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Accession Number ADA564155
Title Rewriting the Histone Code of Breast Cancer Stem Cells.
Publication Date May 2012
Media Count 12p
Personal Author P. Blancafort
Abstract It is perhaps surprising that most of the cells within the bulk of a breast tumor are differentiated cells, which indeed do not have tumorigenic potential at all. The Tumor Initiating Cells (TIC) comprise a small population that can generate tumors with very small amounts (for example, as little as 100 cells) once injected in immunodeficient mice (1-4). These cells, named Cancer Stem Cells (CSCs), are able to sustain self-renewal ability in vitro and have tumorigentic capabilities. CSCs could be visualized as corrupted versions of normal stem cells. Because of their ability to self-renew during a lifetime of an individual, these cells could be primary targets of transformation, by acquisition of genetic defects (for example, mutations in tumor suppressor genes and oncogenes) but also by acquiring transcriptional and epigenetic aberrations (3-4). Like their normal stem cell counterparts (5), CSCs are believed to naturally overexpress proteins in the surface that extrude DNA- damaging agents (like the ones used in chemotherapy for breast cancer) possibly as natural mechanism of stem cells to protect the integrity of their long-life genomes (6-7). Because of their ability to initiate a tumor, their potential to migrate, disseminate and differentiate, and their intrinsic resistance to chemotherapeutic agents, CSCs are primordial targets in breast cancer therapeutics. Recently, the triple negative breast cancer subgroup or basal- like breast cancer, associated with the poorest prognosis in breast cancer patients, has been found enriched in CSCs (8,9) Thus, we are in a critical need for the development of novel technologies to detect and specifically target CSCs, in order to suppress the intrinsic growth capabilities of the tumor.
Keywords Breast cancer
Chemical agents
Coding
Csc(Cancer stem cells)
Damage
Defects(Materials)
Deoxyribonucleic acids
Genes
Genome
Histones
Mammary glands
Neoplasms
Patients
Resistance(Biology)
Stem cells
Tic(Tumor initiating cells)


 
Source Agency Non Paid ADAS
NTIS Subject Category 57E - Clinical Medicine
57F - Cytology, Genetics, & Molecular Biology
Corporate Author North Carolina Univ. at Chapel Hill.
Document Type Technical report
Title Note Annual rept. 1 May 2011-30 Apr 2012.
NTIS Issue Number 1302
Contract Number W81XWH-10-1-0265

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