Glivec Research Today is a free monthly online journal that collates and summarizes the latest research about Glivec, including details on gleevec, imatinib, cancer, treatment, side-effects.

Recommended Books on Glivec

Magic Cancer Bullet: How a Tiny Orange Pill May Rewrite Medical History

The remarkable story behind the revolutionary miracle cure for cancer, Gleevec. Novartis chairman Dr Dan Vasella describes its development and how he and Novartis orchestrated the break–neck approval and massive production of this amazing drug.

Pharmaceutical giant Novartis recently developed Gleevec, one of the first 'smart' drugs created to kill cancer cells without damaging healthy cells in the process. In early tests with a common form of leukemia and other types of cancer, Gleevec has been extraordinarily successful, and side effects have been astoundingly minimal. Gleevec communicates directly with cancer–causing chromosomes and interrupts the signal that causes excessive growth of certain white blood cells. Patients have seen their tumours shrink significantly, and some have disappeared altogether.

This is the inside story of the creation of this miracle drug, and how Novartis CEO and chairman Dan Vasella rallied the company to bring Gleevec to market in mass quantities and record time.

Imatinib mesylate (STI571) abrogates the resistance to doxorubicin in human K562 chronic myeloid leukemia cells by inhibition of BCR/ABL kinase-mediated ... Toxicology and Environmental Mutagenesis] This digital document is a journal article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.

Description:
Imatinib mesylate (STI571), a specific inhibitor of BCR/ABL tyrosine kinase, exhibits potent antileukemic effects in the treatment of chronic myelogenous leukemia (CML). However, the precise mechanism by which inhibition of BCR/ABL activity results in pharmacological responses remains unknown. BCR/ABL-positive human K562 CML cells resistant to doxorubicin (K562DoxR) and their sensitive counterparts (K562DoxS) were used to determine the mechanism by which the STI571 inhibitor may overcome drug resistance. K562 wild type cells and CCRF-CEM lymphoblastic leukemia cells without BCR/ABL were used as controls. The STI571 specificity was examined by use of murine pro-B lymphoid Baf3 cells with or without BCR/ABL kinase expression. We examined kinetics of DNA repair after cell treatment with doxorubicin in the presence or absence of STI571 by the alkaline comet assay. The MTT assay was used to estimate resistance against doxorubicin and Western blot analysis with Crk-L antibody was performed to evaluate BCR/ABL kinase inhibition by STI571. We provide evidence that treatment of CML-derived BCR/ABL-expressing leukemia K562 cells with STI571 results in the inhibition of DNA repair and abrogation of the resistance of these cells to doxorubicin. We found that doxorubicin-resistant K562DoxR cells exhibited accelerated kinetics of DNA repair compared with doxorubicin-sensitive K562DoxS cells. Inhibition of BCR/ABL kinase in K562DoxR cells with 1@mM STI571 decreased the kinetics of DNA repair and abrogated drug resistance. The results suggest that STI571-mediated inhibition of BCR/ABL kinase activity can affect the effectiveness of the DNA-repair pathways, which in turn may enhance drug sensitivity of leukemia cells.

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