ATM functions as a rheostat of metabolic stress in small-cell lung cancer
The metabolic landscape of SCLC remains poorly characterized, particularly its interaction with dysregulated signaling networks, limiting the development of effective strategies to overcome therapeutic resistance. Our work reveals an expanded role for ATM beyond DNA repair, positioning it as a key regulator of metabolic rewiring and highlighting new therapeutic opportunities for SCLC.
Authors
- Mirela Berisa (ORCID: https://orcid.org/0000-0001-7347-9823)
- Tin Htwe Thin (ORCID: https://orcid.org/0000-0002-7891-1459)
- Debdatta Halder
- Kedwin Ventura
- D. Demircioğlu
- Subhamoy Chakraborty
- Vrinda Jethalia
- Hossein Borghaei
- Andrew Elliott
- Triparna Sen
- Utsav Dr. Sen
- Dan Hasson
- Balazs Halmos
- Ari Vanderwalde
- Rachel Brody
- Alan Soto
Institutions
- Fox Chase Cancer Center (US)
- Albert Einstein College of Medicine (US)
- Montefiore Medical Center (US)
- Caris Life Sciences (United States) (US)
- The Ohio State University (US)
- Icahn School of Medicine at Mount Sinai (US)
Publication Details
- Journal
- bioRxiv (Cold Spring Harbor Laboratory)
- Published
- 2026-03-17
- DOI
- https://doi.org/10.64898/2026.03.13.711672
- Primary Topic
- Lung Cancer Research Studies
- Type
- article
- Field-Weighted Citation Impact
- 0.00