In 1972, she identified a genetic glitch
in chronic myelogenous leukemia cells — a swap of genes she called chromosomal translocation — that resulted in the uncontrolled cell growth of cancer.
Brian J. Druker, M.D. Oregon Health Sciences University Mechanism - based therapy for chronic myelogenous leukemia
The team has shown that the microenvironment that controls hematopoietic stem cells can be targeted for the treatment of a set of disorders called myeloproliferative neoplasias, the most prominent of which are chronic myelomonocytic leukemia (CMML), juvenile myelomonocytic leukemia (JMML), and
atypical chronic myelogenous leukemia (CML).
Currently no treatment option is available for five percent of patients suffering
from chronic myelogenous leukemia, since they have developed resistance to conventional medications.
Already, a few examples exist — blood tests for hereditary colon cancer; the design of Herceptin, a breast cancer drug; and Gleevec, a drug used
in chronic myelogenous leukemia — in which the identification of gene alterations translated into clinical applications.
Investigators report that the six - month study of nilotinib, a treatment
for chronic myelogenous leukemia or CML, produced benefit for all study patients who completed the trial (11 of 12), with 11 patients reporting meaningful clinical improvements.
Her research has recently shown that a signaling pathway dubbed «hedgehog» is important not only for normal development of stem cells but also for the growth of cancer cells in
chronic myelogenous leukemia.
For example,
chronic myelogenous leukemia is caused by overproduction of certain white blood cells in the bone marrow.
In both acute and
chronic myelogenous leukemia, immature white blood cells in the bone marrow multiply out of control.
This knowledge laid the foundation for the targeted cancer treatment revolution inaugurated by imatinib (Gleevec ®), which has made another blood cancer,
chronic myelogenous leukemia, a controllable, chronic disease for many patients.
Chronic myelogenous leukemia (CML) is a human disease associated with a consistent chromosomal translocation that results in sequences from the c - abl locus on chromosome 9 being fused to sequences in a breakpoint cluster region (bcr) on chromosome 22.
New treatment strategies to overcome drug resistance in
chronic myelogenous leukemia and other cancers will come from the detailed structure of the enzyme Abl.
• Subject has BCR - ABL - positive leukemia (
chronic myelogenous leukemia in blast crisis).
An exciting development in rational anticancer drug design is Gleevac, a drug that acts on a protein unique to the defective white blood cells in
chronic myelogenous leukemia and on a related protein in a rare form of gastrointestinal cancer.
Immunodeficiency and
chronic myelogenous leukemia - like syndrome in mice with a targeted mutation of the ICSBP gene.
City of Hope researchers may have discovered a more effective treatment for patients with
chronic myelogenous leukemia (CML) according to a study published today in Nature Medicine.
During this time, she worked in the laboratory setting with MAPK signaling pathway in
Chronic Myelogenous Leukemia, for which she received an American Society of Clinical Oncology (ASCO) Young Investigator Award.
In support of the first tenet, both
chronic myelogenous leukemia (11) and acute myelogenous leukemia (12) seem to have arisen from the committed progenitor cells that have acquired self - renewing capabilities.
This work, and that of colleagues Brian Druker and Novartis, led to the development of the kinase inhibitor imatinib (Gleevec) as primary therapy for
chronic myelogenous leukemia (CML), and the discovery that imatinib resistance is caused by BCR - ABL kinase domain mutations.
About Blog I started this blog to keep my friends and family informed about my progress with
Chronic Myelogenous Leukemia (CML).
We have also documented that the same mutations are responsible for the development of certain cancers in humans and dogs, such as the BCR - ABL translocation in
chronic myelogenous leukemia.