Substantial susceptibility of chronic lymphocytic leukemia to BCL2 inhibition: results of a phase I study of navitoclax in patients with relapsed or refractory disease.

By A. Roberts, J. Seymour, Jennifer R. Brown, W. Wierda, T. Kipps, S. Khaw, D. Carney, Simon Z. He, D. Huang, H. Xiong and 6 more. Journal of Clinical Oncology, 2012

827 citations recorded by the source corpus.

Subfields: Genetics, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/400a2134c7be5d12610c35765f4ba7f33209870b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. J. Wells
2. M. Demaria

In Molecular Biology

1. Michelle Arkin
2. Yinyan Tang
3. J. Wells
4. A. Alimonti
5. J. Kohli
6. E. Zagato
7. L. Pellegrini
8. A. Calcinotto

Citations in the corpus

• OncomiR or Tumor Suppressor? The Duplicity of MicroRNAs in Cancer (2016, neutral): “Although the possibility has not been directly investigated, one plausible explanation for this anomaly is that highoverexpression of BCL2, an antiapoptotic target of miR-125b, is a critical hallmark of CLL (5).”
• Targeting BCL2 with Venetoclax in Relapsed Chronic Lymphocytic Leukemia (2015, neutral): “Mutated 6/49 (12) 11/53 (21) 17/102 (17)”
• Small-molecule inhibitors of protein-protein interactions: progressing toward the reality. (2014, background): “ABT-199 is currently in phase 1 trials for CLL, and preliminary results look very promising, with response rates of >80% (Cancer Discovery, 2014).”
• Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “However, these drugs have been associated to severe toxicities in cancer patients (271, 344), and for this reason, new compounds, such as A1331852 and A1155463, have been currently tested in the hope to find better candidates for translation into clinical applications (367).”
• Selectivity by Small-Molecule Inhibitors of Protein Interactions Can Be Driven by Protein Surface Fluctuations (2015, neutral): “One recent cautionary example is ABT-263 (navitoclax), a Bcl-2 inhibitor that exhibited a dose-limiting adverse effect (thrombocytopenia) stemming from its inhibition of Bcl-xL [7,8].”
• Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies (2016, background): “So far, nearly a dozen BH3 mimetics are under investigation as Bcl-2 inhibitors in different phases of human clinical trials such as AT-101 (R-(-)-gossypol) [83,84], ABT199 (venetoclax) [85], ABT-737 [86], ABT-263 (navitoclax, orally available derivative of ABT-737) [87,88], GX15-070 (obatoclax) [89”