Tumor suppressor pathways shape EGFR-driven lung tumor progression and response to treatment

Giorgia Foggetti; Chuan Li; Hongchen Cai; Dmitri A Petrov; Monte M Winslow; Katerina Politi

doi:10.1080/23723556.2021.1994328

Tumor suppressor pathways shape EGFR-driven lung tumor progression and response to treatment

Mol Cell Oncol. 2022 Jan 14;9(1):1994328. doi: 10.1080/23723556.2021.1994328. eCollection 2022.

Authors

Giorgia Foggetti^{1

2}, Chuan Li³, Hongchen Cai⁴, Dmitri A Petrov³, Monte M Winslow^{4

5

6}, Katerina Politi^{1

7

8}

Affiliations

¹ Department of Internal Medicine (Medical Oncology), Yale Cancer Center, Yale School of Medicine, New Haven, Connecticut, USA.
² Department of Medical Oncology, IRCCS Ospedale San Raffaele, Milan, Italy.
³ Departments of Biology, Stanford University School of Medicine, Stanford, California, USA.
⁴ Department of Genetics, Stanford University School of Medicine, Stanford, California, USA.
⁵ Department of Pathology, Stanford University School of Medicine, Stanford, California, USA.
⁶ Stanford Cancer Institute, Stanford University School of Medicine, Stanford, California, USA.
⁷ Department of Pathology, Yale School of Medicine, New Haven, Connecticut, USA.
⁸ Yale Cancer Center, Yale School of Medicine, New Haven, Connecticut, USA.

Abstract

In vivo modeling combined with CRISPR/Cas9-mediated somatic genome editing has contributed to elucidating the functional importance of specific genetic alterations in human tumors. Our recent work uncovered tumor suppressor pathways that affect EGFR-driven lung tumor growth and sensitivity to tyrosine kinase inhibitors and reflect the mutational landscape and treatment outcomes in the human disease.

Keywords: EGFR; Lung cancer; multiplexed in vivo genome editing; targeted therapy; tumor suppressor genes.

Abstract

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