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Pancreatic cancer 'mismatch' in Lynch syndrome

Andrew E Hendifar1, Brent K Larson2, Rebecca Rojansky2

  • 1Department of Gastrointestinal Malignancies, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA.

Abstract

Insights

In Lynch syndrome (LS), mismatch repair (MMR) deficient tumors are treatable with immunotherapy. However, this case shows an MMR-intact pancreatic tumor in an MSH2-LS patient, highlighting the need for individual tumor testing.

Area of Science:

  • Oncology
  • Genetics
  • Immunotherapy

Background:

  • Lynch syndrome (LS) patients have germline mutations in mismatch repair (MMR) genes, predisposing them to MMR-deficient cancers.
  • Pembrolizumab, a PD-1 inhibitor, is approved for unresectable/metastatic solid tumors with MMR deficiency.
  • MMR deficiency status is crucial for determining eligibility for immunotherapy.

Observation:

  • A patient with a pathogenic MSH2 germline mutation and a history of LS-associated cancers presented with pancreatic ductal adenocarcinoma (PDAC).
  • While previous LS-related malignancies (endometrial, colorectal, urothelial) showed MMR deficiency (loss of MSH2/MSH6 expression), the PDAC exhibited intact MSH2 and MSH6 expression.
  • This discordance indicated a sporadic origin for the PDAC, unrelated to the patient's germline MSH2 mutation.

Findings:

  • The PDAC was MMR-intact, making the patient ineligible for pembrolizumab treatment.
  • This represents the first documented case of MMR-intact PDAC in a patient with MSH2-LS.

Implications:

  • Testing MMR protein expression in each malignancy is crucial for LS patients, particularly for pancreatic tumors.
  • Discordant MMR status across tumors can significantly impact treatment options and eligibility for targeted immunotherapies.
  • This case underscores the importance of comprehensive molecular profiling for personalized cancer treatment strategies.

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