Cyclin D-dependent kinases, INK4 inhibitors and cancer.

By Sagrario Ortega, Marcos Malumbres, M. Barbacid. Biochimica et Biophysica Acta, 2002

803 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/890d0cc1e4fd9fa365757001d83495d2f7aa45f0

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. M. Nieto
2. Marcos Malumbres
3. C. Sherr
4. M. Barbacid
5. T. Halazonetis
6. Y. Fouad
7. C. Aanei

In Molecular Biology

1. M. Nieto
2. Marcos Malumbres
3. C. Sherr
4. M. Barbacid
5. F. McCormick
6. Morgane Macheret
7. Jesús Gil
8. José C. R. Silva

In Oncology

1. M. Nieto
2. Marcos Malumbres
3. C. Sherr
4. M. Barbacid
5. F. McCormick
6. Morgane Macheret
7. Jesús Gil
8. L. Vallier

Citations in the corpus

• Cell cycle, CDKs and cancer: a changing paradigm (2009, background): “Deregulation of CDK4 and CDK6 activities have been implicated in a wide variety of tumour”
• DNA replication stress as a hallmark of cancer. (2015, background): “CCNE1, which is amplified in many human cancers and which encodes for cyclin E1, acts directly on Cdk2, whereas certain tumor suppressors, such as CDKN2A and CDKN2B, encode for CDK inhibitors (15, 87).”
• bantam encodes a developmentally regulated microRNA that controls cell proliferation and regulates the proapoptotic gene hid in Drosophila. (2003, neutral): “The human homologs are oncogenes (reviewed by Ortega et al., 2002).”
• The RB and p53 pathways in cancer. (2002, background): “this regulatory machinery act as tumor suppressors or protooncogenes, whose mutations occur so frequently as to prompt speculation that disabling “the RB pathway” may be essential for the formation of cancer cells (Sherr, 1996; Sellers and Kaelin, 1997; Nevins, 2001; Hahn and Weinberg, 2002; Ortega ”
• Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “This region can be subjected to loss of heterozygosity, point mutations or epigenetic alterations, such as promoter hypermethylation, that results in loss of expression (reviewed in Ortega et al., 2002).”
• Snail blocks the cell cycle and confers resistance to cell death. (2004, background): “TGF-␤-induced EMT and survival in both hepatocytes and epithelial cells occurs concomitantly with Snail induction (Valdés et al. 2002; Peinado et al. 2003).”