oncologywatch

Lleonart ME, Artero-Castro A, Kondoh H. Senescence induction; a possible cancer therapy. Mol Cancer. 2009 Jan 8;8(1):3. PMID: 19133111

In normal cells, the ends of chromosomes (telomeres) tend to become shortened with each cell division. When telomeres shorten to a certain length, the cell can no longer replicate and enters senescence. In many cancer cells, a protein normally present in fetal development but not in adults (telomerase) maintains the length of telomeres, effectively conferring immortality. [See CancerQuest for a full explanation, with visuals.]

In Molecular Biology, authors from Fundació Institut de Recerca Hospital Vall d´Hebron in Barcelona and the Graduate School of Medicine, Kyoto University, describe telomerase inhibition and senescence induction as potential strategies for the development of novel cancer therapies. From the paper:

“Cellular senescence has become an attractive therapeutic concept because [it] mimics programmed cell death by excluding cells from active progression through the cell cycle. As an intact apoptotic machinery is unavailable in most established malignancies, a senescence-induced mechanism emerges as a back-up program to substitute for or to reinforce an insufficient apoptotic response. Importantly, the therapeutic potential of senescence induction strongly relies on the irreversibility of this process. Although, it has not been formally tested whether drug-inducible senescence is a complete[ly] reversible process, the acquisition of spontaneous mutations that disable p53 or pRB in a resting cell without DNA replication seems rather unlikely. Thereby it would be very interesting for preclinical investigations to explore future therapies which directly prompt a clear senescence response as those observed in vitro. It would be tempting to speculate that the combination of a senescence induced therapy and a conventional therapy might cooperate to entirely abolish cancer."

[OncologyWatch directory of open-access oncology journals.]

OncologyWatch: Posts about free-access articles on aspects of oncology theory, practice and policy (about the blogger). This blog is not a source for medical advice.

technorati tags: senescence

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McConnell P, Dash RC, Chilukuri R, et al. The Cancer Translational Research Informatics Platform. BMC Med Inform Decis Mak. 2008 Dec 24;8(1):60. PMID: 19108734

Researchers at Duke University Medical Center and SemanticBits (Herndon, Virginia) describe a new outcomes analysis tool that allows oncologists to query clinical data from geographically dispersed patients with similar characteristics to find treatments that were administered with success. The Cancer Translational Research Informatics Platform (caTRIP, https://cabig.nci.nih.gov/tools/caTRIP) facilitates the aggregation of clinical and molecular cancer data which can then be exchanged across institutions.

The authors detail the objectives, overall software architecture, security, implementation, usability, and future development plans for caTRIP. From the paper:

“A motivating use case for the development of caTRIP is one of outcomes analysis, whereby a clinician can query data from a cohort of preexisting patients to help guide treatment of another patient. An oncologist can ask "What are the treatments and outcomes of other patients that have similar characteristics to my patient?" caTRIP makes this possible on multiple levels: local, institutional, regional, national, and beyond by leveraging grid infrastructure to scale beyond traditional query systems."

The tool has the potential to effectively broaden institutional experience with highly atypical cancers:

"The fact of the matter is that even a large tertiary care facility will rarely come across such tumors. caTRIP provides a mechanism to examine all those patients who have been seen at any institution where caTRIP has been deployed and identify the cohort of patients that matches the specified criteria. It is a matter of a few minutes, at most, to construct a query that narrows the cohort to patients that have lobular tumors of the breast, are ER negative, PR negative, and Her-2/neu overexpressed. Furthermore, the type of treatment employed and the time to recurrence or death are easily captured as part of the result set by drawing upon the Tumor Registry as an additional data source. This permits a level of decision in the clinic - heretofore impossible with prior technologies."

caTRIP is available on the U.S. National Cancer Institute’s caBIG™ Community Website.

OncologyWatch: Posts about free-access articles on aspects of oncology theory, practice and policy (about the blogger). This blog is not a source for medical advice.

technorati tags: outcomes analysis

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Lewis MT. Faith, heresy and the cancer stem cell hypothesis. Future Oncol. 2008 Oct;4(5):585-9. PMID: 18922113

Baylor professor Michael Lewis reviews current theory about cancer stem cells, starting from arguments for their existence:

“Arguments for the existence of tumor-initiating ‘cancer stem cells’ are rooted ultimately in cell theory. A central tenet of cell theory states that, other than the first cell, all cells arise from pre-existing cells. Since all cancers are composed of cells, and have, in most cases, been demonstrated to be clonally derived, most cancers must arise from a single, pre-existing cell – a ‘tumor-initiating cell’. The cancer stem cell hypothesis proposes that tumor-initiating ‘cancer stem cells’ arise from cells that either innately possess or acquire the ability to self-renew (reproduce a new tumor-initiating cell) and serve as a precursor cell able to generate all other cell types characteristic of a given tumor. Thus, the term ‘stem cell’ in the ‘cancer stem cell hypothesis’ refers to a defining set of cellular behaviors responsible for tumor formation, and not necessarily to the identity of the cell of origin."

 

OncologyWatch: Posts about free-access articles on aspects of oncology theory, practice and policy (about the blogger). This blog is not a source for medical advice.

technorati tags: cancer stem cells

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