance — domain (amino acids 545-579)127-134 or ITD proximal
activating alterations are associated with sensitivity Mutation of residues within the KIT activation- to the kinase domain (amino acids 569-591)135, such
to TKIs including imatinib, sunitinib, sorafenib, loop (A-loop) has been associated with preclinical as observed here, are predicted to be activating and
dasatinib, nilotinib, pazopanib, regorafenib, and clinical resistance to imatinib77,85-99 and sensitive to imatinib120,136-137. KIT exon 11 deletions
ponatinib, midostaurin, apatinib, avapritinib, and sunitinib77,85,87,92,95,100 in patients with GIST. KIT are frequently observed in the context of
ripretinib50-64. In a Phase 1/2 dose escalation study V654A mutation has been associated with gastrointestinal stromal tumor (GIST)86,121,129 and
of the Type-1 KIT-targeting agent bezuclastinib resistance to imatinib for patients and in cell-based KIT-ITDs in acute myeloid leukemia (AML)136,138-141.
monotherapy or in combination with sunitinib for models77,87,91-93,99,101-103. KIT V654A is associated Extensive clinical and preclinical studies have
patients with heavily pretreated KIT-mutated GIST with resistance to avapritinib55,104-106 and was reported that KIT mutations in exon 17 within the
after progressing on imatinib, sunitinib, or shown to reduce sensitivity to ripretinib based on activation loop (A-loop), including C809, D816,
regorafenib, treatment with the combination clinical and preclinical data56,107-109 and D820, N822, Y823, and A829, have emerged as
therapy resulted in a median PFS (mPFS) of 12.1 preclinical110 as well as regorafenib and ponatinib secondary alterations conferring resistance to
months and a median OS (mOS) of 18.1 months65. in preclinical studies; this mutation still may be imatinib77,86-97, or have shown resistance to
For 11 patients with detectable KIT mutations at inhibited at clinically achievable doses76-77. Clinical sunitinib77,87,92,142. However, KIT A-loop mutations
enrollment, the combination resulted in 1 PR, 8 SD, and preclinical data suggest that mutations located have shown clinical sensitivity to
and 2 PD; the subset of patients with KIT exon 9 or within KIT exons 13 and 14, when co-occurring avapritinib50,53,55,66-67. The V654A exon 13 mutation
exon 11 baseline mutations and KIT secondary with other activating KIT mutations, reduce is located within the kinase domain of KIT and is
mutations in the exon 17 or exon 18 A-loop alone sensitivity to ripretinib56,107-109,111-115. considered activating143. It is also a common
experienced 1 PR and 3 SDs, whereas the patients secondary mutation, acquired in addition to an
with additional exon 13 or exon 14 mutations existing activating mutation in KIT; this mutation
experienced 1 SD and 2 PDs65. Clinical benefit was FREQUENCY & PROGNOSIS
has been associated with resistance to
also observed with bezuclastinib monotherapy KIT mutation has been reported for 54-72% of
imatinib77,87,91-93,101-102 and avapritinib55,104-105
(mPFS 5.8 months and mOS 11.1 months), patients with gastrointestinal stromal tumor
clinically. Based on clinical (2023; AACR Abstract
including 3 SDs and 1 PD for patients with KIT (GIST), and the majority of these mutations affect
3887)56,107-109 data, V654A mutations may be
exon 11 and secondary KIT A-loop mutations, and 1 exon 9 or exon 11116-118. It is estimated that up to
associated with reduced sensitivity to ripretinib;
PD for 1 patient with exon 11 and a secondary KIT 95% of GISTs overexpress the KIT protein, and KIT
preclinical models indicate decreased sensitivity to
D654A mutation in exon 1365. Avapritinib mutation has been reported to be an early event in
regorafenib and ponatinib76-77.
selectively inhibits mutated KIT and PDGFRA55 the development of GIST116,119. Mutations in KIT
and has demonstrated clinical activity against KIT exon 11 are associated with a significantly greater
exon 17 mutations, including KIT D816 response rate to imatinib, compared with POTENTIAL DIAGNOSTIC IMPLICATIONS
mutations50,53,66-67 . In early phase clinical trials, individuals with mutations in exon 9 or without KIT mutations are characteristic drivers of GIST
40% (10/25) of patients with heavily pretreated mutations in KIT120-121. Studies comparing patients and may aid in guiding targeted therapy approaches
KIT-mutated GIST experienced tumor reduction53 with GIST treated with imatinib with those treated in this setting (NCCN GIST Guidelines, v1.2025)144.
and 83% (19/23) of patients with advanced systemic with placebo indicate that the presence of exon 11
mastocytosis responded66. Preclinical68-70 and in-frame deletions is associated with a significantly

PAGE 6 of 32

PATIENT TUMOR TYPE ORDERED TEST #
03-2026-00152703, UA Stomach GIST ORD-2419716-01

REPORT DATE 30 Aug 2026 GENOMIC FINDINGS
SPECIMEN COLLECTION DATE 20 August 2026

GENE 10.4 months compared with patients with non- prognostic implications of BRCA2 alterations in

BRCA2 BRCA mutated disease179. In a Phase 2 study for
patients with PARP-resistant ovarian cancer, the
GIST are limited (PubMed, Jan 2025).

combination of the WEE1 inhibitor adavosertib
ALTERATION FINDING SUMMARY
T3085fs*26 and olaparib elicited improved clinical benefit (ORR
The BRCA2 tumor suppressor gene encodes a
29%; DCR 89%) than adavosertib alone (ORR 23%;
HGVS VARIANT protein that regulates the response to DNA
DCR 63%); however, among patients with BRCA-
NM_000059.3:c.9253dup (p.T3085Nfs*26) damage201. Inactivating BRCA2 alterations can lead
mutated tumors, clinical benefit was comparable
VARIANT CHROMOSOMAL POSITION to homologous recombination deficiency202.
between the combination (ORR 19%) and
chr13:32954272 Alterations such as seen here may disrupt BRCA2
monotherapy (ORR 20%)180. A Phase 1
function or expression201,203-218.
monotherapy trial of adavosertib for BRCA1/
2-mutated solid tumors reported PRs in 2 patients
POTENTIAL GERMLINE IMPLICATIONS
(ovarian serous and oral SCC), while a third patient
POTENTIAL TREATMENT STRATEGIES
One or more of the BRCA2 variants observed here
with BCRA1- and TP53-mutated ovarian serous
— Targeted Therapies — has been described in the ClinVar database as a
carcinoma experienced 14% tumor shrinkage prior
Alterations that inactivate BRCA1 or BRCA2 may to disease progression181. Limited clinical and
likely pathogenic or pathogenic germline mutation
confer sensitivity to PARP inhibitors145-163 or ATR (by an expert panel or multiple submitters)219.
preclinical evidence support the sensitivity of
inhibitors164-169. Clinical responses to PARP Follow-up germline testing would be needed to
BRCA2 inactivating mutations to ATR inhibitors,
inhibitors have been reported for patients with distinguish whether the finding in this patient is
including two responses to berzosertib for patients
either germline or somatic BRCA1/2 mutations with BRCA2 inactivating alterations in somatic or germline. Inactivating germline
mostly in ovarian152,155,162,170, breast149,171-172, neuroendocrine prostate cancer and breast mutations in BRCA1 or BRCA2 are associated with
prostate147,173-174, and pancreatic cancer163, including cancer169,182-185. autosomal dominant hereditary breast and ovarian
patients with platinum-resistant or -refractory cancer220-221, and the lifetime risk of breast and
disease146,151,158,161. Among other tumor types, ovarian cancer in BRCA2 mutation carriers has
— Nontargeted Approaches —
although 1 complete response to olaparib has been been estimated to be as high as >80% and 23%,
reported for 1/3 patients with BRCA2-mutated Inactivation of BRCA2 may also predict sensitivity respectively222. Elevated risk for other cancer types,
colon adenocarcinoma from a basket trial175, Phase to DNA-damaging drugs such as trabectedin,
including gastric, pancreatic, prostate, and
2 and retrospective studies of PARP inhibitors did lurbinectedin, and the platinum chemotherapies
colorectal, has also been identified, with an
cisplatin and carboplatin186-198.
not find clinical benefit for 14 patients with increase in risk ranging from 20 to 60%223. The
BRCA1- or BRCA2-mutated CRC175-178. In the estimated prevalence of deleterious germline
Phase 2 KEYLYNK-007 trial, patients with HRRm/ FREQUENCY & PROGNOSIS BRCA1/2 mutations in the general population is
HRD advanced tumors were treated with the In a genomic study of sarcoma, BRCA2 mutation or between 1:400 and 1:800, with an approximately
combination olaparib and pembrolizumab, and the homozygous deletion was not observed in any of 10-fold higher prevalence in the Ashkenazi Jewish
cohort of patients with BRCA mutated cancer, 22 gastrointestinal stromal tumors (GIST)199. A case population222,224-229. In the appropriate clinical
outside of ovarian and breast cancer, reported report has described a patient with a BRCA2 context, germline testing of BRCA2 is
improved ORR of 27% (36/132) vs. 12% (12/104), mutation who developed GIST, as well as other recommended.
mPFS of 4.4 vs. 3.7 months, and mOS of 14.0 vs. tumors200. Published data investigating the

PAGE 7 of 32

PATIENT TUMOR TYPE ORDERED TEST #
03-2026-00152703, UA Stomach GIST ORD-2419716-01

REPORT DATE 30 Aug 2026 GENOMIC FINDINGS
SPECIMEN COLLECTION DATE 20 August 2026

GENE as a predictive biomarker is not clear. function262-283. One or more alterations seen here

CDKN2A FREQUENCY & PROGNOSIS
are predicted to result in p14ARF loss of
function266,283-286.
ALTERATION Putative concurrent homozygous deletion of
rearrangement intron 2 CDKN2A and CDKN2B was seen in 14% (3/22) of POTENTIAL GERMLINE IMPLICATIONS
REARRANGEMENT DETAILS gastrointestinal stromal tumors (GISTs) in the Germline CDKN2A mutation is associated with
CDKN2A(NM_000077) rearrangement intron 2 Sarcoma Genome Project dataset199. Loss of at least melanoma-pancreatic cancer syndrome, a condition
part of chromosomal region 9p21, which contains marked by increased risk of developing malignant
the CDKN2A/B loci, was reported in 63% of melanoma and/or pancreatic cancer287. Mutation
patient GISTs250. Numerous studies have shown carriers within families may develop either or both
POTENTIAL TREATMENT STRATEGIES that loss of expression of p16INK4a and p14ARF types of cancer, and melanoma cases may be
— Targeted Therapies — correlates with aggressive disease, worse prognosis, referred to as familial or hereditary
Preclinical and clinical data suggest that tumors and shorter survival in patients with GIST250-255. melanoma288-289. CDKN2A is the most implicated
with CDKN2A alterations may predict sensitivity gene in familial melanoma, with germline
mutations present in 16% to 20% of familial
to CDK4/6 inhibitors, such as abemaciclib, FINDING SUMMARY
ribociclib, and palbociclib230-245. Clinical benefit melanoma cases290-292. CDKN2A alteration has also
CDKN2A encodes two different, unrelated tumor
from CDK4/6 inhibitors has been observed for been implicated in familial melanoma-astrocytoma
suppressor proteins, p16INK4a and p14ARF256-257.
patients with B-cell lymphoma, head and neck syndrome, an extremely rare tumor association
Inactivation of p16INK4a leads to dysregulation of
cancer, thymic cancer, NSCLC, sarcoma, characterized by dual predisposition to melanoma
the CDK4/6-cyclin-Rb pathway and loss of cell
mesothelioma, and several other tumor and nervous system tumors293-295. In the
cycle control258-259. The tumor suppressive
types230-232,237-247. Although preclinical studies have appropriate clinical context, germline testing of
functions of p14ARF involve stabilization and
suggested that loss of p14ARF function may be CDKN2A is recommended.
activation of p53, via a mechanism of MDM2
associated with reduced sensitivity to MDM2 inhibition260-261. One or more alterations observed
inhibitors248-249, the clinical relevance of p14ARF here are predicted to result in p16INK4a loss of

GENE been reported in a subset of patients with MTOR- mTOR/AKT pathway is frequently activated in

MTOR mutated solid tumors, most notably RCC298-301, as
well as individual cases of gastric cancer and
GIST tumors, and strategies for targeting this
pathway are under investigation306-310. Activation
ALTERATION
angiosarcoma298. However, multiple retrospective of the PI3K/mTOR/AKT pathway was reported to
A1459D and prospective studies, including NCI-MATCH be more common in GIST with acquired resistance
and analyses of the RECORD-3, GRANITE-1, and to imatinib (53%) when compared to imatinib-
HGVS VARIANT
NM_004958.3:c.4376C>A (p.A1459D)
EVOLVE-1 trials, have not demonstrated a sensitive (27%) and primary resistant GIST (33%)306.
consistent association between MTOR pathway
VARIANT CHROMOSOMAL POSITION
alterations and clinical benefit from
chr1:11217302 FINDING SUMMARY
everolimus302-304.
mTOR encodes an intracellular serine/threonine
kinase that integrates upstream signals, including
FREQUENCY & PROGNOSIS those from the PI3K-AKT pathway to regulate
POTENTIAL TREATMENT STRATEGIES MTOR mutations have been reported in 1.2% of cellular growth, metabolism, and survival311-312.
— Targeted Therapies — gastrointestinal stromal tumors (GIST)305. MTOR mutations such as observed here have
Activating MTOR mutations activate PI3K-AKT- Published data investigating the prognostic shown to be activating and may confer sensitivity
mTOR signaling296-297. Clinical responses to implications of MTOR alterations in GIST are to mTOR inhibitors296-297,313-320.
rapalogs such as everolimus and temsirolimus have limited (PubMed, Feb 2026). However, the PI3K/

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PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 THERAPIES WITH CLINICAL BENEFIT IN PATIENT'S TUMOR TYPE
SPECIMEN COLLECTION DATE 20 August 2026

Regorafenib AREAS OF THERAPEUTIC USE [mPFS]: 5.6 months vs. 4.2 months, HR=0.80)324.
Regorafenib is a small-molecule inhibitor of multiple Regorafenib was superior to avapritinib for patients with
Assay findings association kinases, including RET, VEGFRs, PDGFRs, KIT, and RAF mutations in exons 13 or 14 (mPFS: 7.4 months vs. 1.9
family proteins. It is FDA approved to treat hepatocellular months) or exons 17 or 18 (6.7 months vs. 4.7 months);
KIT carcinoma that has been previously treated with sorafenib, mPFS for patients without secondary mutations in KIT
exon 11 deletion (Q556_V559>H),
exon 13 (V654A), exon 18 metastatic colorectal cancer (CRC), or advanced exons 13 or 14 was similar between the 2 groups (5.6
(A829P) gastrointestinal stromal tumors (GISTs). Please see the months vs. 5.6 months), but avapritinib was inferior to
drug label for full prescribing information. regorafenib for patients with mutations in exons 13 or 14
(1.9 months vs. 7.4 months) or exons 17 or 18 (4.7 months
GENE ASSOCIATION vs. 6.7 months)325. A Phase 2 follow-up study of
On the basis of clinical evidence in gastrointestinal regorafenib treatment for patients with advanced GIST
stromal tumors321-322 and melanoma54, activating KIT and a KIT exon 11 mutation reported a longer median PFS
alterations may predict sensitivity to regorafenib. Limited (13.4 months) compared with patients with KIT/PDGFRA
preclinical data has shown that KIT V654A may reduce wild-type, non-SDH-deficient tumors (1.6 months)321.
sensitivity to regorafenib77. In a study of patients with Regorafenib has shown efficacy in the third line for
GIST, V654A emerged during regorafenib treatment in 4 advanced gastrointestinal stromal tumors (GISTs) based on
patients and increased in allele frequency in 4 additional a Phase 3 randomized study comparing regorafenib to
patients323. placebo; patients who had progressed on imatinib and
sunitinib demonstrated significantly longer median PFS
when treated with regorafenib (4.8 vs. 0.9 months)59. A
SUPPORTING DATA
Phase 2 study of regorafenib in the second-line setting for
In the Phase 3 VOYAGER trial for patients with KIT-
patients with imatinib-resistant advanced GIST reported a
mutated GIST in the third- or fourth-line setting,
median PFS of 36.3 weeks326.
regorafenib was superior to avapritinib (median PFS

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PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 THERAPIES ASSOCIATED WITH UNCLEAR RESISTANCE IN PATIENT'S TUMOR TYPE
SPECIMEN COLLECTION DATE 20 August 2026

Ripretinib AREAS OF THERAPEUTIC USE unclear whether ripretinib would be beneficial in this
Ripretinib is a selective kinase inhibitor of PDGFRA and context.
Resistance of variant(s) to
associated therapy is unclear KIT. It is FDA approved to treat patients with
gastrointestinal stromal tumor (GIST). Please see the drug SUPPORTING DATA
Assay findings association label for full prescribing information. The Phase 3 INVICTUS study comparing ripretinib with
placebo for patients with previously treated advanced
KIT
exon 11 deletion (Q556_V559>H), GENE ASSOCIATION gastrointestinal stromal tumor (GIST) reported improved
exon 13 (V654A), exon 18 On the basis of clinical evidence in KIT-mutated GIST51 as median PFS (mPFS; 6.3 vs. 1.0 months, HR=0.15), median
(A829P) well as strong preclinical evidence106, KIT mutation may OS (15.1 vs. 6.6 months, HR=0.36), and ORR (9.4% vs.
predict sensitivity to ripretinib. On the basis of clinical 0%)328. A Phase 1 study evaluating ripretinib in previously
and preclinical evidence, mutations within KIT exons 13 treated GIST also reported ORRs of 24%, 24%, or 9% as
and 14, when co-occurring with other activating KIT second-line, third-line, or fourth-or-later-line therapies,
mutations, reduce sensitivity to ripretinib56,107-109,111-115 . In respectively51. Intrapatient dose escalation of ripretinib
the Phase 3 INTRIGUE trial of ripretinib versus sunitinib after initial relapse provided a further mPFS of 3.3-5.6
in the second line setting, patients with exon 11 co- months in these studies without additional toxicity329-330 .
mutated with exon 13 or exon 14 mutations experienced The Phase 3 INTRIGUE trial comparing ripretinib with
inferior mPFS on ripretinib (4.0 months vs. 15.0 months, sunitinib in advanced GIST after relapse on imatinib
HR=3.94); however, patients with triplet mutations in reported similar mPFS (8.0 vs. 8.3 months), but ripretinib
exon 11, exon 13 or exon 14, and exon 17 or exon 18 did was associated with a more favorable safety profile as well
not experience significantly poorer mPFS relative to as a higher ORR for patients with KIT exon 11 mutations
patients with triplet mutations treated with sunitinib (8.1 (24% for ripretinib compared with 15% for sunitinib)331.
months vs. 10.9 months, HR=1.07)108. Investigators Outcomes for patients treated with ripretinib in the
reported frequent emergence of KIT exon 13 and 14 INTRIGUE trial differed by co-occurring KIT mutation
mutations at progression on ripretinib treatment111. status: exon 11 and exon 13 or 14 mutations were
Preclinical data suggest that KIT exon 13 and 14 alterations associated with shorter PFS (4 months) than those with
in the absence of other KIT activating mutations may still exon 11 and exon 17 or 18 mutations (14.2 months) .
108

be sensitive to ripretinib treatment 106,111,327 . Therefore, it is

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PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 THERAPIES ASSOCIATED WITH RESISTANCE IN PATIENT'S TUMOR TYPE
SPECIMEN COLLECTION DATE 20 August 2026

Avapritinib AREAS OF THERAPEUTIC USE SUPPORTING DATA
Resistance of variant(s) to Avapritinib is a selective kinase inhibitor of PDGFRA and In the Phase 3 VOYAGER trial for patients with KIT-
associated therapy is likely KIT activating mutations. It is FDA approved to treat mutated GIST in the third- or fourth-line setting,
unresectable or metastatic gastrointestinal stromal tumor avapritinib was not superior to regorafenib (median PFS
Assay findings association (GIST) that is positive for PDGFRA mutation in exon 18, [mPFS] of 4.2 vs. 5.6 months, HR=1.25)324; mPFS for
including the resistance mutation D842V. It is also patients without secondary mutations in the KIT ATP
KIT approved to treat indolent or advanced systemic
exon 11 deletion (Q556_V559>H),
binding pocket (ABP, exons 13 or 14) was similar between
exon 13 (V654A), exon 18 mastocytosis. Please see the drug label for full prescribing the 2 groups (5.6 vs. 5.6 months), but avapritinib was
(A829P) information. inferior to regorafenib for patients with ABP mutations
(1.9 vs. 7.4 months) or activation loop (AL, exons 17 or 18;
GENE ASSOCIATION 4.7 vs. 6.7 months)325. Post hoc analysis of Phase 1 and
On the basis of prospective Phase 1 and Phase 2 studies in Phase 1/2 avapritinib trials showed improved outcomes
KIT-mutated GIST53,55 and systemic mastocytosis for patients with GIST both positive for KIT AL mutations
(SM)332-333 , as well as a case report in metastatic vulvar and negative for KIT ABP mutations relative to patients
melanoma334, KIT mutation may predict sensitivity to with GIST and other KIT mutations (ORR of 27% vs. 12%;
avapritinib. Avapritinib has shown clinical activity against mPFS of 9.1 vs. 3.5 months)336. Avapritinib has primarily
the KIT A-loop mutation D816V in a Phase 1 trial for been studied in the context of PDGFRA- and KIT-mutated
SM335, and against additional KIT A-loop mutations in gastrointestinal stromal tumor (GIST)324,336-339 and KIT-
preclinical studies55. Based on a clinical study for patients mutated mastocytosis50,66,332-333,335 . In the Phase 1
with gastrointestinal stromal tumor (GIST)104 and NAVIGATOR trial in heavily pretreated GIST, patients
preclinical data55,106 , KIT V654A, when co-occurring with with KIT (n=110) or PDGFRA non-D842V (n=3)
alterations experienced a median PFS of 3.7 months and
KIT activating alteration, is associated with resistance to
median OS of 11.6 months337; patients with PDGFRA
avapritinib. The relevance of this therapeutic strategy for
cases in which V654A alteration is seen alone is unclear. D842V-positive GIST experienced an ORR of 88% (49/56;
5 CRs, 44 PRs), a 12-month PFS rate of 81%, and a
24-month OS rate of 81%338.

Imatinib AREAS OF THERAPEUTIC USE clinical evidence in GIST86,91,93,95,98-99,103,352-353,355 .
Resistance of variant(s) to Imatinib targets the BCR-ABL fusion protein, PDGFR,
associated therapy is likely and KIT. It is FDA approved to treat KIT-positive SUPPORTING DATA
gastrointestinal stromal tumors (GISTs), Philadelphia Clinical studies in GIST have reported that imatinib
Assay findings association chromosome-positive chronic myeloid leukemia and acute treatment results in significantly longer recurrence-free
lymphoblastic leukemia, myelodysplastic syndrome/ survival (RFS) and OS123,345 . The Phase 3 BFR14 trial
KIT myeloproliferative syndrome, aggressive systemic
exon 11 deletion (Q556_V559>H), reported improved clinical outcomes for patients with
exon 13 (V654A), exon 18 mastocytosis without a D816V KIT mutation, GIST who continued treatment with imatinib after
(A829P) hypereosinophilic syndrome and/or chronic eosinophilic achieving disease control compared with patients who
leukemia, and dermatofibrosarcoma protuberans. Please discontinued treatment at disease control356. A meta-
see the drug label for full prescribing information. analysis of imatinib clinical trials suggests that patients
with GIST harboring KIT exon 11 mutations respond
GENE ASSOCIATION better to imatinib than those without357. Several Phase 3
On the basis of clinical and preclinical data in KIT- trials of imatinib, including a 10 -year outcomes study,
mutated137,340-342 , KIT-amplified340,342-344 , or KIT- reported significantly increased OS in patients with GIST
expressing tumors141,345-351 , KIT activating alterations may harboring KIT exon 11 mutations relative to those with
confer sensitivity to imatinib. Mutation of residues within KIT exon 9 mutations358-359 . A case study has reported a
or adjacent to the KIT activation loop, as observed here, PR and 5-year disease stabilization upon treatment with
have demonstrated resistance to imatinib in patients with imatinib in a patient with GIST harboring a PDGFRA
GIST86,91,93,95,98-99,102-103,352-354 . The KIT V654A mutation is exon 12 mutation360.
predicted to confer resistance to imatinib based on strong

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PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 THERAPIES ASSOCIATED WITH RESISTANCE IN PATIENT'S TUMOR TYPE
SPECIMEN COLLECTION DATE 20 August 2026

Sunitinib AREAS OF THERAPEUTIC USE months; 56%)92; secondary mutations in KIT V654 in exon
Resistance of variant(s) to Sunitinib is a small-molecule TKI that targets PDGFRs, 13 or T670 in exon 14 were associated with numerically
associated therapy is likely VEGFRs, KIT, FLT3, CSF-1R, and RET. It is FDA approved improved mOS compared with patients carrying
to treat advanced or metastatic pancreatic neuroendocrine secondary activation-loop mutations in exon 17 or exon 18
Assay findings association tumors, gastrointestinal stromal tumors (GISTs) for (13.0 months vs. 4.0 months, n=18 and n=13)92. The
patients who have progressed on or are intolerant to presence of secondary mutations may have impaired the
KIT imatinib, and advanced renal cell carcinoma (RCC) as well
exon 11 deletion (Q556_V559>H),
response of patients with secondary mutations; KIT
exon 13 (V654A), exon 18 as for the adjuvant treatment of patients at high risk of V560D in exon 11 was potently inhibited by sunitinib in
(A829P) recurrent RCC after nephrectomy. Please see the drug label vitro in the absence of secondary KIT mutations92.
for full prescribing information. Biomarker analysis from a Phase 1/2 study of sunitinib in
combination with investigational KIT inhibitor
GENE ASSOCIATION bezuclastinib reported benefit in later lines for patients
On the basis of clinical and preclinical data in KIT- with similar exon 17 or 18 secondary alterations65. In a
mutated92,361-365 or KIT-expressing tumors361,366 , KIT retrospective analysis of second-line sunitinib, patients
activating alterations may predict sensitivity to sunitinib. with advanced gastrointestinal stromal tumor (GIST)
On the basis of retrospective analyses92,100 , case studies367, receiving sunitinib experienced superior median OS
and preclinical evidence in GIST77,92,367 , KIT V654A is (mOS) compared with patients receiving any other
predicted to be sensitive to sunitinib. Mutation of residues second-line treatment (32.4 vs. 27.1 months, n=436 and
within the KIT activation loop (A-loop) is predicted to n=74)368. The median time to progression for patients with
confer resistance to sunitinib based on extensive clinical imatinib-refractory or -intolerant GIST treated with
data in gastrointestinal stromal tumor87,92,95,100 . sunitinib was 27.3 weeks, as compared with 6.4 weeks for
patients treated with placebo369. A Phase 1/2 trial of
SUPPORTING DATA sunitinib in combination with the investigational KIT-
In a Phase 1/2 trial of sunitinib, patients with imatinib- inhibitor bezuclastinib for a population heavily pretreated
resistant GIST harboring KIT exon 11 mutations with KIT-targeted agents reported a median PFS and mOS
experienced worse median OS (mOS, 12.3 months) and of 12.1 months and 18.1 months, respectively; the study
clinical benefit rate (34%) than patients with exon 9 observed 1 CR, 2 PRs, and a clinical benefit rate of 80%
mutations (26.9 months; 58%) or wildtype KIT (30.5 (n=15)65.

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PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 THERAPIES WITH CLINICAL BENEFIT IN OTHER TUMOR TYPE
SPECIMEN COLLECTION DATE 20 August 2026

Dasatinib AREAS OF THERAPEUTIC USE A829, remain sensitive to dasatinib68,373-377 .
Dasatinib is a kinase inhibitor that targets the BCR-ABL
Assay findings association fusion protein, SRC family kinase receptors, KIT, EPHA2, SUPPORTING DATA
and PDGFR-beta. It is FDA approved to treat certain A Phase 2 trial of dasatinib for patients with TKI-naive
KIT subtypes of Philadelphia chromosome-positive (Ph+)
exon 11 deletion (Q556_V559>H), gastrointestinal stromal tumors (GIST) reported an ORR of
exon 13 (V654A), exon 18 chronic myeloid leukemia and Ph+ acute lymphoblastic 74% (31/42, 14 CR) and a median PFS (mPFS) of 13.6
(A829P) leukemia. Please see the drug label for full prescribing months378. A Phase 2 trial of dasatinib for patients with
information. GIST who were refractory to imatinib and sunitinib
reported an mPFS of 3.1 months, and 3.4% (2/58)
GENE ASSOCIATION experienced PRs379; a similar Phase 2 trial reported a PR
On the basis of clinical evidence in melanoma370-371 and rate of 32% (15/47), with 21% of patients demonstrating
preclinical evidence in other cancer types372-373 , activating PFS for >6 months by Choi criteria380. A trial of dasatinib
KIT alterations may confer sensitivity to dasatinib. for patients with GIST previously treated with imatinib
Preclinical and limited clinical data indicate that reported a 25% ORR (12/48, all PR), mPFS of 2.9 months,
secondary imatinib-resistant mutations, including V654A and OS of 19 months by Choi criteria381.
and A-loop alterations at residues D816, D820, N822, and

Nilotinib AREAS OF THERAPEUTIC USE KIT-expressing tumors389, KIT activating alterations may
Nilotinib targets tyrosine kinases such as ABL (including confer sensitivity to nilotinib.
Assay findings association BCR-ABL), PDGFRs, KIT, CSF1R, DDR1, and DDR2. It is
FDA approved to treat newly diagnosed pediatric or adult SUPPORTING DATA
KIT patients with Philadelphia chromosome-positive (Ph+)
exon 11 deletion (Q556_V559>H), The Phase 3 ENESTg3 trial of nilotinib for 240 patients
exon 13 (V654A), exon 18 chronic myeloid leukemia (CML) in chronic phase, adults with advanced gastrointestinal stromal tumors (GIST)
(A829P) with Ph+ CML in chronic or accelerated phase with whose cancer had progressed on prior imatinib and/or
resistance or intolerance to prior therapy including sunitinib treatment showed no significant difference in
imatinib, and pediatric patients with Ph+ CML in chronic PFS between nilotinib and best supportive care, but
phase with resistance or intolerance to prior tyrosine- patients treated with nilotinib showed increased OS390.
kinase inhibitor therapy. Please see the drug label for full The Phase 3 ENESTg1 trial of nilotinib versus imatinib as
prescribing information. a first-line treatment for patients with advanced GIST did
not show clinical improvement for nilotinib; longer OS
GENE ASSOCIATION and PFS were reported for imatinib in the full population
Additionally, imatinib-resistant KIT mutations such as of patients (397), but patients with KIT exon 11 mutations
V654A and A-loop alterations at residues D816, D820, saw similar PFS in both treatment groups387. A Phase 2
N822, and A829 maintain sensitivity to nilotinib as clinical trial showed that nilotinib was well tolerated and
demonstrated in multiple clinical and preclinical suggested that it may be particularly useful in treating a
studies68,143,374-375,382-384 . On the basis of clinical and subset of GIST with KIT exon 17 mutations391.
preclinical data in KIT-mutated384-388 , KIT-amplified385, or

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PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 THERAPIES WITH CLINICAL BENEFIT IN OTHER TUMOR TYPE
SPECIMEN COLLECTION DATE 20 August 2026

Ponatinib AREAS OF THERAPEUTIC USE patients with GIST, KIT V654A emerged during treatment
Ponatinib is a multikinase inhibitor targeting BCR-ABL, in 8 patients394.
Assay findings association RET, KIT, FLT-3, PDGFRs, VEGFRs, FGFRs, and other
tyrosine kinases. It is FDA approved in combination with SUPPORTING DATA
KIT chemotherapy to threat Philadelphia chromosome-
exon 11 deletion (Q556_V559>H), Data from a Phase 2 trial in gastrointestinal stromal
exon 13 (V654A), exon 18 positive (Ph+) acute lymphoblastic leukemia (ALL) or as a tumors (GISTs) indicated that ponatinib induced a clinical
(A829P) monotherapy to treat advanced, T315I-mutated chronic benefit rate (CBR; patients exhibiting CR, PR, or SD for at
myeloid leukemia (CML) and Ph+ ALL, as well as for CML least 16 weeks) in 36% (10/28) of patients with KIT exon
and Ph+ ALL patients for whom no other TKI is indicated. 11 mutations compared with a CBR of 20% (3/15) for
Please see the drug label for full prescribing information. patients lacking mutations in exon 11394. Ponatinib has
also demonstrated robust preclinical activity in patient-
GENE ASSOCIATION derived GIST cell lines against multiple imatinib-resistant
KIT exon 9 and 11 activating mutations have KIT mutations, including the gatekeeper residue, T670I,
demonstrated sensitivity to ponatinib in several and secondary mutations within the activation loop,
preclinical cell models76,78-81,392 , with clinical efficacy including those at residues D816, D820, N822, and A82977.
demonstrated in patients with GIST exhibiting exon 11 Moreover, ponatinib displayed clinical activity in 2/3
mutations77,393 and imatinib resistance52. KIT V654A has patients with refractory GIST, all of whom had been
been shown to result in decreased sensitivity to ponatinib previously treated at a minimum with imatinib, sunitinib,
in a preclinical study76-77 . Additionally, in a study of and regorafenib77.

Sorafenib AREAS OF THERAPEUTIC USE SUPPORTING DATA
Sorafenib is a kinase inhibitor that targets the RAF Phase 2 studies of sorafenib in patients with
Assay findings association kinases, KIT, FLT3, RET, VEGFRs, and PDGFRs. It is FDA gastrointestinal stromal tumors (GIST) previously treated
approved to treat unresectable hepatocellular carcinoma, with imatinib and sunitinib have reported PRs in 10-13%
KIT advanced renal cell carcinoma (RCC), and recurrent or of patients and SDs in 52-57% of patients397,403 . A
exon 11 deletion (Q556_V559>H),
exon 13 (V654A), exon 18 metastatic differentiated thyroid carcinoma. Please see the retrospective analysis of sorafenib in 124 patients with
(A829P) drug label for full prescribing information. GIST previously treated with imatinib and sunitinib
reported that 57% (70/124) of patients achieved disease
GENE ASSOCIATION stabilization and 10% (12/124) achieved PR404. A real-
On the basis of clinical and preclinical data in KIT- world evidence study of patients with advanced GIST
mutated68,70-72,395-398 or KIT-expressing tumors399-402 , KIT treated with sorafenib reported median overall survival
activating alterations may predict sensitivity to sorafenib. (mOS) of 17.4 months405. One study of 60 patients who
On the basis of preclinical68-70 and limited clinical71-73 had progressed on imatinib or sunitinib reported 3 PRs to
data, mutations of residues within the KIT activation loop sorafenib treatment, and median PFS (mPFS) of 7.7
(A-loop) are predicted to be sensitive to sorafenib, months and mOS of 13.5 months406.
although preclinical evidence of potential resistance has
been reported specifically for the D816V mutation69,74-75 .

NOTE Genomic alterations detected may be associated with activity of certain US FDA or other specific country approved therapies; however, the therapies
listed in this report may have varied evidence in the patient’s tumor type. The listed therapies are not ranked in order of potential or predicted efficacy for this
patient or in order of level of evidence for this patient's tumor type. The therapies listed in this report may not be complete and/or exhaustive. Furthermore, the
listed therapies are limited to US FDA approved pharmaceutical drug products that are linked to a specific genomic alteration. There may also be US FDA
approved pharmaceutical drug products that are not linked to a genomic alteration. Further there may also exist pharmaceutical drug products that are not
approved by the US FDA or other national authorities. There may also be other treatment modalities available than pharmaceutical drug products.

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PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 CLINICAL TRIALS
SPECIMEN COLLECTION DATE 20 August 2026

IMPORTANT Clinical trials are ordered by gene and research staff. This is not a comprehensive list of all in order of level of evidence for this patient's tumor type.
prioritized by: age range inclusion criteria for pediatric available clinical trials. There may also be compassionate Clinical trials listed here may have additional enrollment
patients, proximity to ordering medical facility, later trial use or early access programs available, which are not listed criteria that may require medical screening to determine
phase, and verification of trial information within the last in this report. Foundation Medicine displays a subset of final eligibility. For additional information about listed
two months. While every effort is made to ensure the trial options and ranks them in this order of descending clinical trials or to conduct a search for additional trials,
accuracy of the information contained below, the priority: Qualification for pediatric trial → Geographical please see clinicaltrials.gov. However, clinicaltrials.gov does
information available in the public domain is continually proximity → Later trial phase. Clinical trials are not ranked not list all clinical trials that might be available.
updated and should be investigated by the physician or in order of potential or predicted efficacy for this patient or

GENE RATIONALE

BRCA2 BRCA2 loss or inactivating alterations may predict may serve as inclusion criteria for 1 or more
sensitivity to PARP inhibitors or to ATR clinical trials listed below.
ALTERATION
inhibitors. The genomic finding observed here

T3085fs*26

NCT05797168 PHASE 1/2

Phase I/IIa Study for AZD5335 as Monotherapy and in Combination With Anti-cancer Agents in TARGETS
Participants With Solid Tumors PARP1

LOCATIONS: Istanbul (Turkey (Türkiye)), Ankara (Turkey (Türkiye)), Berlin (Germany), Leipzig (Germany), Regensburg (Germany), Hanover (Germany),
Mannheim (Germany), Freiburg im Breisgau (Germany), Cambridge (United Kingdom), London (United Kingdom)

NCT04341181 PHASE 2

ProTarget - A Danish Nationwide Clinical Trial on Targeted Cancer Treatment Based on Genomic TARGETS
Profiling ALK, RET, PD-L1, VEGFRs, EGFR, PARP,
FGFR1, FGFR2, FGFR3, ERBB2, MEK,
BRAF, SMO

LOCATIONS: Copenhagen (Denmark)

NCT04817956 PHASE 2

Improving Public Cancer Care by Implementing Precision Medicine in Norway TARGETS
PD-L1, VEGFA, ERBB2, ALK, RET, PARP,
SMO, TRKB, TRKC, ROS1, TRKA, MEK,
BRAF, PI3K-alpha, FGFR1, FGFR2,
FGFR3, MET, KIT, ABL

LOCATIONS: Fredrikstad (Norway), Oslo (Norway), Skien (Norway), Drammen (Norway), Hamar (Norway), Kristiansand (Norway), Trondheim (Norway),
Stavanger (Norway), Bergen (Norway), Førde (Norway)

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REPORT DATE 30 Aug 2026 CLINICAL TRIALS
SPECIMEN COLLECTION DATE 20 August 2026

NCT02925234 PHASE 2

The Drug Rediscovery Protocol (DRUP Trial) TARGETS
EGFR, PARP, BRAF, ABL, KIT, MEK,
ERBB2, SMO, VEGFRs, RET, PD-1,
ERBB4, FGFR1, FGFR2, FGFR3, MET,
ROS1, PD-L1, VEGFA, TRKB, ALK, TRKC,
TRKA, FGFRs, PDGFRA, CDK4, CDK6,
AXL, FLT3, CSF1R, CTLA-4, PI3K-alpha

LOCATIONS: Almelo (Netherlands), Groningen (Netherlands), Hoogeveen (Netherlands), Deventer (Netherlands), Drachten (Netherlands), Zwolle
(Netherlands), Venlo (Netherlands), Apeldoorn (Netherlands), Arnhem (Netherlands), Leeuwarden (Netherlands)

NCT04657068 PHASE 1/2

A Study of ART0380 for the Treatment of Advanced or Metastatic Solid Tumors TARGETS
ATR

LOCATIONS: Paris (France), Villejuif (France), Marseille (France), London (United Kingdom), Manchester (United Kingdom), Girona (Spain), Glasgow
(United Kingdom), Badalona (Spain), Sabadell (Spain), Barcelona (Spain)

NCT05691491 PHASE 1/2

Testing the Combination of the Anti-Cancer Drugs Temozolomide and M1774 to Evaluate Their Safety TARGETS
and Effectiveness ATR

LOCATIONS: Connecticut, Maryland, Pennsylvania, Tennessee, Missouri, Kansas

NCT05327010 PHASE 2

Testing the Combination of the Anti-cancer Drugs ZEN003694 (ZEN-3694) and Talazoparib in Patients TARGETS
With Advanced Solid Tumors, The ComBET Trial BRD4, BRDT, BRD2, BRD3, PARP

LOCATIONS: Maryland, Pennsylvania, Virginia, Illinois, North Carolina, Kentucky, Georgia, Missouri

NCT02693535 PHASE 2

TAPUR: Testing the Use of Food and Drug Administration (FDA) Approved Drugs That Target a Specific TARGETS
Abnormality in a Tumor Gene in People With Advanced Stage Cancer CDK4, CDK6, FLT3, VEGFRs, CSF1R,
KIT, RET, mTOR, ERBB2, MEK, BRAF,
PARP, PD-1, CTLA-4, PD-L1, TRKB, ALK,
TRKC, ROS1, TRKA, FGFRs

LOCATIONS: Maine

NCT06074692 PHASE 2

PARP Inhibition, Stereotactic Body Radiotherapy and Immunotherapy for Metastatic or Advanced TARGETS
Sarcoma (PRIMA): a Prospective Phase 2 Trial PARP, PD-1

LOCATIONS: Shanghai (China)

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PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 CLINICAL TRIALS
SPECIMEN COLLECTION DATE 20 August 2026

NCT05035745 PHASE 1/2

Selinexor & Talazoparib in Advanced Refractory Solid Tumors; Advanced/Metastatic Triple Negative TARGETS
Breast Cancer (START) XPO1, PARP

LOCATIONS: Singapore (Singapore)

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PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 CLINICAL TRIALS
SPECIMEN COLLECTION DATE 20 August 2026

GENE RATIONALE

CDKN2A CDKN2A alterations may predict sensitivity to
CDK4/6 inhibitors such as palbociclib, ribociclib,
here may serve as inclusion criteria for 1 or more
clinical trials listed below.
ALTERATION
and abemaciclib. The genomic finding observed

rearrangement intron 2

NCT02925234 PHASE 2

NCT02693535 PHASE 2

LOCATIONS: Maine

NCT04282031 PHASE 1/2

A Study of BPI-1178 in Patients With Advanced Solid Tumor and HR+/HER2- Breast Cancer TARGETS
CDK6, CDK4, ER, Aromatase

LOCATIONS: Shanghai (China)

NCT05953350 PHASE 1/2

A Phase Ib/II Study Confirmed Inhibition of Autophagy Synergizes Anti-tumor Effect of High Dose TARGETS
CDK4/6i CDK4, CDK6

LOCATIONS: Guangzhou (China)

NCT03454035 PHASE 1

Ulixertinib/Palbociclib in Patients With Advanced Pancreatic and Other Solid Tumors TARGETS
CDK4, CDK6, ERK2, ERK1

LOCATIONS: North Carolina

PAGE 18 of 32

PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 CLINICAL TRIALS
SPECIMEN COLLECTION DATE 20 August 2026

NCT04693468 PHASE 1

Talazoparib and Palbociclib, Axitinib, or Crizotinib for the Treatment of Advanced or Metastatic Solid TARGETS
Tumors, TalaCom Trial PARP, CDK4, CDK6, VEGFRs, ALK,
ROS1, AXL, TRKA, MET, TRKC

LOCATIONS: Texas

PAGE 19 of 32

PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 CLINICAL TRIALS
SPECIMEN COLLECTION DATE 20 August 2026

GENE RATIONALE

KIT Activating mutations in KIT may confer
sensitivity to Type-1 inhibitors of KIT such as
genomic finding observed here may serve as
inclusion criteria for 1 or more clinical trials listed
ALTERATION
bezuclastinib, based on clinical and pre-clinical below. Mutation of residues within or adjacent to
evidence of benefit for patients with activating the KIT activation loop, as observed here, have
exon 11 deletion (Q556_V559>H), exon 13 mutations in KIT exon 11- and KIT exon demonstrated resistance to imatinib and sunitinib
(V654A), exon 18 (A829P) 17-mutated GIST. KIT amplification or activating in patients with GIST. Mutations in KIT exons 13
mutations may predict sensitivity to small- and 14 may be associated with reduced sensitivity
molecule TKIs. Also, because KIT activation leads to ripretinib. The KIT V654A mutation is
to activation of the PI3K-AKT-mTOR pathway, associated with resistance to imatinib and
PI3K and mTOR pathway inhibitors may be avapritinib and decreased sensitivity to
relevant in a tumor with KIT activation. The regorafenib, ponatinib, and ripretinib.

NCT05957367 PHASE 1/2

A Study of DCC-3116 in Combination With Anticancer Therapies in Participants With Advanced TARGETS
Malignancies KIT, PDGFRA, ULK1, ULK2, MEK, BRAF,
EGFR

LOCATIONS: Frankfurt (Germany), Hamburg (Germany), Aarhus (Denmark), Florence (Italy), Milan (Italy), Nijmegen (Netherlands), Bern (Switzerland),
Genova (Italy), Amsterdam (Netherlands), Paris (France)

NCT05159245 PHASE 2

The Finnish National Study to Facilitate Patient Access to Targeted Anti-cancer Drugs TARGETS
BRAF, VEGFRs, RET, KIT, ERBB2, TRKB,
ALK, TRKC, ROS1, TRKA, SMO, PD-L1,
MEK, CDK4, CDK6

LOCATIONS: Helsinki (Finland), Turku (Finland), Tampere (Finland), Kuopio (Finland), Oulu (Finland)

NCT05443087 PHASE NULL

TARGETed Therapy Drug MONITOring in DIGestive Oncology TARGETS
BRAF, VEGFRs, RET, KIT, mTOR, FLT3,
CSF1R, MET, ROS1, MEK, EGFR

LOCATIONS: Strasbourg (France), Nancy (France), Dijon (France), Reims (France), Lille (France), Auxerre (France), Amiens (France), Paris (France), Villejuif
(France), Clichy (France)

NCT04116541 PHASE 2

A Study Evaluating the Activity of Anti-cancer Treatments Targeting Tumor Molecular Alterations/ TARGETS
Characteristics in Advanced / Metastatic Tumors. CDK6, CDK4, MDM2, MET, ROS1, RET,
VEGFRs, ALK, BRAF, KIT, MEK,
PDGFRA

LOCATIONS: Strasbourg (France), Lyon (France), Marseille (France), Nice (France), Villejuif (France), Caen (France), Toulouse (France), Bordeaux (France)

PAGE 20 of 32

PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 CLINICAL TRIALS
SPECIMEN COLLECTION DATE 20 August 2026

NCT02925234 PHASE 2

NCT05024214 PHASE 1/2

Phase Ib/II Trial of Envafolimab Plus Lenvatinib for Subjects With Solid Tumors TARGETS
PD-L1, FGFRs, RET, PDGFRA, VEGFRs,
KIT, FLT3, CSF1R

LOCATIONS: Ürümqi (China), Taiyuan (China), Beijing (China), Tianjin (China), Kunming (China), Zhengzhou (China), Jinan (China), Shenyang (China),
Dalian (China), Bengbu (China)

NCT04199026 PHASE NULL

Implantable Microdevice for the Delivery of Drugs and Their Effect on Tumors in Patients With TARGETS
Metastatic or Recurrent Sarcoma TOP1, mTOR, IGF1R, FGFR3, KIT, FGFR1,
VEGFRs, FGFR2

LOCATIONS: Texas

NCT07379047 PHASE 2/3

Efficacy and Safety of NB003 in Patients With Advanced Gastrointestinal Stromal Tumors (GIST) TARGETS
KIT, PDGFRA, BRAF, VEGFRs, RET

LOCATIONS: Beijing (China), Qingdao (China), Wuhan (China), Hefei (China)

NCT02693535 PHASE 2

LOCATIONS: Maine

PAGE 21 of 32

PATIENT TUMOR TYPE ORDERED TEST #
03-2026-00152703, UA Stomach GIST ORD-2419716-01

REPORT DATE 30 Aug 2026 CLINICAL TRIALS
SPECIMEN COLLECTION DATE 20 August 2026

NCT06081907 PHASE 1/2

The Efficacy and Safety of IBI363 in Solid Tumors. TARGETS
IL-2R, PD-1, CD73, FGFRs, RET,
PDGFRA, VEGFRs, KIT

LOCATIONS: Changsha (China)

PAGE 22 of 32

PATIENT TUMOR TYPE ORDERED TEST #
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REPORT DATE 30 Aug 2026 CLINICAL TRIALS
SPECIMEN COLLECTION DATE 20 August 2026

GENE RATIONALE

MTOR MTOR mutation may lead to activation of the
mTOR pathway, and may therefore indicate
finding observed here may serve as inclusion
criteria for 1 or more clinical trials listed below.
ALTERATION
sensitivity to mTOR inhibitors. The genomic

A1459D

NCT04199026 PHASE NULL

Implantable Microdevice for the Delivery of Drugs and Their Effect on Tumors in Patients With TARGETS
Metastatic or Recurrent Sarcoma TOP1, mTOR, IGF1R, FGFR3, KIT, FGFR1,
VEGFRs, FGFR2

LOCATIONS: Texas

NCT07109726 PHASE 1/2

A Phase 1/2 Trial of TER-2013 in Patients With Solid Tumors Harboring AKT/PI3K/PTEN Pathway TARGETS
Alterations AKT1, ER

LOCATIONS: Massachusetts, Virginia, Ohio, Wisconsin, Illinois, Minnesota, North Carolina, Missouri, Nebraska, Tennessee

NCT02693535 PHASE 2

LOCATIONS: Maine

NCT05036226 PHASE 1/2

COAST Therapy in Advanced Solid Tumors and Prostate Cancer TARGETS
DDR2, ABL, SRC, KIT, mTOR

LOCATIONS: South Carolina

PAGE 23 of 32

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REPORT DATE 30 Aug 2026 APPENDIX Variants of Unknown Significance
SPECIMEN COLLECTION DATE 20 August 2026

NOTE One or more variants of unknown significance (VUS) were detected in this patient's tumor. These variants may not have been adequately characterized in
the scientific literature at the time this report was issued, and/or the genomic context of these alterations makes their significance unclear. We choose to
include them here in the event that they become clinically meaningful in the future.

AR CDKN2C ERBB4 IGF1R
NM_000044.2: c.2668G>C NM_001262.2: NM_005235.2: c.284G>A NM_000875.3: c.4082T>G
(p.V890L) c.204_211delinsCA (p.R95H) (p.L1361R)
chrX:66943588 (p.T69_F71delinsI) chr2:212812292 chr15:99500649
0.21% VAF chr1:51439639-51439646 48.4% VAF 51.1% VAF
5.8% VAF

MLH1 ZNF703
NM_000249.3: c.25C>T NM_025069.1:
(p.R9W) c.1204_1205insN[42]
chr3:37035063 (p.A401_H402insX[14])
0.35% VAF chr8:37555584
42.6% VAF

APPENDIX - PAGE 24 of 32

PATIENT TUMOR TYPE ORDERED TEST #
03-2026-00152703, UA Stomach GIST ORD-2419716-01

REPORT DATE 30 Aug 2026 APPENDIX Genes assayed in FoundationOne®Liquid CDx
SPECIMEN COLLECTION DATE 20 August 2026

FoundationOne Liquid CDx interrogates 324 genes, including 309 genes with complete exonic (coding) coverage and 15 genes with only select non-coding
coverage (indicated with an *) ; 75 genes (indicated in bold) are captured with increased sensitivity and have complete exonic (coding) coverage unless otherwise
noted.

ABL1 ACVR1B AKT1 AKT2 AKT3 ALK ALOX12B AMER1 APC
Exons 4-9 Exon 3 Exons 20-29, Introns (FAM123B or WTX)
18, 19

AR ARAF ARFRP1 ARID1A ASXL1 ATM ATR ATRX AURKA
Exons 4, 5, 7, 11, 13, 15,
16

AURKB AXIN1 AXL BAP1 BARD1 BCL2 BCL2L1 BCL2L2 BCL6

BCOR BCORL1 BCR* BRAF BRCA1 BRCA2 BRD4 BRIP1 BTG1
Introns 8, 13, 14 Exons 11-18, Introns 7-10 Introns 2, 7, 8, 12, 16, 19, 20 Intron 2

BTG2 BTK CALR CARD11 CASP8 CBFB CBL CCND1 CCND2
Exons 2, 15

CCND3 CCNE1 CD22 CD70 CD74* CD79A CD79B CD274 CDC73
Introns 6-8 (PD-L1)

CDH1 CDK12 CDK4 CDK6 CDK8 CDKN1A CDKN1B CDKN2A CDKN2B

CDKN2C CEBPA CHEK1 CHEK2 CIC CREBBP CRKL CSF1R CSF3R

CTCF CTNNA1 CTNNB1 CUL3 CUL4A CXCR4 CYP17A1 DAXX DDR1
Exon 3

DDR2 DIS3 DNMT3A DOT1L EED EGFR EMSY EP300 EPHA3
Exons 5, 17, 18 Introns 7, (C11orf30)
15, 24-27

EPHB1 EPHB4 ERBB2 ERBB3 ERBB4 ERCC4 ERG ERRFI1 ESR1
Exons 3, 6, 7, 8, 10, 12, Exons 4-8
20, 21, 23, 24, 25

ETV4* ETV5* ETV6* EWSR1* EZH2 EZR* FANCA FANCC FANCG
Intron 8 Introns 6, 7 Introns 5, 6 Introns 7-13 Exons 4, 16, 17, 18 Introns 9-11

FANCL FAS FBXW7 FGF10 FGF12 FGF14 FGF19 FGF23 FGF3

FGF4 FGF6 FGFR1 FGFR2 FGFR3 FGFR4 FH FLCN FLT1
Introns 1, 5, Intron 17 Intron 1, Intron 17 Exons 7, 9 (alternative
designation exon 10),
14, 18, Intron 17
FLT3 FOXL2 FUBP1 GABRA6 GATA3 GATA4 GATA6 GID4 GNA11
Exons 14, 15, 20 (C17orf39) Exons 4, 5

GNA13 GNAQ GNAS GRM3 GSK3B H3-3A HDAC1 HGF HNF1A
Exons 4, 5 Exons 1, 8 (H3F3A)

HRAS HSD3B1 ID3 IDH1 IDH2 IGF1R IKBKE IKZF1 INPP4B
Exons 2, 3 Exon 4 Exon 4

IRF2 IRF4 IRS2 JAK1 JAK2 JAK3 JUN KDM5A KDM5C
Exon 14 Exons 5, 11, 12, 13, 15,
16

KDM6A KDR KEAP1 KEL KIT KLHL6 KMT2A KMT2D KRAS
Exons 8, 9, 11, 12, 13, 17, (MLL) Introns 6, 8-11, (MLL2)
Intron 16 Intron 7

APPENDIX - PAGE 25 of 32

PATIENT TUMOR TYPE ORDERED TEST #
03-2026-00152703, UA Stomach GIST ORD-2419716-01

REPORT DATE 30 Aug 2026 APPENDIX Genes assayed in FoundationOne®Liquid CDx
SPECIMEN COLLECTION DATE 20 August 2026

LTK LYN MAF MAP2K1 MAP2K2 MAP2K4 MAP3K1 MAP3K13 MAPK1
(MEK1) Exons 2, 3 (MEK2) Exons 2-4, 6, 7

MCL1 MDM2 MDM4 MED12 MEF2B MEN1 MERTK MET MITF

MKNK1 MLH1 MPL MRE11 MSH2 MSH3 MSH6 MST1R MTAP
Exon 10 (MRE11A) Intron 5

MTOR MUTYH MYB* MYC MYCL MYCN MYD88 NBN NF1
Exons 19, 30, 39, 40, Intron 14 Intron 1 (MYCL1) Exon 4
43-45, 47, 48, 53, 56

NF2 NFE2L2 NFKBIA NKX2-1 NOTCH1 NOTCH2 NOTCH3 NPM1 NRAS
Intron 26 Exons 4-6, 8, 10 Exons 2, 3

NSD2 NSD3 NT5C2 NTRK1 NTRK2 NTRK3 NUTM1* P2RY8 PALB2
(WHSC1 or MMSET) (WHSC1L1) Exons 14, 15, Introns Intron 12 Exons 16, 17 Intron 1
8-11

PARP1 PARP2 PARP3 PAX5 PBRM1 PDCD1 PDCD1LG2 PDGFRA PDGFRB
(PD-1) (PD-L2) Exons 12, 18, Introns 7, Exons 12-21, 23
9, 11

PDK1 PIK3C2B PIK3C2G PIK3CA PIK3CB PIK3R1 PIM1 PMS2 POLD1
Exons 2, 3, 5-8, 10, 14,
19, 21 (Coding Exons 1,
2, 4-7, 9, 13, 18, 20)
POLE PPARG PPP2R1A PPP2R2A PRDM1 PRKAR1A PRKCI PRKN PTCH1
(PARK2)

PTEN PTPN11 PTPRO QKI RAC1 RAD21 RAD51 RAD51B RAD51C

RAD51D RAD52 RAD54L RAF1 RARA RB1 RBM10 REL RET
Exons 3, 4, 6, 7, 10, 14, Intron 2 Introns 7, 8, Exons 11,
15, 17, Introns 4-8 13-16, Introns 9-11

RICTOR RNF43 ROS1 RPTOR RSPO2* SDC4* SDHA SDHB SDHC
Exons 31, 36-38, 40, Intron 1 Intron 2
Introns 31-35

SDHD SETD2 SF3B1 SGK1 SLC34A2* SMAD2 SMAD4 SMARCA4 SMARCB1
Intron 4

SMO SNCAIP SOCS1 SOX2 SOX9 SPEN SPOP SRC STAG2

STAT3 STK11 SUFU SYK TBX3 TEK TENT5C TERC* TERT*
(FAM46C) ncRNA Promoter

TET2 TGFBR2 TIPARP TMPRSS2* TNFAIP3 TNFRSF14 TP53 TSC1 TSC2
Introns 1-3

TYRO3 U2AF1 VEGFA VHL WT1 XPO1 XRCC2 ZNF217 ZNF703

ADDITIONAL ASSAYS: FOR THE DETECTION OF SELECT CANCER BIOMARKERS
Microsatellite (MS) status
Blood Tumor Mutational Burden (bTMB)
ctDNA Tumor Fraction

APPENDIX - PAGE 26 of 32

PATIENT TUMOR TYPE ORDERED TEST #
03-2026-00152703, UA Stomach GIST ORD-2419716-01

REPORT DATE 30 Aug 2026 APPENDIX About FoundationOne®Liquid CDx
SPECIMEN COLLECTION DATE 20 August 2026

FoundationOne Liquid CDx fulfills the exclusively as a laboratory service using circulating repeatability of equivocal calls may be lower than
requirements of the European Directive 98/79 EC cell-free DNA (cfDNA) isolated from plasma derived non-equivocal calls.
for in vitro diagnostic medical devices and is from anti-coagulated peripheral whole blood from
registered as a CE-IVD product by Foundation patients with solid malignant neoplasms. The assay COPY NUMBER LOSS CALLS
Medicine's EU Authorized Representative, Qarad employs a single DNA extraction method to obtain The FoundationOne Liquid CDx assay detects copy
b.v.b.a, Cipalstraat 3, 2440 Geel, Belgium. The CE- cfDNA from plasma from whole blood. Extracted number loss in the following genes: BRCA1, BRCA2,
IVD regulatory status of FoundationOne Liquid cfDNA undergoes whole-genome shotgun library and PTEN.
CDx is applicable in countries that accept and/or construction and hybridization-based capture of
recognize the CE mark. 324 cancer-related genes including coding exons RANKING OF THERAPIES AND CLINICAL
Foundation Medicine GmbH is accredited by and select introns of 309 genes, as well as only TRIALS
DAkkS according to DIN EN ISO 15189:2024. The select intronic regions or non-coding regions of 15 Ranking of Therapies in Summary Table
accreditation only applies to the scope of genes. Hybrid-capture selected libraries are Therapies are ranked based on the following
accreditation listed in certificate D- sequenced with deep coverage using the NovaSeq® criteria: Therapies with clinical benefit (ranked
ML-21105-01-00. 6000 platform. Sequence data are processed using a alphabetically within each evidence category),
customized analysis pipeline designed to accurately followed by therapies associated with resistance
detect genomic alterations, including base (when applicable).
substitutions, indels, select copy number variants,
Ranking of Clinical Trials
and select genomic rearrangements. Substitutions
ABOUT FOUNDATIONONE LIQUID CDx Pediatric trial qualification → Geographical
and insertion and deletion alterations (indels) are
FoundationOne Liquid CDx was developed and its proximity → Later trial phase.
reported in 311 genes, copy number alterations
performance characteristics determined by (CNAs) are reported in 310 genes, and gene
LIMITATIONS
Foundation Medicine, Inc. (Foundation Medicine). rearrangements are reported in 324 genes. The assay
FoundationOne Liquid CDx may be used for 1. For in vitro diagnostic use.
also reports ctDNA tumor fraction, and genomic
clinical purposes and should not be regarded as 2. For prescription use only. This test must be
signatures including MSI and bTMB. A subset of
purely investigational or for research only. ordered by a qualified medical professional in
targeted regions in 75 genes is baited for increased
Foundation Medicine's clinical reference accordance with clinical laboratory regulations.
sensitivity.
laboratories are qualified to perform high- 3. A negative result does not rule out the presence
complexity clinical testing. THE REPORT of a mutation below the limits of detection of
the assay. Patients for whom no companion
Incorporates analyses of peer-reviewed studies and
Please refer to technical information for diagnostic alterations are detected should be
other publicly available information identified by
performance specification details. considered for confirmation with an
Foundation Medicine; these analyses and
appropriately validated tumor tissue test, if
information may include associations between a
INTENDED USE available.
molecular alteration (or lack of alteration) and one
FoundationOne Liquid CDx is a next generation 4. The FoundationOne Liquid CDx assay does not
or more drugs with potential clinical benefit (or
sequencing based in vitro diagnostic device that detect heterozygous deletions.
potential lack of clinical benefit), including drug
analyzes 324 genes. Substitutions and insertion and 5. The test is not intended to provide information
candidates that are being studied in clinical
deletion alterations (indels) are reported in 311 on cancer predisposition.
research. Note: A finding of biomarker alteration
genes, copy number alterations (CNAs) are reported 6. Performance has not been validated for cfDNA
does not necessarily indicate pharmacologic
in 310 genes, and gene rearrangements are reported input below the specified minimum input.
effectiveness (or lack thereof) of any drug or
in 324 genes. The test also detects the genomic 7. Tissue TMB and blood TMB (bTMB) are
treatment regimen; a finding of no biomarker
signatures blood tumor mutational burden (bTMB), estimated from the number of synonymous and
alteration does not necessarily indicate lack of
microsatellite instability (MSI), and ctDNA tumor nonsynonymous single-nucleotide variants
pharmacologic effectiveness (or effectiveness) of any
fraction. FoundationOne Liquid CDx utilizes (SNVs) and insertions and deletions (indels) per
drug or treatment regimen.
circulating cell-free DNA (cfDNA) isolated from area of coding genome sampled, after the
plasma derived from the anti-coagulated peripheral DISEASE AND TUMOR TYPE removal of known and likely oncogenic driver
whole blood of cancer patients. The test is intended The ‘DISEASE’ and ‘TUMOR TYPE’ fields in this events and germline SNPs. Tissue TMB is
to be used as a companion diagnostic to identify report represent a standardized term mapped from calculated based on variants with an allele
patients who may benefit from treatment with the diagnosis submitted by the ordering physician frequency of ≥5%, and bTMB is calculated based
targeted therapies in accordance with the approved and may be adjusted at the discretion of a on variants with an allele frequency of ≥0.5%.
therapeutic product labeling. Additionally, Foundation Medicine pathologist. This service is 8. ctDNA tumor fraction is the percentage of
FoundationOne Liquid CDx is intended to provide not accredited under ISO15189. circulating tumor DNA (ctDNA) present in a
tumor mutation profiling to be used by qualified cell-free DNA (cfDNA) sample. The ctDNA
health care professionals in accordance with QUALIFIED ALTERATION CALLS tumor fraction estimate integrates multiple
professional guidelines in oncology for patients (EQUIVOCAL) distinct genomic features, including modeled
with malignant neoplasms. All equivocal calls, regardless of alteration type, aneuploidy and the observed allele frequencies
imply that there is adequate evidence to call the of somatic short variants and rearrangements.
TEST PRINCIPLES
alteration with confidence. However, the
The FoundationOne Liquid CDx assay is performed

APPENDIX - PAGE 27 of 32

PATIENT TUMOR TYPE ORDERED TEST #
03-2026-00152703, UA Stomach GIST ORD-2419716-01

REPORT DATE 30 Aug 2026 APPENDIX About FoundationOne®Liquid CDx
SPECIMEN COLLECTION DATE 20 August 2026

9. Microsatellite instability (MSI) is a condition of ClinVar genomic database (Landrum et al., 2018; the NCCN Compendium®. Referenced with
genetic hypermutability that generates excessive 29165669) as Pathogenic, Pathogenic/Likely permission from the NCCN Clinical Practice
amounts of short insertion/deletion mutations Pathogenic, or Likely Pathogenic (by an expert Guidelines in Oncology (NCCN Guidelines®). ©
in the tumor genome; it generally occurs at panel or multiple submitters), 2) associated with National Comprehensive Cancer Network, Inc.
microsatellite DNA sequences and is caused by a hereditary cancer-predisposing disorder(s), 3) 2023. All rights reserved. To view the most recent
deficiency in DNA mismatch repair (MMR) in detected at an allele frequency of >30%, and 4) in and complete version of the guidelines, go online to
the tumor. The MSI algorithm is based on select genes informed by the ESMO Precision NCCN.org. NCCN makes no warranties of any kind
genome wide analysis of 1765 microsatellite loci Medicine Working Group (Kuzbari et al., 2023; whatsoever regarding their content, use or
and not based on the 5 or 7 MSI loci described 36529447) and ASCO Guidelines (Tung et al., 2024; application and disclaims any responsibility for
in current clinical practice guidelines for solid 38759122). The selected genes are ATM, BAP1, their application or use in any way.
tissue testing. BARD1, BRCA1, BRCA2, BRIP1, CHEK2, FH, FLCN,
10. Genomic findings from circulating cell-free MLH1, MSH2, MSH6, MUTYH, PALB2, PMS2, POLD1, LEVEL OF EVIDENCE NOT PROVIDED
DNA (cfDNA) may originate from circulating POLE, PTCH1, RAD51C, RAD51D, RET, SDHA, SDHB, Drugs with potential clinical benefit (or potential
tumor DNA fragments, germline alterations, or SDHC, SDHD, SMARCB1, SUFU, TSC2, and VHL, and lack of clinical benefit) are not evaluated for source
non-tumor somatic alterations, such as clonal are not inclusive of all cancer susceptibility genes. or level of published evidence.
hematopoiesis of indeterminate potential The content in this report should not substitute for
(CHIP). Genes with alterations that may be genetic counseling or follow-up germline testing, NO GUARANTEE OF CLINICAL BENEFIT
derived from CHIP include, but are not limited which is needed to distinguish whether a finding in This report makes no promises or guarantees that a
to: ASXL1, ATM, CBL, CHEK2, DNMT3A, JAK2, this patient’s tumor sequencing is germline or particular drug will be effective in the treatment of
KMT2D (MLL2), MPL, MYD88, SF3B1, TET2, somatic. Interpretation should be based on clinical disease in any patient. This report also makes no
TP53, and U2AF1. context. promises or guarantees that a drug with potential
11. Alterations reported may include somatic (not lack of clinical benefit will in fact provide no
inherited) or germline (inherited) alterations; VARIANTS THAT MAY REPRESENT clinical benefit.
however, the test does not distinguish between CLONAL HEMATOPOIESIS
germline and somatic alterations. If a reported Variants that may represent clonal hematopoiesis NO GUARANTEE OF REIMBURSEMENT
alteration is suspected to be germline, (CH) are limited to select reportable short variants Foundation Medicine makes no promises or
confirmatory testing should be considered in in defined genes identified in solid tumors only. guarantees that a healthcare provider, insurer or
the appropriate clinical context. Variant selection was determined based on gene other third party payor, whether private or
12. The test is not intended to replace germline tumor-suppressor or oncogene status, known role governmental, will reimburse a patient for the cost
testing or to provide information about cancer in solid tumors versus hematological malignancies, of FoundationOne Liquid CDx.
predisposition. and literature prevalence. The defined genes are
ASXL1, ATM, CBL, CHEK2, DNMT3A, IDH2, JAK2, TREATMENT DECISIONS ARE THE
KMT2D (MLL2), MPL, MYD88, SF3B1, TET2, and RESPONSIBILITY OF PHYSICIAN
REPORT HIGHLIGHTS Drugs referenced in this Report may not be suitable
U2AF1 and are not inclusive of all CH genes. The
The Report Highlights includes select genomic and for a particular patient. The selection of any, all or
content in this report should not substitute for
therapeutic information with potential impact on none of the drugs associated with potential clinical
dedicated hematological workup. Comprehensive
patient care and treatment that is specific to the benefit (or potential lack of clinical benefit) resides
genomic profiling of solid tumors detects nontumor
genomics and tumor type of the sample analyzed. entirely within the discretion of the treating
alterations that are due to CH. Patient-matched
This section may highlight information including physician. Indeed, the information in this Report
peripheral blood mononuclear cell sequencing is
targeted therapies with potential sensitivity or must be considered in conjunction with all other
required to conclusively determine if this alteration
resistance; evidence-matched clinical trials; and relevant information regarding a particular patient,
is present in tumor or is secondary to CH.
variants with potential diagnostic, prognostic, before the patient's treating physician recommends
Interpretation should be based on clinical context.
nontargeted treatment, germline, or clonal a course of treatment. Decisions on patient care and
hematopoiesis implications. Information included NATIONAL COMPREHENSIVE CANCER treatment must be based on the independent
in the Report Highlights is expected to evolve with NETWORK® (NCCN®) CATEGORIZATION medical judgment of the treating physician, taking
advances in scientific and clinical research. Biomarker and genomic findings detected may be into consideration all applicable information
Findings included in the Report Highlights should associated with certain entries within the NCCN concerning the patient's condition, such as patient
be considered in the context of all other Drugs & Biologics Compendium® (NCCN and family history, physical examinations,
information in this report and other relevant Compendium®) (www.nccn.org). The NCCN information from other diagnostic tests, and patient
patient information. Decisions on patient care and Categories of Evidence and Consensus indicated preferences, in accordance with the standard of care
treatment are the responsibility of the treating reflect the highest possible category for a given in a given community. A treating physician's
physician. therapy in association with each biomarker or decisions should not be based on a single test, such
genomic finding. Please note, however, that the as this test or the information contained in this
VARIANTS TO CONSIDER FOR FOLLOW-
accuracy and applicability of these NCCN categories report.
UP GERMLINE TESTING
within a report may be impacted by the patient’s
The variants indicated for consideration of follow- Certain sample of variant characteristics may result
clinical history, additional biomarker information,
up germline testing are 1) limited to reportable in reduced sensitivity. These include: low sample
age, and/or co-occurring alterations. For additional
short variants with a protein effect listed in the quality, deletions and insertions >40bp, or
information on the NCCN categories, please refer to

APPENDIX - PAGE 28 of 32

PATIENT TUMOR TYPE ORDERED TEST #
03-2026-00152703, UA Stomach GIST ORD-2419716-01

REPORT DATE 30 Aug 2026 APPENDIX About FoundationOne®Liquid CDx
SPECIMEN COLLECTION DATE 20 August 2026

repetitive/high homology sequences.
FoundationOne Liquid CDx is performed using
cell-free DNA, and as such germline events may not
be reported.

SELECT ABBREVIATIONS
ABBREVIATION DEFINITION
CR Complete response
ctDNA Circulating tumor DNA
DCR Disease control rate
DFS Disease-free survival
DOR Duration of response
EFS Event-free survival
ER Estrogen receptor
HR +/- Hormone-receptor positive/negative
ITD Internal tandem duplication
MR Molecular response
MMR Mismatch repair
Muts/Mb Mutations per megabase
NOS Not otherwise specified
ORR Objective response rate
OS Overall survival
mOS Median overall survival
PD Progressive disease
PFS Progression-free survival
mPFS Median progression-free survival
PR Partial response
PSA Prostate-specific antigen
R/R Relapsed or refractory
SD Stable disease
TKI Tyrosine kinase inhibitor
CRC Colorectal cancer
HCC Hepatocellular carcinoma
HNSCC Head and neck squamous cell carcinoma
NSCLC Non-small cell lung cancer
RCC Renal cell carcinoma
SCC Squamous cell carcinoma

REFERENCE SEQUENCE INFORMATION
Sequence data is mapped to the human genome,
Genome Reference Consortium Human Build 37
(GRCh37), also known as hg19.

SOFTWARE VERSION INFORMATION
MR Suite Version (RG) 10.0.1
MR Reporting Config Version 91
Analysis Pipeline Version v3.47.0
Computational Biology Suite Version 7.5.1

APPENDIX - PAGE 29 of 32

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REPORT DATE 30 Aug 2026 APPENDIX References
SPECIMEN COLLECTION DATE 20 August 2026

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REPORT DATE 30 Aug 2026 APPENDIX References
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SPECIMEN COLLECTION DATE 20 August 2026

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