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Hepatitis B- and C-associated hepatocellular carcinoma in a large U.S. cancer center: Do clinicopathologic features or patient outcomes differ by the potentially causative viruses?
Background: Hep B virus (HBV) and hep C virus (HCV) are the main viral causes of hepatocellular carcinoma (HCC) development and are responsible for ~50% of USA cases. Because HBV is a DNA virus (Hepadna family) and HCV is an RNA virus (flavivirus family), it is unclear whether such virologic differences influence clinico-pathologic features of HCC or patient outcomes. We evaluated such differences in a large-scale, single-center study. Methods: Between 1992 to 2011, 815 HCC patients (HCV = 472, HBV = 343) were referred for treatment at the Univ. of Texas MD Anderson Cancer Center. Under IRB approval, detailed patient characteristics at time of diagnosis were documented. Chi-square tests were used to assess the significance of differences in the distributions of categorical variables between HBV and HCV groups. Median survival (mos.) was calculated using Kaplan Meier product-limit method and survival rates were compared using the log rank test. Results: 63% of patients were Texas residents with male to female ratio = 3:1. Patients with HBV were more likely to develop HCC at younger age than HCV patients, with poorly differentiated tumor (PDT), portal thrombosis (PT), larger tumor size (> 5 cm), extensive liver involvement (> 50%), high alpha-fetoprotein, and advanced CLIP stage (3-6). On the other hand, patients with HCV were more likely to exhibit underlying cirrhosis, have a history of greater alcohol and cigarette use, and had higher co-occurrence of diabetes mellitus (DM). One-year survival rates were similar between both groups (43.3%) and median survivals were 10.9 and 9.3 mos. for HCV and HBV, respectively (P = 0.9). Conclusions: Significant clinico-pathologic variations exist in HCC patients associated with HCV vs HBV, which may impact patients’ eligibility for treatment, but not prognosis.
|Age||PDT||PT||> 5cm||> 50%||Cirrhosis||CLIP(3-6)||Smoke||Alcohol||DM||STT||LAT||AFP|
|HCV||61.3 ± 10||18.8||30.2||35.2||26.6||86||36.9||73||70.1||23.5||27.5||27.4||17894 ± 4662|
|HBV||57.4 ± 14||26.5||35.7||49.4||42.9||59.5||44||56.4||49.3||18.3||36.9||17.2||55708 ± 1095|
|p||<.001||.001||.05||.02||< .001||< .001||.03||< .001||< .001||.05||< .001||< .001||< .001|
Abstracts by Marc Isamu Uemura:
Intratumoral (i.t.) IMO-2125 (IMO), a TLR9 agonist, in combination with ipilimumab (ipi) in PD-(L)1 refractory melanoma (RM).Meeting: 2017 ASCO-SITC Clinical Immuno-Oncology Symposium | Abstract No: 136
Retrospective study of non-mucinous appendiceal adenocarcinomas: Role of systemic chemotherapy and cytoreductive surgery.Meeting: 2016 Gastrointestinal Cancers Symposium | Abstract No: 263
Presentations by Marc Isamu Uemura:
Hepatitis B and C Associated Hepatocellular Carcinoma in a Large U.S. Cancer Center: Do Clinicopathologic Features or Patient Outcomes Differ by the Potentially Causative Viruses?Meeting: 2015 ASCO Annual Meeting Abstract No: 4011Session: To Lump or To Split: Molecular, Anatomic, and Etiologic Subtyping of Noncolorectal Gastrointestinal Malignancies and Potential Therapeutic Implications (Clinical Science Symposium)