CTIC attempting to make hay of its AACR presentations. Going to hang in there for now, as it's only up a tenth of a point this morning. I doubt they'll have much to add until ASCO.
>>SEATTLE, April 9 /PRNewswire-FirstCall/ -- In a plenary minisymposium on
intracellular signaling published in the April 2003 issue of the Proceedings
of the Annual Meeting of the American Association for Cancer Research (AACR),
Cell Therapeutics, Inc. (CTI) (Nasdaq: CTIC) presented data on a novel cancer
target, LPAAT-beta. The data suggest that the inhibition of LPAAT-beta may
impede the growth of tumors on two fronts, by restricting the growth of
supporting tissues such as blood vessels and by removing a cofactor essential
to tumor cell growth and proliferation. Existing therapies typically use a
single mechanism to fight cancer, whereas, LPAAT-beta inhibitors appear to
have a dual function.
In the published proceedings, CTI highlighted research on signaling
pathways which showed that inhibition of LPAAT-beta by genetic knockdown with
RNAi or with specific inhibitors of the enzyme leads to tumor cell death
through apoptosis. CTI's research also suggests the enzyme plays an important
role in cell types that are critical in the formation of the support tissues
(stroma) and the abnormal blood vessels which support tumor growth and provide
tumor blood supply.
"The discovery of a gene product that has critical functions in the
regulation of the Raf and other cancer-related pathways as well as in the
tissues supporting the tumor is intriguing and suggests LPAAT-beta inhibition
may be particularly effective in treating cancer where therapies that use only
a single mechanism for fighting cancer have failed," said Jack W. Singer, M.D.
and Research Program Chair of CTI.
LPAAT-beta produces a lipid called phosphatidic acid (PA), an essential
cofactor for molecules in two important pathways, Raf and mTOR, that are
overactive and critical to tumor growth. CTI scientists have found that
although LPAAT-beta is minimally expressed in most normal tissue, it is highly
expressed in most cancers including lung, ovarian, prostate, bladder and
cervical cancer as well as leukemias and lymphomas. Now, scientists have shown
that stromal tissue is one of the few normal tissues to express high levels of
LPAAT-beta and that PA may be critical to the growth and function of
endothelial and smooth muscle cells that make up the supporting tissue of
tumors. Additionally, small molecule inhibitors of LPAAT-beta are found to
slow the growth of normal endothelial and smooth muscle cells but are not
found to have the cytotoxic effect that is seen in tumor cells.
were published on LPAAT-beta
inhibition in the AACR proceedings. These posters can also be seen on the
Company web site at ctiseattle.com. CTI will continue its investigation of
LPAAT-beta inhibitors with its research partner, The Hope Heart Institute.
"We look forward to further characterizing the effects of LPAAT-beta
inhibition on tumor stroma and working with our partners at The Hope Heart
Institute to evaluate the effects of LPAAT-beta inhibitors in animal models
specifically developed to evaluate angiogenesis and other stromal tissues,"
stated Singer.
About LPAAT-beta
LPAAT-beta is an enzyme, initially cloned by CTI scientists, that
regulates the production of a lipid known as phosphatidic acid (PA), shown to
be critical for the activation of several key oncologic pathways, including
the Ras/Raf/ERK pathway and the Akt/mTOR pathway. Enhanced expression of
LPAAT-beta is associated with increased tumorigenicity while its inhibition
induces tumor cell death through apoptosis.<< |
