The changing treatment landscape of EGFR-mutant non-small-cell lung cancer

F Zhou, H Guo, Y **a, X Le, DSW Tan… - Nature Reviews …, 2024 - nature.com
The discovery of the association between EGFR mutations and the efficacy of EGFR tyrosine-
kinase inhibitors (TKIs) has revolutionized the treatment paradigm for patients with non …

Epidermal growth factor receptor targeting in colorectal carcinoma: Antibodies and patient-derived organoids as a smart model to study therapy resistance

S Tardito, S Matis, MR Zocchi, R Benelli… - International Journal of …, 2024 - mdpi.com
Colorectal cancer (CRC) is the second leading cause of cancer-related death worldwide.
Therefore, the need for new therapeutic strategies is still a challenge. Surgery and …

Alveolar Differentiation Drives Resistance to KRAS Inhibition in Lung Adenocarcinoma

Z Li, X Zhuang, CH Pan, Y Yan, R Thummalapalli… - Cancer …, 2024 - aacrjournals.org
Lung adenocarcinoma (LUAD), commonly driven by KRAS mutations, is responsible for 7%
of all cancer mortality. The first allele-specific KRAS inhibitors were recently approved in …

[HTML][HTML] Homopolymer switches mediate adaptive mutability in mismatch repair-deficient colorectal cancer

H Kayhanian, W Cross, SEM van der Horst… - Nature Genetics, 2024 - nature.com
Mismatch repair (MMR)-deficient cancer evolves through the stepwise erosion of coding
homopolymers in target genes. Curiously, the MMR genes MutS homolog 6 (MSH6) and …

The SMC5/6 complex prevents genotoxicity upon APOBEC3A-mediated replication stress

DF Fingerman, DR O'Leary, AR Hansen, T Tran… - The EMBO …, 2024 - embopress.org
Mutational patterns caused by APOBEC3 cytidine deaminase activity are evident throughout
human cancer genomes. In particular, the APOBEC3A family member is a potent genotoxin …

Differentiation signals induce APOBEC3A expression via GRHL3 in squamous epithelia and squamous cell carcinoma

NJ Smith, I Reddin, P Policelli, S Oh, N Zainal… - The EMBO …, 2025 - embopress.org
Two APOBEC DNA cytosine deaminase enzymes, APOBEC3A and APOBEC3B, generate
somatic mutations in cancer, thereby driving tumour development and drug resistance. Here …

APOBEC3 upregulation drives gemcitabine resistance

J Maciejowski, T Mohamed - Nature Cancer, 2024 - nature.com
Gemcitabine is a widely used chemotherapy drug that acts by targeting DNA replication.
Understanding why many tumors are unresponsive to gemcitabine is a clinical challenge. A …

ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts

B Hu, M Wiesehöfer, FJ de Miguel, Z Liu… - Cancer …, 2024 - aacrjournals.org
The majority of EGFR mutant lung adenocarcinomas respond well to EGFR tyrosine kinase
inhibitors (TKI). However, most of these responses are partial, with drug-tolerant residual …

Targeting APOBECs in cancer: It's about timing

AN Hata, M Larijani - Cancer Cell, 2024 - Elsevier
APOBEC3 cytidine deaminases have emerged as key drivers of mutagenesis in a wide
spectrum of tumor types and are now appreciated to play a causal role in driving tumor …

APOBEC Mutagenesis in Cancer Development and Susceptibility

A Dananberg, J Striepen, JS Rozowsky, M Petljak - Cancers, 2024 - mdpi.com
Simple Summary APOBEC cytosine deaminases represent potent mutational sources in
over 50% of human cancers and are linked to tumor heterogeneity and therapy responses …