title: Clinicopathologic Features of Colorectal Carcinoma in HIV-Positive Patients.
abstract: Emerging evidence suggests differences in colorectal cancer in HIV-infected patients (HIV(+)) compared with HIV(-) patients. Microsatellite instability (MSI), occurring in a subset of colorectal cancer, is present at a higher rate in certain cancers in HIV(+) patients. Colorectal cancer with MSI share some characteristics with those reported for HIV(+) colorectal cancer. On this premise, we studied clinical and pathologic features of HIV(+) colorectal cancer and evaluated for MSI using matched HIV(-) colorectal cancer controls.
  
  
  
  Two nested, matched cohorts were identified from a hospital-based cohort of colorectal cancer patients. HIV(+) colorectal cancers were identified and random control patients were matched for selected characteristics. Mismatch repair protein (MMR) IHC was performed as the detection method for MSI. Variables were compared between cases and controls using fixed-effects logit modeling to account for matching.
  
  
  
  We included 184 colorectal cancer samples (38 HIV(+), 146 HIV(-) control). Median patient age at colorectal cancer onset was 55. When compared with HIV(-) colorectal cancer, HIV(+) patients were more likely to have smoked (P = 0.001), have right-sided colorectal cancer (37% vs. 14%; P = 0.003), and tumor-infiltrating lymphocytes (TIL) above 50/10 high-power fields (21% vs. 7%). There was no difference in MMR protein expression (P = 0.6). HIV(+) colorectal cancer patients had reduced overall survival (P = 0.02) but no difference in progression-free survival.
  
  
  
  HIV(+) patients developed colorectal cancer at a lower median age than population estimates, had a higher frequency of right-sided disease, and increased TILs, suggesting potential biologic differences compared with uninfected patients.
  
  
  
  Clinicopathologic differences in colorectal cancer of HIV(+) persons may have implications for tumor pathogenesis. Cancer Epidemiol Biomarkers Prev; 25(7); 1098-104. ©2016 AACR.
authors.affiliation: Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York.
authors.forename: Carlie
authors.initials: C
authors.lastname: Sigel
authors.affiliation: Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York.
authors.forename: Marcela S
authors.initials: MS
authors.lastname: Cavalcanti
authors.affiliation: Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York.
authors.forename: Tanisha
authors.initials: T
authors.lastname: Daniel
authors.affiliation: Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York.
authors.forename: Efsevia
authors.initials: E
authors.lastname: Vakiani
authors.affiliation: Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York.
authors.forename: Jinru
authors.initials: J
authors.lastname: Shia
authors.affiliation: Division of General Internal Medicine, Mount Sinai School of Medicine, New York, New York. sigelc@mskcc.org.
authors.forename: Keith
authors.initials: K
authors.lastname: Sigel
mesh_terms: D000230:Adenocarcinoma / Q000150:complications* / Q000473:pathology; D000328:Adult; D000367:Age Factors; D000368:Aged; D014408:Biomarkers, Tumor / Q000235:genetics / Q000378:metabolism; D016022:Case-Control Studies; D015331:Cohort Studies; D015179:Colorectal Neoplasms / Q000150:complications* / Q000473:pathology; D005260:Female; D015658:HIV Infections / Q000150:complications*; D006801:Humans; D008297:Male; D053842:Microsatellite Instability; D008875:Middle Aged; D000070957:MutL Protein Homolog 1 / Q000235:genetics; D012307:Risk Factors
chemical_list: D014408:Biomarkers, Tumor; D000070957:MutL Protein Homolog 1