TP53 mutations confer resistance to hypomethylating agents and BCL-2 inhibition in myeloid neoplasms

Blood Adv. 2022 Jun 14;6(11):3201-3206. doi: 10.1182/bloodadvances.2021005859.

Authors

Roman R Schimmer^{1

2}, Larisa V Kovtonyuk^{1

2}, Nancy Klemm^{1

2}, Jonas Fullin^{1

2}, Sebastian M Stolz^{1

2}, Jan Mueller^{1

2}, Francisco Caiado^{1

2}, Kari J Kurppa^{3

4}, Benjamin L Ebert⁵, Markus G Manz^{1

2}, Steffen Boettcher^{1

2}

Affiliations

¹ Department of Medical Oncology and Hematology, University of Zurich and University Hospital Zurich, Zurich, Switzerland.
² Comprehensive Cancer Center Zurich, Zurich, Switzerland.
³ Institute of Biomedicine and MediCity Research Laboratories, University of Turku, Turku, Finland.
⁴ Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland; and.
⁵ Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.

No abstract available

MeSH terms

Humans
Mutation
Neoplasms* / genetics
Proto-Oncogene Proteins c-bcl-2* / genetics
Tumor Suppressor Protein p53 / genetics

Substances

Proto-Oncogene Proteins c-bcl-2
TP53 protein, human
Tumor Suppressor Protein p53