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Old 09-11-2009, 12:38 AM   #38
Rich66
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Re: Novel Cancer Therapies Aim to Destroy the Disease at Its Root: The Cancer Stem Ce

GENova files patent for new breast cancer treatment

Thu Sep 10, 2009 6:01am EDT

NEW YORK, NY, Sept. 10 /PRNewswire-FirstCall/ - (OTCBB: GVBP.OB) - GENova
Biotherapeutics, Inc., ("GENova"), a biotechnology company that identifies,
acquires, and develops novel drug targets that disrupt the advance of
life-threatening diseases, today announced it has filed a patent for a
potential blockbuster drug target that combats breast cancer.
The target, Tetanolic acid, is a tailor-made lipid which induces cell death in
breast cancer cells, thus curtailing development of the harmful cancer.
This novel approach - using proteins to stop cancer - is based on recent
discoveries that indicate that most tumors are derived from a cancer stem
cell. The technology behind Tetanolic acid involved identifying specific
characteristics of these cancer stem cells and then tailoring a lipid
(Tetanolic acid) that can identify these characteristics and then attack the
malignant cells whilst leaving healthy cells intact.
This tailor-made cancer
treatment strategy is far superior to any existing therapies, as it terminates
the cancer at the source, with no side effects, and no harm to surrounding
healthy tissues.
"This target has tremendous market potential, as it can ultimately eliminate
the need for surgery and chemotherapy," says Aaron Whiteman for GENova.
Worldwide, breast cancer is the fifth most common cause of cancer death, and
is the most common cancer (and cause of cancer death) in women. The demand for
new and better treatments for the disease is as urgent as ever.
Whiteman explains GENova's novel approach: "If you compared this disease to a
tree, so far, treatments have only treated the crown of the tree - its
branches and leaves, and even tried to hit the stem, but no treatment has
penetrated its roots. Now that we can identify cancer stem cells, we can
remove the root at its formation, and therefore eliminate all sources of life
to the tumor. That is the potential behind Tetonolic acid."


http://www.genovabio.com/pipeline.html
Tetanolic acid: Promising novel lipid molecule for breast cancer
Known as an alpha hydroxyoleic acid, tetanolic acid is a form of a lipid which is also found as a main component of olive oil. Alpha hydroxyoleic acids are able to interact with the cell membrane in order to control its composition or structure with affect on the receptors on the membrane. This control mechanism affects the growth and proliferation of cells – and seeing that cancer is characterised as a normal proliferation of cells, these lipids can potentially prevent cancer spread (Ohba et al., 2007 Int. J. Cancer 121 (1)).
Tests have been shown that such analogues of oleic acid are able to prevent the growth and spread of cancers, including breast cancer, in mice. That is why GENova's Tetanolic acid is a candidate for development of an anti-cancer medicament in humans.




Proc Natl Acad Sci U S A. 2009 Aug 18;106(33):13754-8. Epub 2009 Aug 3.
Pivotal role of dihydrofolate reductase knockdown in the anticancer activity of 2-hydroxyoleic acid.

Lladó V, Terés S, Higuera M, Alvarez R, Noguera-Salva MA, Halver JE, Escribá PV, Busquets X.
Laboratory of Cell Biology and Laboratory of Molecular Cell Biomedicine, Department of Biology, Institut Universitari d'Investigacions en Ciències de la Salut, University of the Balearic Islands, E-07122 Palma de Mallorca, Spain.
alpha-Hydroxy-9-cis-octadecenoic acid, a synthetic fatty acid that modifies the composition and structure of lipid membranes. 2-Hydroxyoleic acid (HOA) generated interest due to its potent, yet nontoxic, anticancer activity. It induces cell cycle arrest in human lung cancer (A549) cells and apoptosis in human leukemia (Jurkat) cells. These two pathways may explain how HOA induces regression of a variety of cancers. We showed that HOA repressed the expression of dihydrofolate reductase (DHFR), the enzyme responsible for tetrahydrofolate (THF) synthesis. Folinic acid, which readily produces THF without the participation of DHFR, reverses the antitumor effects of HOA in A549 and Jurkat cells, as well as the inhibitory influence on cyclin D and cdk2 in A549 cells, and on DNA and PARP degradation in Jurkat cells. This effect was very specific, because either elaidic acid (an analog of HOA) or other lipids, failed to alter A549 or Jurkat cell growth. THF is a cofactor necessary for DNA synthesis. Thus, impairment of DNA synthesis appears to be a common mechanism involved in the different responses elicited by cancer cells following treatment with HOA, namely cell cycle arrest or apoptosis. Compared with other antifolates, such as methotrexate, HOA did not directly inhibit DHFR but rather, it repressed its expression, a mode of action that offers certain therapeutic advantages. These results not only demonstrate the effect of a fatty acid on the expression of DHFR, but also emphasize the potential of HOA to be used as a wide-spectrum drug against cancer.

PMID: 19666584 [PubMed - indexed for MEDLINE]
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