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In This Issue of JAMA Oncology
April 2019

Highlights

JAMA Oncol. 2019;5(4):451. doi:10.1001/jamaoncol.2018.4749

Research

In this case series, Abida and colleagues prospectively evaluated prostate tumors for microsatellite instability-high (MSI-H) or mismatch repair–deficient (dMMR) biomarkers to assess the use of immune checkpoint blockade in patients with MSI-H or dMMR disease. Results showed that although the MSI-H/dMMR molecular phenotype is uncommon, there is potential for durable responses to immune checkpoint blockade. Reichert et al provide an Invited Commentary.

Invited Commentary

Ramsey and colleagues performed a multicenter cohort study to investigate the prevalence of hepatitis B virus (HBV), hepatitis C virus (HCV), and HIV in patients with newly diagnosed cancer. Results showed that many patients were unaware of their viral infection status at the time of diagnosis and had no identifiable risk factors for infection. The low rate of infection does not support universal screening in this population, but screening would be important to health care workers obtaining venous access.

Kim and colleagues performed a noninferiority randomized clinical trial to assess the long-term survival of patients with stage I gastric cancer treated with laparoscopic distal gastrectomy vs open distal gastrectomy. Results showed comparable overall survival rates in both groups. Intention-to-treat analysis confirmed the noninferiority of the laparoscopic approach compared with the open approach. Overall cancer-specific survival rates were similar as well.

AlDubayan and colleagues performed a case-control enrichment analysis to systematically compare the enrichment of germline pathogenic variants in the predisposition DNA repair genes in 205 unselected men with testicular germ cell tumors (TGCTs). Results showed that unselected men with TGCTs were 4 times more likely to carry germline loss-of-function CHEK2 variants compared with cancer-free individuals. Individuals with the pathogenic CHEK2 loss-of-function variants developed TGCTs 6 years earlier than those with CHEK2 wild-type alleles.

Cohen and colleagues performed a post hoc analysis of a cohort study to identify the possible mechanisms underlying primary resistance to immune checkpoint inhibitors (ICIs) in patients with metastatic colorectal cancer and microsatellite instability (MSI) or mismatch repair–deficient (dMMR) biomarkers. Results showed that primary resistance of tumors with MSI or dMMR to ICIs was due to misdiagnosis of MSI or dMMR status. Therefore, this status should be tested with both immunohistochemistry and polymerase chain reaction methods prior to ICI treatment.

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