New roles for the RB tumor suppressor protein.
ABSTRACT For a gene whose existence was first postulated in 1971, was cloned in 1986 and whose functions have been extensively characterized ever since, you might be inclined to think there was not much new to report regarding the retinoblastoma tumor suppressor gene (RB)--but you would be wrong to make such an assumption. RB is still piquing our interest with several activities defined over the past year that reveal new and exciting roles for this key tumor suppressor gene. These functions include regulation of senescence through specific gene silencing mechanisms, control of developmental processes in extra-embryonic tissues, maintaining tissue homeostasis and determining survival responses to chemotherapy.
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ABSTRACT: Silvio Gutkind – National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA Pancreatic cancer has one of the poorest prognoses among human neoplasms, with an overall five-year survival rate of 3%. It usually occurs without appreciable symptoms and can remain undetected until the tumor is at an advanced stage. Pancreatic cancer tumors are highly resistant to conventional chemotherapy and radiation treatments. Although the use of combined modality therapy has produced modest increases in survival, significant advances in the treatment of this cancer have not been made. In this article, Martin E. Fernandez-Zapico and Raul Urrutia discuss the signaling pathways that control cell growth, differentiation and migration, which are dysregulated in this cancer, and the potential there is to manipulate these pathways for therapeutic purposes.Drug Discovery Today Disease Mechanisms 11/2004; 1(2):247–252. DOI:10.1016/j.ddmec.2004.09.003
Tribology and Interface Engineering Series 01/2000; 38:203-213. DOI:10.1016/S0167-8922(00)80126-1
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ABSTRACT: Despite decades of research, ovarian cancer is still associated with unacceptably high mortality rates, which must be addressed by novel therapeutic approaches. One avenue through which this may be achieved is targeting of tumor-initiating 'Cancer Stem Cells' (CSCs). CSCs are sufficient to generate primary and recurrent disease through extensive rounds of asymmetric division, which maintain the CSC pool while producing the tissues that form the bulk of the tumor. CSCs thrive in the harsh tumor niche, are generally refractory to therapeutic intervention and closely-linked to the Epithelial-Mesenchymal Transition process, which facilitates invasion and metastasis. While it is well-accepted that CSC-targeting must be assessed as a novel therapeutic avenue, few ovarian CSC models have been developed due to perceived and actual difficulties associated with the process of 'CSC Discovery'. In this article we review contemporary approaches to CSC Discovery and argue that this process should start with an understanding of the specific challenges associated with clinical intervention, laying the pipeline backwards towards CSC Discovery. Such an approach would expedite the bridging of the gap between laboratory isolation and clinical targeting of ovarian CSCs.Molecular Cancer 12/2014; 13(1):262. DOI:10.1186/1476-4598-13-262 · 5.40 Impact Factor