Cancer discovery
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Several retrospective studies have examined whether patients with cancer who develop COVID-19 may be at risk of more severe viral disease if their therapy includes immune checkpoint inhibition. Although the data are not uniform, for now, halting or modifying cancer treatment decisions is unnecessary; meanwhile, vigilance with testing for COVID-19 in this population is recommended.
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The COVID-19 pandemic has caused widespread disruption of cancer clinical trials due to the restrictions on nonessential services and the reallocation of resources, and at the same time the urgent global effort toward discovering therapies that treat or prevent COVID-19 infection has led to shortening of traditional regulatory timelines. This experience should stimulate similar urgency in the way future cancer research is conducted.
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Due to the COVID-19 pandemic, oncologists have had to balance patients' need for treatment with their risk of contracting the disease, sometimes leading them to adjust standard treatment and/or rethink its timing. These decisions have been largely informed by guidelines, research, and shared decision-making-and their complexity led one group to develop a tool that might help.
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Most patients with KRAS G12C-mutant non-small cell lung cancer (NSCLC) experience clinical benefit from selective KRASG12C inhibition, whereas patients with colorectal cancer bearing the same mutation rarely respond. To investigate the cause of the limited efficacy of KRASG12C inhibitors in colorectal cancer, we examined the effects of AMG510 in KRAS G12C colorectal cancer cell lines. Unlike NSCLC cell lines, KRAS G12C colorectal cancer models have high basal receptor tyrosine kinase (RTK) activation and are responsive to growth factor stimulation. ⋯ EGFR and KRASG12C should be concomitantly inhibited to overcome resistance to KRASG12C blockade in colorectal tumors. See related commentary by Koleilat and Kwong, p. 1094. This article is highlighted in the In This Issue feature, p. 1079.
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TMPRSS2 is both the most frequently altered gene in primary prostate cancer and a critical factor enabling cellular infection by coronaviruses, including SARS-CoV-2. The modulation of its expression by sex steroids could contribute to the male predominance of severe infections, and given that TMPRSS2 has no known indispensable functions, and inhibitors are available, it is an appealing target for prevention or treatment of respiratory viral infections.