Diagnosing and exploiting cancer's addiction to blocks in apoptosis

By A. Letai. Nature Reviews. Cancer, 2008

601 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/52c60aa6c4dd36c0904b4cf1d7fbc927477bd85e

How researchers see this paper

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

In Cell Biology

1. John Calvin Reed
2. Douglas R. Green
3. Thomas G. Cotter

In Molecular Biology

1. Douglas R. Green
2. F. Llambi
3. J. Chipuk
4. John Calvin Reed
5. Eric S. Lander
6. Thomas G. Cotter
7. Todd R. Golub
8. Yan W. Asmann

In Oncology

1. Douglas R. Green
2. John Calvin Reed
3. Nicolas Stransky
4. Thomas G. Cotter
5. F. Llambi
6. Eric S. Lander
7. Guido Kroemer

Citations in the corpus

• Discovery and prioritization of somatic mutations in diffuse large B-cell lymphoma (DLBCL) by whole-exome sequencing (2012, background): “To address this, we focused on the BCL2 BH domains that mediate interactions with proapoptotic proteins (37).”
• Synthetic Lethality of Combined Bcl-2 Inhibition and p53 Activation in AML: Mechanisms and Superior Antileukemic Efficacy (2017, background): “For most cancer treatments, including chemotherapy, radiotherapy, and targeted therapies, induction of apoptosis represents the principal mechanism by which malignant cells are eliminated (Delbridge et al., 2016; Hata et al., 2015; Letai, 2008).”
• The BCL-2 Family Reunion (2010, background): “Examples of increased BCL-2 or BCL-xL Molecular Cell 37, February 12, 2010 ª2010 Elsevier Inc. 307 levels in human malignancy include lymphoma and epithelial cancers, and are generally predictive of aggressive disease, poor prognosis, and chemotherapeutic resistance (reviewed in Letai, 2008).”
• When NRF2 Talks, Who's Listening? (2010, neutral): “p53 regulates a host of processes within the cell, both directly, including the induction of apoptosis through the permeabilization of the outer mitochondrial membrane through interaction with proapoptotic factors (43, 89, 100), and indirectly, through the transcription of genes that effect changes ”
• Apoptosis and cancer: the genesis of a research field (2009, background): “Such findings probably result from the fact that the sensitivity of cancer cells to specific drugs can be regulated through the expression patterns of the BH3-only family members and not simply through the expression levels of BAX and BCL-2 (Ref”