Guest Editor(s)
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- Dr. Lucio Crinò
- Department of Medical Oncology, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori, Meldola, Italy.
Website | E-mail
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- Dr. Angelo Delmonte
- Department of Medical Oncology, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori, Meldola, Italy.
Website | E-mail
Special Issue Introduction
KRAS represents an oncogene of the RAS family. When mutated, KRAS acts as a driver oncogene in a number of different cancers; in particular it constitutes the most common mutation in lung adenocarcinoma (25%-30%), in colorectal cancer (30%-40%) and in pancreatic cancer (approximately 90%), being present also in bladder, head and neck cancers and in melanoma. Furthermore the variants encoded by KRAS gene are considered ubiquitous and expressed in different cancer cell lines and in tumor microenvironment. Mutant KRAS proteins activate downstream signalling, through the MAPK and PI3K signalling cascade and induce continuous, unregulated cell proliferation and cell immortalization by evading apoptosis.
Because of their widespread expression in human cancers and their critical role in cancer cell proliferation, mutant KRAS protein represents an ideal and crucial target for the molecular treatment strategies in cancer precision medicine. Today after years of unsuccessful trials, a number of KRAS specific inhibitors are tested in RAS-driven tumors and preliminary results in lung cancer appear very promising to open the way to develop an efficacious strategy for treating KRAS-driven tumors.
The current special issue will highlight the recent key findings in the field of KRAS-mutant cancers and new strategies to improve the therapy for these diseases.
Submission Deadline
28 Feb 2021
Journal of Cancer Metastasis and Treatment
jcmtjournal.com
