oncopro tmb & msi profile - lal pathlabs

Name : DUMMY N210 Collected : 29/07/2020 Lab No. : 153672450 Age: 35 years Gender: Male Received : 29/07/2020 Status : F Ref By : UNKNOWN Reported : 01/08/2020

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CLINICAL INDICATION Breast Cancer

GENOMIC HIGHLIGHTS

Pathways driving cancer

Cell cycle control pathway

Beta catenin/ Wnt signaling pathway

DNA damage/ repair pathway

DNA mismatch repair pathway

Receptor tyrosine kinase pathway

Driver mutations BRCA2, TP53, APC, POLE, PMS2, BAP1, NTRK1,

STK11 and NF1 genes

Gene variants with therapy BRCA2 (A2513E) and TP53 (C238F)

Tumor Mutation Burden (TMB) Low TMB score, which is associated with better response

rate with immune-checkpoint inhibitor.

Microsatellite Instability (MSI)

MSI STABLE, which represents phenotypic evidence that DNA

mismatch repair (MMR) is functioning normally.

Clinically actionable mutation We found FDA-approved therapies with the drugs, Olaparib and

Bevacizumab, as maintenance treatment for Ovarian cancer.

Clinical trial

We found a clinical trial investigating the action of high- dose

alkylating chemotherapy in patients with oligo- metastatic breast

cancer harboring homologous recombination deficiency.

ONCOPRO TMB & MSI PROFILE

No clinically actionable mutations or driver mutations identified


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IMPLICATION TO IMMUNOTHERAPY

VARIANTS WITH CLINICALLY RELEVANT THERAPIES

Summary of Relevant Therapies in same cancer type

Gene Therapy Evidence Reference

BRCA2(A2513E) Carboplatin, Thiotepa, and Cyclophosphamide Late trials NCT01646034

Summary of Relevant Therapies in other cancer types

Gene Therapy Cancer type Evidence Reference

BRCA2

(A2513E)

Olaparib Ovarian cancer FDA FDA guidelines

Olaparib; Bevacizumab Ovarian cancer FDA FDA guidelines

TP53

(C238F)

Olaparib; Adavosertib Ovarian cancer Early trials NCT02576444

Cetuximab Colorectal Carcinoma Late trials NCT02942706

Pembrolizumab Gastro-esophageal Junction

Adenocarcinoma

Early trials NCT02589496

Adavosertib; Paclitaxel Early trials NCT02448329

Tumor mutational burden Tumor mutational burden (TMB) is a measure of the mutation load in a tumor sample. TMB for this tumor sample is determined to fall in the Low TMB category. High TMB is associated with production of more neo-antigens which may be recognized by the immune system and inciting an anti-tumor response. High TMB is associated with better response rate with immune-checkpoint inhibitor

Microsatellite Instability

Microsatellite Instability (MSI) refers to a type of genomic instability in tumor tissue caused by the failure of the DNA mismatch repair system to repair errors during DNA replication. This process results in accumulation of various mutations including alterations in the length of small repetitive microsatellite sequences. MSI for this tumor sample is found to fall in the MSI-Stable category.


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CLINICAL TRIAL We found a clinical trial investigating the effect of high-dose alkylating chemotherapy compared with

standard chemotherapy as part of a multimodality treatment approach in patients with oligo-metastatic breast cancer harboring homologous recombination deficiency.

These high- alkylating chemotherapy regimens contain potent inducers of DNA double-strand breaks (DSB), which are highly effective in tumors with an inadequate DNA repair system. The tumor suppressor genes BRCA1 and BRCA2 are involved in the repair of DNA DSB via homologous recombination. When this mechanism is inactivated, tumor cells rely on less adequate repair mechanisms. This is called homologous recombination deficiency (HRD) and causes genome instability and consequently apoptosis of tumor cells. Hence, targeting BRCA2 mutation with an altered chemotherapy regime is recommended to treat breast cancer.


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CLINICAL TRIAL

Study Title

High-dose Alkylating Chemotherapy in Oligo-metastatic Breast Cancer Harboring Homologous

Recombination Deficiency

Brief Summary

This study investigates the effect of high-dose alkylating chemotherapy compared with standard

chemotherapy as part of a multimodality treatment approach in patients with oligo-metastatic breast

cancer harboring homologous recombination deficiency.

Study phase Phase 3

Condition

Breast cancer

NCT Number NCT01646034

Intervention

Experimental: intensified alkylating chemotherapy

a course chemotherapy with high dose cyclophosphamide, G-CSF and peripheral blood progenitor cell (PBPC) harvest followed by tandem intermediate-dose alkylating therapy (miniCTC, carboplatin 800 mg/m2, thiotepa 240 mg/m2, and cyclophosphamide 3000 mg/m2) with PBPC-reinfusion.

Intervention: Drug: carboplatin, thiotepa, and cyclophosphamide

Active Comparator: three cycles of chemotherapy

three cycles of chemotherapy depending on previously received agents

chemotherapy naïve;three cycles of docetaxel, doxorubicin, and cyclophosphamide previously received anthracyclines without taxanes;three cycles of carboplatin and paclitaxel previously received anthracyclines and taxanes;three cycles of carboplatin and gemcitabine

Intervention: Drug: chemotherapy (docetaxel, doxorubicin, cyclofosfamide, carboplatin, paclitaxel, gemcitabine)

Last updated July 2, 2018


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RELEVANT THERAPIES IN SAME CANCER TYPE

BRCA2 – Breast cancer 2

Variant details

Drug details –

Carboplatin, Thiotepa, and Cyclophosphamide

This study investigates the effect of high-dose alkylating chemotherapy compared with standard chemotherapy as part of a multimodality treatment approach in patients with oligo-metastatic breast cancer harboring homologous recombination deficiency.

Studies have shown that patients with high-risk breast cancer and a BRCA1- or BRCA2-like profile derive important benefit from high-dose, alkylating chemotherapy in comparison to conventional chemotherapy (hazard ratio (HR) for overall survival: 0.19, 95% confidence interval (CI): 0.08 to 0.48). It is suggested that selecting oligo-metastatic patients based on HRD for high-dose chemotherapy can improve outcome for more patients.


Variant details Gene Genomic alteration Impact Mutation ID Clinical significance

BRCA2 chr13:g.32930667C>A,p.A2513E Missense rs1060502401 Likely pathogenic

Drug Details –

Olaparib

Olaparib is a small molecule inhibitor of the nuclear enzyme poly (ADP-ribose) polymerase (PARP) with potential

chemosensitizing, radiosensitizing, and antineoplastic activities. It selectively binds to and inhibits PARP, inhibiting

PARP-mediated repair of single strand DNA breaks; PARP inhibition may enhance the cytotoxicity of DNA-

damaging agents and may reverse tumor cell chemoresistance and radioresistance. PARP catalyzes post-

translational ADP-ribosylation of nuclear proteins and can be activated by single-stranded DNA breaks.

Gene Genomic alteration Impact Mutation ID Clinical significance

BRCA2 chr13:g.32930667C>A,p.A2513E Missense rs1060502401 Likely pathogenic


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On December 19, 2018, the Food and Drug Administration approved olaparib (LYNPARZA®, AstraZeneca

Pharmaceuticals LP) for the maintenance treatment of adult patients with deleterious or suspected deleterious

germline or somatic BRCA-mutated (gBRCAm or sBRCAm) advanced epithelial ovarian, fallopian tube or primary

peritoneal cancer who are in complete or partial response to first-line platinum-based chemotherapy.

https://www.fda.gov/drugs/fda-approved-olaparib-lynparza-astrazeneca-pharmaceuticals-lp- maintenance-

treatment-adult-patients

Olaparib; Bevacizumab

Olaparib is a small molecule inhibitor of the nuclear enzyme poly (ADP-ribose) polymerase (PARP) with potential

chemosensitizing, radiosensitizing, and antineoplastic activities.

On May 8, 2020, the Food and Drug Administration expanded the indication of olaparib (LYNPARZA, AstraZeneca

Pharmaceuticals, LP) to include its combination with bevacizumab for first-line maintenance treatment of adult

patients with advanced epithelial ovarian, fallopian tube, or primary peritoneal cancer who are in complete or

partial response to first-line platinum-based chemotherapy and whose cancer is associated with homologous

recombination deficiency positive status defined by either a deleterious or suspected deleterious BRCA mutation,

and/or genomic instability.

https://www.fda.gov/drugs/drug-approvals-and-databases/fda-approves-olaparib-plus-bevacizumab- maintenance-

treatment-ovarian-fallopian-tube-or-primary

TP53 – Tumor suppressor protein 53

Variant details

Gene Genomic alteration Impact Mutation ID Clinical significance

TP53 chr17:g.7577568C>A,p.C238F Missense rs730882005 Pathogenic

Drug Details -

Olaparib and Adavosertib

Olaparib (AZD-2281, MK-7339 trade name Lynparza) is an FDA-approved targeted therapy for cancer. It is a PARP inhibitor, inhibiting poly ADP ribose polymerase (PARP), an enzyme involved in DNA repair. Adavosertib (AZD1775) is a first-in-class, potent, and selective inhibitor of WEE1 with proof of chemo- potentiation in p53-deficient tumors in preclinical models. (Chen, Dongshao, 2018)

https://www.fda.gov/drugs/fda-approved-olaparib-lynparza-astrazeneca-pharmaceuticals-lp-maintenance-treatment-adult-patients



https://www.fda.gov/drugs/drug-approvals-and-databases/fda-approves-olaparib-plus-bevacizumab-maintenance-treatment-ovarian-fallopian-tube-or-primary




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Given that PARP inhibition by olaparib results in DNA double-strand breaks in S phase, it is hypothesized that combined Wee1 kinase and PARP inhibition could induce tumor cell death. Remarkable synergy was observed using an AZD1775/olaparib combination in small-cell lung cancer (SCLC) xenograft models (O’Connor, EORTC 2015).

Cetuximab

This study aims at evaluating the effect of cetuximab monotherapy as maintenance treatment, versus continuation after 8 courses of

induction therapy with cetuximab plus standard chemotherapy regimen (FOLFIRI or mFOLFOX6）in metastatic colorectal cancer (mCRC) patients.

The maintenance treatments are continued until disease progression or untolerated toxicity. The aim of this study is to demonstrate that cetuximab monotherapy is non-inferior to continuation treatment, in those mCRC patients who responded to induction therapy (SD, PR, or CR), and carry biomarker-panels (KRAS, NRAS, BRAF, and PIK3CA) favor EGFR antibody. (Details of clinical trial on page 4) (NCT02942706)

Pembrolizumab

Pembrolizumab is a highly selective IgG4-kappa humanized monoclonal antibody against PD-1 receptor. Pembrolizumab targets and blocks a protein called PD-1 on the surface of certain immune cells called T-cells. Blocking PD-1 triggers the T-cells to find and kill cancer cells. Pembrolizumab is very well tolerated so many patients who have difficulty tolerating chemotherapy may be able to handle this medication,

In the phase Ib KEYNOTE-012 study which evaluated pembrolizumab monotherapy at 10 mg/kg ever 2 weeks in patients with gastric cancer were recently reported. Most patients had two or more prior lines of therapy. In the study, 41% of evaluable patients showed tumor shrinkage. The overall response rate in 39 patients were 31%.

Adavosertib, Paclitaxel

This study is a single arm, single center phase II study of AZD1775 in combination with paclitaxel in patients with

advanced gastric adenocarcinoma harboring TP53 mutation as a second-line chemotherapy.

AZD1775 is an inhibitor of Wee1, a protein tyrosine kinase. Wee1 phosphorylates and inhibits cyclin- dependent

kinases 1 (CDK1) and 2 (CDK2), and is involved in regulation of the intra-S and G2 cell cycle checkpoints.

In in-vitro and in-vivo preclinical models, AZD1775 selectively enhanced chemotherapy induced death of cells deficient in p53 signaling. Tumor context-specific sensitization to the DNA damaging agents, gemcitabine and platinum, was observed in TOV21G (ovarian carcinoma) cell lines matched for wild type and knock down of p53


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DRIVER MUTATIONS

GENES OVERVIEW

Variant details

TP53 – Tumor suppressor protein 53

TP53 is a well-known tumor suppressor gene and has various mechanisms of anticancer function and plays

significant role in maintenance of genome integrity, apoptosis, genomic stability, and inhibition of angiogenesis

etc. Loss of TP53 function allows deregulated survival of genetically impaired abnormal cells which can lead to

neoplastic conversion of later on. It is altered in 39.49% of all cancers with mutations in 32.77% of breast carcinoma patients.

Gene Genomic alteration Clinical Significance Variant Reference

BRCA2 chr13:g.32930667C>A,p.A2513E Likely pathogenic Missense rs1060502401

TP53 chr17:g.7577568C>A,p.C238F Pathogenic Missense rs730882005

APC chr5:112173704C>T,p.R805* Pathogenic Stop gained rs587779783

APC chr5:g.112170823G>A,p.R640Q VUS Missense rs1273594465

POLE chr12:g.133244124G>A,p.R762W VUS Missense rs1064794759

PMS2 chr7:g.6043354C>T,p.R107Q VUS Missense rs63751284

BAP1 chr3:g.52436326G>A,p.P723L VUS Missense rs1559584547

NTRK1 chr1:g.156834587C>T,p.R119C VUS Missense rs757031354

STK11 chr19:g.1226569C>T,p.R409W VUS Missense rs368466538

NF1 chr17:g.29541476C>T,p.T467I Likely pathogenic Missense In-silico prediction tools

APC chr5:g.112176446G>A,p.E1719K VUS Missense

BRCA2 chr13:g.32930697T>A,p.L2523Q VUS Missense


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APC- Adenomatous polyposis coli

APC is a gene that encodes a tumor suppressor protein that acts as an antagonist of the Wnt signaling pathway.

It is also involved in other processes including cell migration and adhesion, transcriptional activation, and

apoptosis .Defects in this gene cause familial adenomatous polyposis (FAP), an autosomal dominant pre-

malignant disease that usually progresses to malignancy. APC also play a rate-limiting role in the majority of

sporadic colorectal cancers.

APC is altered in 10.55% of all cancers with mutations in 2.04% of breast carcinoma patients.


BRCA2 is a gene that encodes a protein that functions in maintaining genomic stability and as a tumor suppressor.

BRCA2 is a mediator of the core mechanism of homologous recombination. BRCA2 loss- of-function truncation

mutant display some defects in replication and checkpoint control.

BRCA2 alterations allow cells to bypass checkpoint controls and evade apoptosis, and thereby initiate

tumorigenesis. BRCA2 is altered in 4.63% of all cancers with mutations in 3.95% of breast carcinoma patients.

POLE – Polymerase (DNA directed), epsilon, catalytic subunit

POLE is a gene that encodes a protein that is a catalytic component of DNA polymerase epsilon. The enzymatic

protein functions in DNA repair and chromosomal DNA replication. Polε is also involved in DNA repair pathways

such as mismatch repair (MMR), base excision repair (BER), nucleotide excision repair (NER) or double-strand

break repair. (Guerro J et al, 2017)

Pathogenic somatic mutations in the proofreading domain of POLE have been found in some tumour types at

moderate or rare frequencies. Some mutations in the polymerase domain have been suggested to be drivers.

POLE is altered in 3.43% of all cancers with mutations in 1.78% of breast carcinoma patients

PMS2 – Post-meiotic segregation increased 2

PMS2 is a gene that encodes a protein that functions in DNA mismatch repair that functions to correct DNA

mismatches and small insertions and deletions that can occur during DNA replication and homologous

recombination. Also implicated in DNA damage signalling, a process which induces cell cycle arrest and can lead

to apoptosis in case of major DNA damages.

PMS2 is altered in 1.38% of all cancers with mutations in 0.81% of breast carcinoma patients.


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BAP1 – BRCA1 associated protein 1

BAP1 is a tumor suppressor gene important to the development and prognosis of many cancers, especially uveal

melanoma (UM). BAP1 is a scavenger protein that regulates cell cycle, cellular differentiation, and DNA damage

response. BAP1 was first shown to act as a tumor suppressor in cultured cells, where its deubiquitinase (UCH)

domain and nuclear localization sequences were required for BAP1 to suppress cell growth. BAP1 is altered in

2.04% of all cancers.

NTRK1 – Neurotrophic receptor tyrosine kinase 1

The NTRK1 gene provides instructions for making a protein that is essential for the development and survival of

nerve cells (neurons), especially those that transmit information about sensations such as pain, temperature,

and touch (sensory neurons). The NTRK1 protein is found on the surface of cells, particularly sensory neurons.

Trk (neurotrophin) receptors are single transmembrane catalytic receptors with intracellular tyrosine kinase

activity.

NTRK1 is altered in 2.21% of all cancers with mutations in 1.71% of breast carcinoma patients.

STK11- Serine/threonine kinase 11

STK11 is a gene that encodes a protein that belongs to the serine/threonine kinase family. The protein functions

in the regulation of cell polarity and is also a tumor suppressor. STK11 has been reported to play a critical role in

P53-mediated cell apoptosis. STK11 gene is involved in cell cycle regulation and apoptosis, whose abnormality

can induce and promote tumorigenesis.

STK11 is altered in 2.56% of all cancers with mutations in 1.23% of breast carcinoma patients.

NF1 – Neurofibromin 1

NF1 is a gene that codes for neurofibromin, a tumor suppressor protein. NF1 suppresses the function of the Ras

protein, which promotes cell growth and differentiation. In cancer, the tumor suppression function of the gene

is impaired, leading to conditions favorable for uncontrolled cell growth. NF1 mutations have been observed in

multiple cancer types, including myelodysplastic syndromes.

NF1 is altered in 6.78% of all cancers with mutations in 4.83% of breast carcinoma patients.


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Cell Cycle Control Pathway

GENES OVERVIEW

CDK4/6 inhibitors

targeting

pathway -

CDK1 inhibitors,

CDK2 inhibitors,

CDK inhibitors,

Genomic alteration in TP53

gene

Pathway driving cancer- Cell

Cycle Control

Pathway


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Beta-catenin/ Wnt Signaling Pathway

DNA Damage/Repair Pathway

FZD inhibitors

GSK inhibitors

targeting Therapies

pathway –

Genomic alteration in

APC gene

Pathway driving cancer-

Beta catenin/ Wnt

signaling pathway


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DNA Damage/Repair Pathway


BRCA2 and POLE genes

Pathway driving cancer- DNA damage/

repair pathway Therapies pathway – targeting

PARP inhibitors


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DNA Mismatch repair pathway

PARP inhibitors

targeting

pathway -


PMS2 gene


DNA mismatch repair

Pathway


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Receptor Tyrosine Kinase Pathway


NTRK1 and NFI genes


Receptor tyrosine kinase

pathway

Therapies targeting pathway- Therapeutic antibodies

Tyrosine kinase inhibitors


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Websites

COSMIC - Catalogue Of Somatic Mutations in Cancer - https://cancer.sanger.ac.uk/cosmic

ClinVar https://www.ncbi.nlm.nih.gov/clinvar

NIH- Clinical Trials - https://clinicaltrials.gov/

NIH- National Cancer Institute - https://www.cancer.gov/

https://www.mycancergenome.org/

https://www.drugbank.ca/

https://www.cancer.net/cancer-types

http://www.cancer-genetics.org/

https://www.cancerresearchuk.org/

https://www.genecards.org/

https://pubchem.ncbi.nlm.nih.gov/

http://atlasgeneticsoncology.org/

https://cancer.sanger.ac.uk/cosmic

https://www.ncbi.nlm.nih.gov/clinvar

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https://www.cancer.net/cancer-types/colorectal-cancer/medical-illustrations

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TEST DESCRIPTION

Somatic Genomic Test- Target Focus is a Next Generation Sequencing based test which identifies genetic alterations in a comprehensive panel of well curated 352 tumor genes which can impact response to approved therapy for a particular cancer type. Some of the alterations detected may have bearing on prognosis and/or therapeutic options and may provide relevant information that allows doctor to consider various lines of targeted treatment for the patient.

Sample preparation and Library preparation:

DNA isolated from FFPE or any other fresh tumor tissue source was used to perform targeted gene capture using a custom capture kit. The libraries were sequenced to mean >100X coverage on Illumina sequencing platform.

Bioinformatics Analysis and Reporting:

The sequences obtained are aligned to human reference genome (GRCh37/hg19) and variant analysis was performed using set of Bioinformatics Pipeline. Clinically relevant mutations were annotated using published variants in literature and a set of databases – ClinVar, COSMIC Drugs and Clinical Trials, FDA Approval Drugs. Common variants are filtered based on allele frequency in 1000 Genome Phase 3, ExAC, EVS, dbSNP147, etc. Non-synonymous variants effect is calculated using multiple algorithms such as PolyPhen-2, SIFT, MutationTaster2, Mutation Assessor and LRT. Only non-synonymous and splice site variants found in the clinical exome panel consisting of specific set of genes were used for clinical interpretation. Silent variations that do not result in any change in amino acid in the coding region are not reported.

Tumor Mutation Burden (TMB) is an evolving and promising biomarker for predicting a response to immunotherapy treatment. TMB is calculated by estimating the somatic non synonymous coding mutation as identified by Whole Exome Sequencing. A sample is categorized as High TMB if the TMB is found to be ≥20 mutations / megabase.


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LIMITATIONS AND DISCLAIMER

DNA studies do not constitute a definitive test for the selected condition(s) in all individuals. It should be

realized that there are possible sources of error. Errors can result from trace contamination, rare technical errors,

rare genetic variants that interfere with analysis, recent scientific developments, and alternative classification

systems. This test should be one of the many aspects used by the healthcare provider to help with a diagnosis and

treatment plan.

The contents of this test should be carefully assessed by the treating physician and further interpreted

along with clinical, histopathological findings, contraindications and guidelines before deciding the course of

therapy.

Most recent block is recommended for testing as the mutation profile may change in response to treatment

and hence differ at different sampling points.

Somatic Genomic Test has not been cleared or approved by the FDA.

Large deletions of more than 10 bp or copy number variations /chromosomal rearrangements cannot be

assessed using this method.

Certain genes may not be covered completely, and few mutations could be missed. A negative result

cannot rule out the possibility that the tested tumor sample carries mutations not previously associated with

cancer and hence not included in the panel.

The following table represents the panel of 352 genes, evaluated in the Target Focus test, commonly known to be

associated with different cancers and cancer syndromes.

ABCB1 BRAF CDKN2C EPHA3 FGF3 HSD3B1 MAP3K1 NFE2L2 PIM1 RNF43 SUFU

ABCC1 BRCA1 CEBPA EPHB1 FGF4 103 MAP3K13 NFKBIA PLK1 ROS1 SULT1A1

ABL1 BRCA2 CHEK1 EPHB4 FGF6 IDH1 MAPK1 NKX2-1 PMS2 RPTOR SYK

ACVR1B BRD4 CHEK2 ERBB2 FGFR1 IDH2 MCL1 NOTCH1 POLD1 RRM1 TBX3

AKT1 BRIP1 CIC ERBB3 FGFR2 IGF1R MDM2 NOTCH2 POLE RSP02 TEK

AKT2 BTG1 CREBBP ERBB4 FGFR3 IKBKE MDM4 NOTCH3 PPARG SDC4 TGFBR2

AKT3 BTG2 CRKL ERCC1 FGFR4 IKZF1 MED12 NPM1 PPP2R1A SDHA TIPARP

ALK BTK CSF1R ERCC2 FH INPP4B MEF2B NRAS PPP2R2A SDHB TMPRSS2

ALOX12B CALR CSF3R ERCC4 FLCN IRF2 MEN1 NTSC2 PRDM1 SDHC TNFAIP3

AMER1 CARD11 CTCF ERCC5 FLT1 IRF4 MERTK NTRK1 PRKAR1

A SOHO TNFRSF14

APC CASP8 CTNNA1 ERG FLT3 IRS2 MET NTRK2 PRKCD SETD2 TOP1

AR

CBFB CTNNB1 ERRFl1 FLT4 JAK1 MITF NTRK3 PRKCI SF3B1 TOP2A

GENES EVALUATED


of 21

ARAF CBL CUL3 ESR1 FOXL2 JAK2 MKNK1 NUTM1 PTCH1 SGK1 TOP2B

ARFRP1 CCND1 CUL4A ETV4 FUBP1 JAK3 MLH1 P2RY8 PTEN SLC29A1 TP53

ARID1A CCND2 CXCR4 ETV5 GABRA6 JUN MPL PALB2 PTPN11 SLC34A2 TPMT

ASXL1 CCND3 CYP17A1 ETV6 GATA1 KDM5A MRE11A PARK2 PTPRO SLC01B1 TSC1

ATM CCNE1 CYP2B6 EWSR1 GATA3 KDM5C MSH2 PARP1 QKI SMAD2 TSC2

ATR CD22 CYP2C19 EZH2 GATA4 KDM6A MSH3 PARP2 RAC1 SMAD4 TYMP

ATRX CD274 CYP2C8 EZR GATA6 KOR MSH6 PARP3 RAD21 SMARCA4 TYR03

AURKA CD70 CYP206 FAM46C GID4 KEAP1 MST1R PAX5 RAD5O SMARCB1 U2AF1

AURKB CD74 DAXX FANCA GNA11 KEL MTAP PBRM1 RAD51 SMO VEGFA

AXIN1 CD79A DDR1 FANCC GNA13 KIT MTHFR PDCD1 RAD51B SNCAIP VHL

AXL CD79B DDR2 FANCD2 GNAQ KLHL6 MTOR PDCD1LG2 RAD51C SOCS1 WHSC1

BAP1 CDC73 DHFR FANCG GNAS KMT2A MUTYH PDGFRA RAD52 SOX9 WHSC1L1

BARD1 CDH1 DIS3 FANCL GRM3 KMT2D MYB PDGFRB RAD54L SPARC WT1

BCL2 CDK12 DNMT3A FAS GSK3B KRAS MYC PDK1 RAF1 SPEN XPA

BCL2L1 CDK4 DOT1L FBXW7 GSTP1 LTK MYCL PIK3C2B RARA SPOP XPC

BCL2L2 CDK6 OPYD FGF10 H3F3A LYN2 MYCN PIK3C2G RB1 SRC XP01

BCL6 CDK8 EEO FGF12 HDAC1 MAF MYD88 PIK3CA RBM10 STAG2 XRCC1

BCOR CDKN1A EGFR FGF14 HGF MAP2K1 NBN PIK3CB REL STAT3 XRCC2

BCORL1 CDKN1B EMSY FGF19 HNF1A MAP2K2 NF1 PIK3R1 RET STK11 ZNF217

BCR CDKN2A EP300 FGF23 HRAS MAP2K4 NF2 PIK3R2 RICTOR STK11IP ZNF703

Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6030806/

--- End of report ----

Dr. Anand C Annan

MD (Path), PhD (Molecular & Cellular Pathology),

Head Oncopathology

NRL, Dr Lal PathLabs Ltd.

Dr. Atul Thatai PhD, National

Head R&D Molecular

Diagnostics, NRL, Dr Lal

PathLabs Ltd.

Dr. Gaurav Verma PhD (Clinical Genetics)

Sr. Manager – Scientific Affairs,

NRL, Dr Lal PathLabs Ltd.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6030806/

oncopro tmb & msi profile - lal pathlabs

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