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Sent on Sunday, 2008 Oct 19.
Search breast cancer
Click on the following url to view complete results in pubmed. (Results may change over time.)
http://www.ncbi.nlm.nih.gov/entrez/cubby.fcgi?call=0bkg6reh3dXqE9WIXqD1ekzsVNzXvD90_VypYFFo8rVDD1A4ElaTC23c-KjA7sC&WebCubbyUser=08aoOpvcIcDEes6aEPvgjBME%401FC06D428FAD9DE0_0012SID
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==================== Entrez pubmed Results ======================
Items 1 - 5 of 44
1: PLoS Genet. 2008 Oct;4(10):e1000227. Epub 2008 Oct 17.
Depletion of human histone h1 variants uncovers specific roles in gene
expression and cell growth.
Sancho M, Diani E, Beato M, Jordan A.
Centre de Regulacio Genomica (CRG-UPF), Barcelona, Spain.
At least six histone H1 variants exist in somatic mammalian cells that bind to
the linker DNA and stabilize the nucleosome particle contributing to higher
order chromatin compaction. In addition, H1 seems to be actively involved in the
regulation of gene expression. However, it is not well known whether the
different variants have distinct roles or if they regulate specific promoters.
We have explored this by inducible shRNA-mediated knock-down of each of the H1
variants in a human breast cancer cell line. Rapid inhibition of each H1 variant
was not compensated for by changes of expression of other variants. Microarray
experiments have shown a different subset of genes to be altered in each H1
knock-down. Interestingly, H1.2 depletion caused specific effects such as a cell
cycle G1-phase arrest, the repressed expression of a number of cell cycle genes,
and decreased global nucleosome spacing. On its side, H1.4 depletion caused cell
death in T47D cells, providing the first evidence of the essential role of an H1
variant for survival in a human cell type. Thus, specific phenotypes are
observed in breast cancer cells depleted of individual histone H1 variants,
supporting the theory that distinct roles exist for the linker histone variants.
PMID: 18927631 [PubMed - in process]
2: Cancer Gene Ther. 2008 Oct 17; [Epub ahead of print]
Imaging of cationic multifunctional liposome-mediated delivery of COX-2 siRNA.
Mikhaylova M, Stasinopoulos I, Kato Y, Artemov D, Bhujwalla ZM.
1JHU ICMIC Program, The Russell H Morgan Department of Radiology and
Radiological Science, The Johns Hopkins University School of Medicine,
Baltimore, MD, USA.
Liposomes are a useful means of delivering molecular targeting agents such as
small interfering RNA (siRNA) to downregulate specific pathways important in
cancer growth and progression. The ability to non-invasively image these
carriers is important to ascertain their delivery within the tumor. As
cyclooxygenase-2 (COX-2) is an important therapeutic target in cancer, we
investigated loading COX-2-specific siRNA into cationic liposomes containing MR
contrast agents for imaging delivery in cancer cells and tumors. COX-2 and GAPDH
siRNA, as well as Magnevist or Feridex, were loaded directly into the liposomes.
These lipoplexes were used for cell transfection of the poorly differentiated
and highly metastatic breast cancer cell line MDA-MB-231. PEGylated liposomes
loaded with Feridex and fluorescently labeled COX-2 siRNA were used for in vivo
delivery of lipoplexes in MDA-MB-231 breast cancer xenografts in female SCID
mice. Transient transfection assays demonstrated potent and specific
downregulation of the COX-2 protein in cells in culture. Tail vein injections of
PEGylated COX-2 lipoplexes resulted in intratumoral delivery of siRNA.
Biodistribution studies showed significant localization in the lung, liver and
kidney at 24 h. These data demonstrate the feasibility of liposomal-mediated
delivery of COX-2-specific siRNA to downregulate COX-2 in cancer cells, and
multi-modality imaging of the delivery of specific siRNA in tumors.Cancer Gene
Therapy advance online publication, 17 October 2008; doi:10.1038/cgt.2008.79.
PMID: 18927599 [PubMed - as supplied by publisher]
3: Panminerva Med. 2008 Sep;50(3):247-54.
Is there a place for postmenopausal hormone therapy use in women with lupus?
Gompel A, Piette JC.
Unit of Endocrinological Gynecology, Paris Descartes University, Hotel Dieu de
Paris, APHP, Paris, France anne.gompel@htd.aphp.fr.
The Women Health Initiative (WHI) randomized trials have reported increase in
cardiovascular and breast cancer risks from the use of post-menopausal hormone
therapy (HT). A striking decrease of HT use has been observed worldwide despite
the fact that other regimens in younger post-menopausal women could be safer.
Systemic lupus erythematosis (SLE) is considered as estrogen sensitive. HT is
generally considered as contraindicated in these women who are especially at
risk for cardiovascular diseases and osteoporosis. However, recent randomized
trials have raised the question of a lack of deleterious effects of estrogen
containing oral contraceptives. In view of the recent knowledge and
understanding in the field of menopause the authors were interested to examine
the HT effects in women with SLE by analysis the published cases control,
observational studies and randomized trials. The randomized trials and large
observational studies showed a mild increase risk in flares and thrombotic
events, whereas retrospective studies did not show increase in these risks but
suggesting selection bias. A better profile on the blood clotting parameters and
surrogate markers of the arterial risk can be obtained by transdermal estrogen
and natural progesterone in non SLE women. Less venous thrombotic events are
observed in women at risk for thrombosis with the transdermal estradiol
administration in a case control study. However no randomized trial is still
available and no epidemiological data are reassuring on the arterial risk.
Prescription of HT has to remain especially prudent in women with SLE. If a
decision of treatment is taken transdermal estradiol and progesterone or close
pregnane derivatives should be probably most valuable but also used at the
minimal dose.
PMID: 18927529 [PubMed - in process]
4: Cancer Biol Ther. 2008 Dec 7;7(12) [Epub ahead of print]
A survivin specific T-cell clone from a breast cancer patient display universal
tumor cell lysis.
Sorensen RB, Svane IM, Straten PT, Andersen MH.
Centre for Cancer Immune therapy (CCIT), Department of Hematology, Herlev
University Hospital, Herlev, Denmark.
Survivin is an attractive candidate for cancer immunotherapy since it is
overexpressed in most common human cancers, poorly expressed in most normal
adult tissues and is essential for cancer cell survival. Previously, we and
others have demonstrated that survivin-specific immune responses are present in
cancer patients. However, a significant limitation of these findings has been
that antigen-specific lysis of tumors was achieved using polyclonal T-cell lines
rather than a specific T cell clone. In the present study we isolated and
expanded survivin specific cytotoxic T lymphocyte (CTL) clones from the
peripheral blood of cancer patients. The survivin specific CTL clones
efficiently lysed a large panel of tumor cells of different origin, i.e., breast
cancer, colon cancer and melanoma cells. The data support the notion that
survivin may serve as a universal target antigen for anti-cancer immunotherapy.
PMID: 18927499 [PubMed - as supplied by publisher]
5: Cancer Biol Ther. 2008 Oct 19;7(10) [Epub ahead of print]
Regulation of centrosomes by the BRCA1-dependent ubiquitin ligase.
Kais Z, Parvin JD.
Department of Biomedical Informatics, The Ohio State University Comprehensive
Cancer Center, Columbus, Ohio, USA.
Centrosomes are the organelles that organize microtubule networks and establish
the bipolar mitotic spindle, which is essential for the segregation of
chromosomes during cell division. Proper duplication of centrosomes is necessary
to prevent genetic instability, thus control of this organelle is important in
the suppression of tumorigenesis. The BRCA1 dependent ubiquitination activity
regulates centrosome number in breast derived cell lines and this activity is
likely critical for the tumor suppression activity of BRCA1. This review will
focus on the importance of controlling centrosome number and on the effect of
BRCA1 on the centrosome duplication cycle in mammary cells.
PMID: 18927495 [PubMed - as supplied by publisher]