Triple blockade of EGFR, MEK and PD-L1 has antitumor activity in colorectal cancer models with constitutive activation of MAPK signaling and PD-L1 overexpression
Stefania Napolitano; Nunzia Matrone; A. L. Muddassir; Giulia Martini; Alexey V. Sorokin; Vincenzo De Falco; Emilio Francesco Giunta; Davide Ciardiello · 2019 · Journal of Experimental & Clinical Cancer Research
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
BACKGROUND: Molecular mechanisms driving acquired resistance to anti-EGFR therapies in metastatic colorectal cancer (mCRC) are complex but generally involve the activation of the downstream RAS-RAF-MEK-MAPK pathway. Nevertheless, even if inhibition of EGFR and MEK could be a strategy for overcoming anti-EGFR resistance, its use is limited by the development of MEK inhibitor (MEKi) resistance. METHODS: We have generated in vitro and in vivo different CRC models in order to underline the mechanisms of MEKi resistance. RESULTS: The three different in vitro MEKi resistant models, two generated by
Abstract by Stefania Napolitano; Nunzia Matrone; A. L. Muddassir; Giulia Martini; Alexey V. Sorokin; Vincenzo De Falco; Emilio Francesco Giunta; Davide Ciardiello, Journal of Experimental & Clinical Cancer Research (2019) — licensed CC BY 4.0.
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Metadata source: OpenAlex · DOI 10.1186/s13046-019-1497-0
