Study Shows PCI-32765 Selectively Targets Malignant B Cells In Chronic Leukemia

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BlankStudy Shows Agent Selectively Targets Malignant B Cells In Chronic Leukemia

04 May 2011

A new experimental drug selectively kills the cancerous cells that cause chronic

lymphocytic leukemia, according to a new study by researchers at the Ohio State

University Comprehensive Cancer Center - Arthur G. Cancer Hospital and

J. Solove Research Institute (OSUCCC - ).

The study shows that the experimental agent PCI-32765 selectively kills the

malignant B lymphocytes that cause chronic lymphocytic leukemia (CLL).

The researchers say the findings, published online in the journal Blood, are

important because current CLL therapies kill T lymphocytes along with the

cancerous B lymphocytes.

T lymphocytes and B lymphocytes make up the adaptive immune system. When CLL

treatment destroys them both, patients become highly susceptible to

life-threatening infections.

" A drug that kills malignant B lymphocytes and spares T lymphocytes could

dramatically improve outcomes for CLL patients, " says study leader Dr. C.

Byrd, director, division of hematology and professor of medicine, of medicinal

chemistry and of veterinary biosciences at the OSUCCC - .

" Our collective results indicate that PCI-32765 is an outstanding candidate for

further development as a therapeutic for CLL, " says study co-director Dr. Amy J.

, assistant professor of hematology and medicinal chemistry, and a CLL

researcher with the OSUCCC-.

The research by Byrd, and a group of colleagues used CLL cells from ten

patients. It had several key findings related to PCI-32765:

a.. The agent specifically targets an important signaling molecule called

Bruton's tyrosine kinase, which is overexpressed in CLL cells and absent in T

cells.

b.. The agent inhibits the proliferation of CLL cells in laboratory culture

and promotes their death by self-destruction (apoptosis).

c.. It blocks survival signals from cells in the surrounding microenvironment,

including soluble factors such as IL-6, IL-4, and TNF-a, and stromal-cell

contact.