Nature Communications (Aug 2020)
Enhancing chemotherapy response through augmented synthetic lethality by co-targeting nucleotide excision repair and cell-cycle checkpoints
- Yi Wen Kong,
- Erik C. Dreaden,
- Sandra Morandell,
- Wen Zhou,
- Sanjeev S. Dhara,
- Ganapathy Sriram,
- Fred C. Lam,
- Jesse C. Patterson,
- Mohiuddin Quadir,
- Anh Dinh,
- Kevin E. Shopsowitz,
- Shohreh Varmeh,
- Ömer H. Yilmaz,
- Stephen J. Lippard,
- H. Christian Reinhardt,
- Michael T. Hemann,
- Paula T. Hammond,
- Michael B. Yaffe
Affiliations
- Yi Wen Kong
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Erik C. Dreaden
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Sandra Morandell
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Wen Zhou
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Sanjeev S. Dhara
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Ganapathy Sriram
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Fred C. Lam
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Jesse C. Patterson
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Mohiuddin Quadir
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Anh Dinh
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Kevin E. Shopsowitz
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Shohreh Varmeh
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Ömer H. Yilmaz
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Stephen J. Lippard
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- H. Christian Reinhardt
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Michael T. Hemann
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Paula T. Hammond
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- Michael B. Yaffe
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
- DOI
- https://doi.org/10.1038/s41467-020-17958-z
- Journal volume & issue
-
Vol. 11,
no. 1
pp. 1 – 12
Abstract
Cell cycle checkpoint kinase, MK2, is in synthetic relationship with p53 in the DNA damage response to chemotherapeutic agents. Here, the authors report XPA as a third gene in which simultaneous targeting of MK2 and XPA further enhances sensitivity to cisplatin in p53-deficient tumours.
