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  9. Predictive And Prognostic Markers
  11. Methylthioadenosine Phosphorylase Genomic Loss In Advanced Gastrointestinal Cancers

Methylthioadenosine Phosphorylase Genomic Loss in Advanced Gastrointestinal Cancers

Natalie Y L Ngoi1,2, Tin-Yun Tang3, Catia F Gaspar1

  • 1Department of Investigational Cancer Therapeutics, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

The Oncologist
|February 8, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Methylthioadenosine phosphorylase (MTAP)-loss occurs in 8.3% of gastrointestinal cancers, particularly pancreatic cancer. This genomic alteration impacts treatment strategies and prognostic outcomes in GI tumors.

Area of Science:

  • Oncology
  • Genomics
  • Cancer Research

Background:

  • 9p21 deletion, a common cancer event, includes methylthioadenosine phosphorylase (MTAP), CDKN2A, and CDKN2B genes, linked to poor prognosis and immunotherapy resistance.
  • MTAP-loss is an emerging drug target, with inhibitors exploiting synthetic lethality.

Purpose of the Study:

  • To determine the prevalence and genomic characteristics of MTAP-loss in advanced gastrointestinal (GI) cancers.
  • To evaluate MTAP-loss as a prognostic biomarker in GI tumors.

Main Methods:

  • Next-generation sequencing and comparative genomic analysis of 64,860 tumors across 5 GI cancer types.
  • Retrospective analysis comparing clinical outcomes of MTAP-loss versus MTAP-intact GI tumors.

Main Results:

Keywords:
9p21 lossMTAP lossbiomarkerscholangiocarcinoma

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  • MTAP-loss was found in 8.3% of GI cancers, most frequent in pancreatic ductal adenocarcinoma (PDAC) (21.7%) and least in colorectal carcinoma (CRC) (1.1%).
  • MTAP-loss tumors showed distinct genomic alterations and lower rates of microsatellite instability or high tumor mutational burden.
  • PD-L1 expression was less frequent in MTAP-loss intrahepatic cholangiocarcinoma (IHCC).

Conclusions:

  • MTAP-loss, part of 9p21 loss, has an 8% prevalence in GI cancers, with significant variation by subtype (e.g., 22% in PDAC, 1.1% in CRC).
  • MTAP-loss is not mutually exclusive with other targetable mutations, suggesting complex therapeutic implications.
genomics
tumor