Programmed cell death ligand‐1 (PD‐L1) detection assays have not been standardized for patients with colorectal cancer, and the prognostic value of PD‐L1 expression is unclear. We compared the PD‐L1 expression patterns in colorectal cancer samples using various immunohistochemical assays using 3 primary PD‐L1 antibodies (assay 1, MIH1; assay 2, E1L3; and assay 3, 22C3) and investigated the prognostic implication of PD‐L1 expression using each. Additionally, PD‐L1 gene amplification was evaluated using FISH. The percentage scorings and positivity rates of the 3 assays differed; the degrees of correlation and concordance between assays 2 and 3 were relatively high, whereas assay 1 was an outlier. Multivariate analyses indicated that PD‐L1 positivity in tumor cells and its negativity in tumor‐infiltrating lymphocytes were independent predictors of poorer overall and disease‐free survival in patients with colorectal cancer. PD‐L1 gene amplification was found in 2 patients (PD‐L1/CEP ratio, 5.60 and 5.84, respectively); both had strong PD‐L1 expression according to immunohistochemistry. Overall, our study showed that PD‐L1 expression status in tumor and immune cells is an independent prognostic factor in patients with colorectal cancer. Standardizations of both PD‐L1 detection using immunohistochemistry and the cut‐off for positivity are necessary. Finally, PD‐L1 gene amplification was found in a small fraction of samples, suggesting the possibility of an ancillary test for PD‐L1 evaluation.

The aim of the current study is to evaluate the prognostic value of anemia, an easily estimable parameter in patients with diffuse large B‐cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (R‐CHOP) immunochemotherapy. A total of 157 patients with newly diagnosed diffuse large B‐cell lymphoma treated with ≥1 cycle of R‐CHOP were included. Hemoglobin level without red cell transfusion within 7 days of initiation of treatment was chosen as a parameter of baseline cancer‐induced anemia. To investigate the clinical significance of chemotherapy‐induced anemia and its recovery after completion of treatment, 87 patients in complete remission for ≥6 months from the time of the last cycle of R‐CHOP were grouped and analyzed separately. Patients with a cancer‐induced anemia of hemoglobin <10 g/dL showed inferior event‐free and disease‐free survival compared to those with hemoglobin ≥10 g/dL. This finding was observed irrespective of the status of pre‐treatment bone marrow involvement. In multivariate analysis, hemoglobin <10 g/dL was found to be an international prognostic index‐independent prognostic factor. Risk of relapse was significantly higher for patients who were still anemic at 6 months after R‐CHOP, compared to those who achieved complete recovery from chemotherapy‐induced anemia within 6 months.

Lee JA, et al. J Breast Cancer. 2011 Jun;14(2):104-111. http://dx.doi.org/10.4048/jbc.2011.14.2.104

Hepatocellular carcinoma (HCC) is one of the most common cancers with a high mortality rate. Constitutive activation of STAT3 is found in various types of tumors, including HCC. In addition, suppressors of cytokine signaling 3 (SOCS3) signals for negative feedback to STATs, and is found to be inversely correlated with STAT3 expression. However, the exact role of SOCS3 in the tumorigenesis and progression of HCC is not fully understood. In this study we intended to show that SOCS3 inhibition promotes proliferation, migration, and invasion of HCC cells. HepG2, a human HCC cell line, was grown with SOCS3 siRNA or negative control (NC) transfection to assess the involvement of SOCS3 in cell proliferation, migration, and invasion by MTT, migration, and invasion assays, respectively. Western blot analysis was performed to examine the expression of STAT3, SOCS3, c-myc, matrix metalloproteinase (MMP)-2, and MMP-9 after transfection with either SOCS3 or NC siRNAs. A diethylnitrosamine (DEN)-induced HCC mouse model was assessed with or without injection of NSC 74859, a STAT3 inhibitor, to show accompanied changes among the expressions of STAT3, SOCS3, c-myc, MMP-2, and MMP-9. Inhibition of SOCS3 expression promoted the proliferation, migration, and invasion of HepG2 cells and increased the expression of c-myc, MMP-2, and MMP-9. HCC tumors developed in mice by DEN-induction with administration of NSC 74859 resulted in decreased expression of c-myc, MMP-2, and MMP-9, but not SOCS3. Loss of SOCS3 increased tumor growth, migration, and invasion and resulted in accompanied changes in expression of STAT3 and its target oncoproteins.