H. Varmus

LKB1 suppresses growth and promotes the internalization of EGFR through the PIKFYVE lipid kinase

This study identifies LKB1's role in suppressing growth by activating PIKFYVE to promote EGFR internalization in LUAD.

FORMATION OF MALIGNANT, METASTATIC SMALL CELL LUNG CANCERS THROUGH OVERPRODUCTION OF cMYC PROTEIN IN TP53 AND RB1 DEPLETED PULMONARY NEUROENDOCRINE CELLS DERIVED FROM HUMAN EMBRYONIC STEM CELLS

This study shows that overproducing cMYC in TP53 and RB1-depleted hESC-derived PNECs leads to aggressive SCLC-like tumors with metastatic properties and NEUROD1 expression.

Lineage-specific intolerance to oncogenic drivers restricts histological transformation

The paper models histological transformation of lung cancer and identifies neuroendocrine-specific tolerance to Myc as an oncogenic driver.

Non-conserved metabolic regulation by LKB1 distinguishes human and mouse lung adenocarcinoma

This study identifies a metabolic divergence between human and mouse lung adenocarcinomas due to LKB1-dependent regulation of TPI1 phosphorylation, highlighting limitations of mouse models for studying human cancer.

A novel small molecule that induces cytotoxicity in lung cancer cells inhibits disulfide reductases GSR and TXNRD1

The paper identifies LCS3, a compound that induces oxidative stress in lung cancer cells by inhibiting disulfide reductases GSR and TXNRD1, and shows its synergistic effect with glutathione and thioredoxin pathway inhibition.

Impaired hematopoiesis and leukemia development in mice with a conditional \"knock-in\" allele of a mutant splicing factor gene U2af1

This paper generates a mouse model with a conditional knock-in of the U2af1(S34F) mutation to study its role in hematopoiesis and leukemia, finding that it requires additional mutations for leukemogenesis.

Generation of pulmonary neuro-endocrine cells and tumors resembling small cell lung cancers from human embryonic stem cells

The paper develops a model for studying small cell lung cancers by generating pulmonary neuro-endocrine cells and tumors from human embryonic stem cells through genetic manipulation.

YES1 amplification: a mechanism of acquired resistance to EGFR inhibitors identified by transposon mutagenesis and clinical genomics

This study identifies YES1 amplification as a novel mechanism of resistance to EGFR inhibitors in lung cancer using transposon mutagenesis and clinical genomic analysis.

How Cancer Genomics Drives Cancer Biology: Does Synthetic Lethality Explain Mutually Exclusive Oncogenic Mutations?

The paper investigates mutual exclusivity of KRAS and EGFR mutations in lung adenocarcinomas, suggesting synthetic lethality explains their absence in co-occurring tumors.