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HCV with 1p36.3 mutation may contribute to cancer risk

The combination of hepatitis C virus, Ki-67 positivity and 1p36.3 deletion may be associated with the development of certain cancers, according to recent findings.

Researchers suggested that the core protein found in HCV infection can accumulate mutations in p53 and may therefore have co-oncogenic properties. In the current analysis, they aimed to determine the role of 1p36.3 telomere deletion among patients with B-cell non-Hodgkin’s lymphoma. They used fluorescence in situ hybridization (FISH) in relation to survival to evaluate antigen expression in Ki-67.

The analysis included 50 patients with HCV who served as the study group and 50 patients without HCV who served as controls. Sixty bone marrow biopsies also were collected from participants. All patients underwent FISH for assessment of 1p36.3 and immunohistochemical staining with Ki-67 antigens, according to the results.

Forty percent of patients in the study group demonstrated 1p36.3 deletion vs. 0% among controls. Immunohistochemical staining results showed that 74% of samples contained Ki-67 expression.

An overall survival of 25 months was reported for patients without HCV with positive FISH results vs. 40.78 months in FISH-negative patients without HCV (P=.0001).

Ki-67 positivity yielded an OS of 30.67 months vs. 46.5 months for Ki-67 negativity (P=.001).

For those with positive FISH results, an OS of 15.31 months was reported in the Ki-67–positive group vs. 31 months in the Ki-67–negative group.

HCV plus Ki-67 positivity was associated with an OS of 14.16 months among patients with positive FISH results and 19 months among patients with negative FISH results (P=.05).

Among the positive FISH group, an OS of 16.36 months was reported for Ki-67 positivity and 26.67 months for Ki-67 negativity. Also, among the positive FISH group, the presence of HCV infection was associated with 15.71 months vs. 29 months in patients without HCV.

“A significant difference was found between positive and negative HCV patients in their OS, the qualitative expression of Ki-67 and the quantitative detection of 1p36.3 deletion by FISH,” the researchers wrote. “We concluded that the coexistence of Ki-67 positivity, HCV positivity and 1p36.3 deletion may contribute to infection-related cancers at the 1p36.3 locus.”

Disclosure: The researchers report no relevant financial disclosures.