Issue 2:6 of Cancer Medicine is live and available to read online. A great range of articles in this collection, but here are some top articles which Editor-in-Chief Prof. Qingyi Wei has highlighted from the issue:
Phenotypic modifications in ovarian cancer stem cells following Paclitaxel treatment
Vinicius Craveiro, Yang Yang-Hartwich, Jennie C. Holmberg, Natalia J. Sumi, John Pizzonia, Brian Griffin, Sabrina K. Gill, Dan-Arin Silasi, Masoud Azodi, Thomas Rutherford, Ayesha B. Alvero and Gil Mor
Summary: We demonstrate that putative ovarian cancer cells with tumor initiating capacity that survive chemotherapy acquire molecular phenotypic modifications, which makes them distinct from the original tumor-initiating cells. The modifications that occur may not be the same in every patient. This suggests that treatment modalities should be modified to each individual patient. Further studies using our models will identify biomarkers for personalized treatment.
ADAM17-mediated CD44 cleavage promotes orasphere formation or stemness and tumorigenesis in HNSCC
Pachiyappan Kamarajan, Jae M Shin, Xu Qian, Bibiana Matte, Joey Yizhou Zhu and Yvonne L. Kapila
Summary: Our data demonstrate, for the first time that CD44 cleavage by ADAM17 is a critical determinant of orasphere formation or stemness and tumorigenesis in oral cancer. Our data support the concept that therapeutics that target CD44 cleavage mechanisms within the stem cell compartment can impair stemness and thus hold promise for treating aggressive oral cancer.
BRD4 associates with p53 in DNMT3A-mutated leukemia cells and is implicated in apoptosis by the bromodomain inhibitor JQ1
Helen Jayne Susan Stewart, Gillian Abigail Horne, Sarah Bastow and Timothy James Telfer Chevassut
Summary: The bromodomain inhibitor JQ1 blocks BRD4 binding to acetylated histones leading to apoptosis of acute myeloid leukemia cells. We find JQ1 exhibits synergistic activity with histone deacetylase inhibitors, Nutlin-3 and daunorubicin suggesting involvement of p53. We show that BRD4 interacts with p53, suggesting a role in DNA damage repair response that is disrupted by JQ1 in DNMT3A/NPM1-mutated OCI-AML3 leukemia cells.