Expression of p16(INK4A) but not hypoxia markers or poly adenosine diphosphate-ribose polymerase is associated with improved survival in patients with pancreatic adenocarcinoma

Cancer. 2010 Nov 15;116(22):5179-87. doi: 10.1002/cncr.25481.

Abstract

Background: Pancreatic cancer is associated with mutations in the tumor suppressor gene cyclin-dependent kinase inhibitor 2A (p16(INK4A) ), a regulator of the cell cycle and apoptosis. This study investigates whether immunohistochemical expression of p16(INK4A) as well as hypoxia markers and poly adenosine diphosphate-ribose polymerase (PARP) correlates with survival in patients with resected pancreatic adenocarcinoma.

Methods: Seventy-three patients with pancreatic adenocarcinoma who underwent curative resection at Stanford University were included. From the surgical specimens, a tissue microarray was constructed using triplicate tissue cores from the primary tumor and used for immunohistochemical staining for the following markers: carbonic anhydrase IX, dihydrofolate reductase, p16(INK4A) , and PARP1/2. Staining was scored as either positive or negative and percentage positive staining. Staining score was correlated with overall survival (OS) and progression-free survival (PFS).

Results: Of the markers tested, only immunohistochemical expression of p16(INK4A) correlated with clinical outcome. On univariate analysis, p16(INK4A) expression in the tumor was associated with improved OS (P = .038) but not PFS (P = .28). The median survival for patients with positive versus negative p16(INK4A) staining was 28.8 months versus 18 months. On multivariate analysis, p16(INK4A) expression was associated with improved OS (P = .026) but not PFS (P = .25). Age (P = .0019) and number of nodes involved (P = .025) were also significant for OS. Adjuvant chemotherapy and margin status did not correlate with OS or PFS.

Conclusions: Expression of p16(INK4A) is associated with improved OS in patients with resected pancreatic adenocarcinoma. Further investigation is needed for validation, given conflicting data in the published literature. .

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / metabolism*
  • Adenocarcinoma / mortality
  • Adult
  • Aged
  • Aged, 80 and over
  • Antigens, Neoplasm / metabolism
  • Biomarkers, Tumor / metabolism
  • Carbonic Anhydrase IX
  • Carbonic Anhydrases / metabolism
  • Cell Hypoxia*
  • Cyclin-Dependent Kinase Inhibitor p16 / metabolism*
  • Disease-Free Survival
  • Female
  • Humans
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Pancreatic Neoplasms / metabolism*
  • Pancreatic Neoplasms / mortality
  • Poly(ADP-ribose) Polymerases / metabolism*
  • Prognosis
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins p21(ras)
  • Tetrahydrofolate Dehydrogenase / metabolism
  • Tissue Array Analysis
  • ras Proteins / genetics

Substances

  • Antigens, Neoplasm
  • Biomarkers, Tumor
  • Cyclin-Dependent Kinase Inhibitor p16
  • KRAS protein, human
  • Proto-Oncogene Proteins
  • Tetrahydrofolate Dehydrogenase
  • Poly(ADP-ribose) Polymerases
  • Proto-Oncogene Proteins p21(ras)
  • ras Proteins
  • CA9 protein, human
  • Carbonic Anhydrase IX
  • Carbonic Anhydrases