A Worldwide Support Network For Chronic Myelogenous Leukemia
Posted by rob on November 30, 2004 under Uncategorized | 
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Clione or ’sea angels’ swim in a Tokyo aquarium. The Clione, which lives mostly in temperate waters, can be found in the Okhotsk Sea, off the northeastern part of Hokkaido in Japan.
Posted by rob on November 29, 2004 under Uncategorized | Be the First to Comment
- Results Will Be Presented Dec. 5 at Annual American Society
of Hematology Conference -
WHITE PLAINS, N.Y., NOV. 29 /PRNewswire/ — Alan Kinniburgh, Senior Vice
President for Research for The Leukemia & Lymphoma Society, is available to
discuss clinical findings showing the overwhelming success of a new drug,
BMS-354825, in overcoming resistance to Gleevec, the frontline therapy for
chronic myelogenous leukemia.
Dr. Kinniburgh will be available at the American Society of Hematology
conference in San Diego on Sunday, Dec. 5, when the findings of the Phase I
clinical trial will be presented by Charles Sawyers, M.D., the lead
investigator of the team.
The Leukemia & Lymphoma Society led the way in funding the research that
led up to this clinical trial, with a $7.5 million Specialized Center of
Research (SCOR) grant over a 5-year period.
To arrange an interview with Dr. Kinniburgh, contact him on his cell phone
at 914-837-6650, or contact Jennifer Corrigan at 732-382-8898 (office), or
732-742-7148 (cell).
http://www.prnewswire.com/cgi-bin/stories.pl?ACCT=109&STORY=/www/story/11-29-2004/0002550970&EDATE=
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Researchers at the National Cancer Institute (NCI), part of the National Institutes of Health (NIH), have found that inhibition of the same protein produces different effects in mouse cell lines depending on whether those cell lines express normal or cancerous forms of Kit, a cell surface receptor critical for the development of some kinds of blood cells. These findings, appearing in the journal Blood online*, November 2004, reveal a potential new target for treating certain blood cell disorders.
From U.S. NIH:
Protein Plays Different Roles in Growth of Normal and Cancerous Mouse Cell Lines
Researchers at the National Cancer Institute (NCI), part of the National Institutes of Health (NIH), have found that inhibition of the same protein produces different effects in mouse cell lines depending on whether those cell lines express normal or cancerous forms of Kit, a cell surface receptor critical for the development of some kinds of blood cells. These findings, appearing in the journal Blood online*, November 2004, reveal a potential new target for treating certain blood cell disorders.
A specific mutation affecting the catalytic domain of the Kit receptor results in a cancerous form of Kit found in patients with mast cell disease and some forms of acute myeloid leukemia. This particular Kit mutant, known as D814Y, is resistant to Gleevecâ?¢, a drug used to treat a variety of diseases associated with Kit and related proteins. Other types of cancer, including gastrointestinal stromal cell tumors, have different Kit mutations that are sensitive to Gleevec. One potential way to circumvent the Gleevec-resistant form of Kit is to target one or more of the proteins that are activated by Kit.
NCI researchers Diana Linnekin, Ph.D., and Tanya Jelacic, Ph.D., found that inhibition of one such Kit-activated protein, PKCδ (a member of a family of protein kinases involved in cell signaling), reduced the growth of a mouse mast cell line expressing the D814Y mutant Kit by approximately 40 percent. In contrast, PKCδ inhibition did not suppress the growth of normal mast cells. ”This is the first demonstration of a function change in PKCδ resulting from a cancerous mutation in a growth factor receptor,” said Linnekin.
Because anti-PKCδ drugs would specifically inhibit the growth of mutated cells and not affect normal ones, these results suggest that PKCδ may be a therapeutic target for mast cell disease associated with the D814Y mutation in Kit and possibly for other disorders associated with Kit catalytic domain mutations. ”This work is a promising study on cancer inhibition,” said Linnekin. ”Dr. Jelacic and I believe that follow-up work with human cell lines, as well as work in mouse models of cancer, would be definitely worthwhile.”
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Title: Pic Of The Day
Date: 11/28/2004 9:12:17 PM
A supporter of Ukrainian opposition leader Viktor Yushchenko holds a rose during a rally in Kiev.
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A supporter of Ukrainian opposition leader Viktor Yushchenko holds a rose during a rally in Kiev.
Posted by rob on November 28, 2004 under Uncategorized | Be the First to Comment
Story last updated at 7:28 a.m. Sunday, November 28, 2004
Minority marrow donors in short supply
Matches are usually dictated by race, leaving many who need transplants at a disadvantage
BY HOLLY AUER
Of The Post and Courier Staff
If you’re white and need a bone marrow transplant, your chances of finding a nonrelated donor who’s a perfect genetic match are about one in a million. It may sound unlikely, but you’ll probably get one, since there are more than 5 million people enrolled as potential donors in the National Bone Marrow Donor Program.
If you’re black, Asian or Native American, though, the odds plummet, because there aren’t enough people in those groups in the national registry. The genes that correlate to donor matches are usually tied to race, so minorities are at a disadvantage when awaiting a transplant.
Siblings offer the greatest chance for a genetic match, but only 30 percent of people who need transplants, most of whom have leukemia, are able to find a donor in their family. As family size continues to decrease — the average number of children per family is now 1.86 according to the 2000 Census — doctors expect more people will need to tap into the registry.
Each year, about 35,000 people in the United States are diagnosed with diseases for which a marrow or blood cell transplant could be a cure.
“A bone marrow transplant used to be a treatment of last resort,” said Dr. George Geils Jr., medical director of Roper Hospital’s blood and marrow transplant program. “But improving technologies and improving mortality rates have really made it the best option for a lot of patients.”
When Janie Goodin, a 62-year-old Awendaw resident who is black, learned she had chronic myelogenous leukemia in 2002, her doctor put her on Gleevec, what many called a leukemia wonder drug. For her, though, the side effects were almost worse than the disease itself, and it became clear that she would need a bone marrow transplant.
She hoped one of her four sisters would be a match, but weeks went by before she found out. The whole time, she worried that she’d have to seek out that perfect match from the donor registry.
“The doctor told me my chances wouldn’t be as good that way,” she said. “The anxiety is unbelievable. Day by day, you don’t know what’s going to happen.”
One of her sisters did prove to be a match, and Goodin had her transplant in late September.
Today, she’s back on her feet and encouraging everyone who will listen to get on the marrow donor registry.
“If you get this disease, what are you going to do if you don’t have a donor?” she said. “You can die while you wait.”
Seventy-eight people turned out at Roper Hospital’s bone marrow donor registration drive last week, and 30 percent of those were minorities, which is more than the national average of 25 percent, noted Sarah Hathcock, a registered nurse who organized the drive.
Getting the word out to black churches has been a crucial way to draw more minority donors, she said.
“They have a lot of questions, but if we can get them in here, we can give them all the information,” Hathcock said. “The more people we have on the registry, the better chance somebody has … of matching.”
Goodin said she believes the minority donor shortage stems from a lack of education about the process. Two of her four sisters were afraid even to be tested, because they believed donating marrow is like donating a kidney, with many risks and a long recovery time.
“One sister said, ‘What’s gonna happen to my hip?’ One said, ‘Are they going to take all my blood?’” I couldn’t convince them,” Goodin said. “They didn’t believe that you can do this and not be sick.”
Doctors need blood stem cells, the tiniest building blocks of blood, from the bone marrow to conduct a transplant, which then leads to regeneration of healthy marrow in sick patients. Although donating marrow once required a procedure under general anesthesia, people now may donate stem cells through an IV catheter during a short, painless outpatient procedure.
Goodin said her sister went right back to work after her donation.
“It was so easy, she didn’t even have an ache or a pain,” she said. “It’s a shame that black people don’t realize that this thing is nothing that’s going to destroy them. It’s not a big deal.”
Free registration drives are offered several times a year throughout the Lowcountry. For more information about bone marrow donation, call the Red Cross at 744-8021, ext. 371, or visit www.marrow.org.
Holly Auer covers health and medicine. Reach her at (843) 937-5560 or hauer@postandcourier.com.
Copyright c 2004, The Post and Courier, All Rights Reserved.
Comments about our site, write: webmaster@postandcourier.com
http://www.charleston.net/stories/112804/loc_28marrow.shtml
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Leukemia. 2004 Dec; 18(12): 1951-63
Weisberg E, Catley L, Kujawa J, Atadja P, Remiszewski S, Fuerst P, Cavazza C, Anderson K, Griffin JD
NVP-LAQ824 is a novel potent hydroxamic acid-derived histone deacetylase inhibitor that induces apoptosis in nanomolar concentrations in myeloid leukemia cell lines and patient samples. Here we show the activity of NVP-LAQ824 in acute myeloid leukemia cells and BCR/ABL-expressing cells of mouse and human origin, both sensitive and resistant to imatinib mesylate (Gleevec, STI-571). Whereas imatinib inhibited overall cellular tyrosine phosphorylation in Ba/F3.p210 cells, NVP-LAQ824 did not inhibit tyrosine phosphorylation, and did not affect BCR/ABL or ABL protein expression. Neither compound was able to inhibit cellular tyrosine phosphorylation in the imatinib-resistant Ba/F3.p210-T315I cell line. These data taken together suggest that BCR/ABL kinase activity is not a direct target of NVP-LAQ824. Synergy between NVP-LAQ824 and imatinib was demonstrated against BCR/ABL-expressing K562 myeloid leukemia cell lines. In addition, we show that NVP-LAQ824 was well tolerated in vivo in a pre-clinical murine leukemia model, with antileukemia activity resulting in significant prolongation of the survival of mice when treated with NVP-LAQ824 compared to control mice. Taken together, these findings provide the framework for NVP-LAQ824 as a novel therapeutic in myeloid malignancies.Leukemia (2004) 18, 1951-1963. doi:10.1038/sj.leu.2403519 Published online 21 October 2004.
http://www.hubmed.org/display.cgi?issn=08876924;uids=15496979
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Acta Haematol. 2004; 112(4): 225-226
Matsumoto Y, Nomura K, Shimizu D, Takeshima Y, Ueda K, Nakao M, Morita M, Yokota S, Horiike S, Taniwaki M
http://www.hubmed.org/display.cgi?issn=00015792;uids=15564738
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Acta Haematol. 2004; 112(4): 217-218
Arimura K, Arima N, Ohtsubo H, Matsushita K, Kukita T, Ayukawa T, Kuroki T, Tei C
Interferon (IFN)-alpha is a leukocyte-derived cytokine and is used to treat several hematopoietic malignancies. The most common adverse effects of IFN-alpha are flu-like symptoms and usually insignificant. However, adverse effects due to autoimmune mechanisms are often hazardous and irreversible, although their frequency is low. In the present report, we describe a 55-year-old female with chronic myelogenous leukemia who developed severe autoimmune thrombocytopenia during IFN-alpha therapy. The lowest platelet count was 6 x 10(9)/l with severe hemorrhagic tendency. The present report strongly suggests the clinical importance of autoimmune thrombocytopenia as an adverse effect of IFN-alpha. Copyright (c) 2004 S. Karger AG, Basel.
http://www.hubmed.org/display.cgi?issn=00015792;uids=15564735
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Hematology (Am Soc Hematol Educ Program). 2004; 146-62
O’brien S, Tefferi A, Valent P
In Section I, Dr. Stephen O’Brien reviews the latest data on the clinical use of imatinib (STI571, Gleevec, Glivec) in CML. His review focuses on the use of imatinib in newly diagnosed chronic phase patients and summarizes cytogenetic and molecular response data, as well as use of the agent at high doses and in combination with other drugs. A brief summary of the prospective international Phase III studies that are currently ongoing is also provided, and the issues of resistance and definition of suboptimal therapeutic response are also covered. Finally, therapeutic decision-making and treatment strategy are considered. In Section II, Dr. Ayalew Tefferi considers the latest developments in the biology and therapy of myeloid metaplasia/myelofibrosis. Dr. Tefferi covers what is currently understood of the biology of the disease and reviews established therapies for the condition as well as novel agents that are being used in clinical trials. The development of optimal management strategies for the disease is considered. In Section III, Dr. Peter Valent reviews the classification of mast cell proliferative disorders and covers the clinical and pathological presentation of this group of neoplasms. He reviews the state-of-the-art regarding the molecular biology of mastocytosis along with diagnostic criteria and novel treatment concepts.
http://www.hubmed.org/display.cgi?issn=15204391;uids=15561681
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http://www.hubmed.org/display.cgi?issn=1607551X;uids=15553811
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http://www.hubmed.org/display.cgi?issn=04851439;uids=15553045
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A man travels in a bus decorated by an advertisement promoting shopping in Hong Kong.
Posted by rob on November 27, 2004 under Uncategorized | Be the First to Comment
A supporter of Ukrainian opposition leader Viktor Yushchenko attends a rally in Kiev’s main square to protest against the presidential election results.
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A balloon flies next to the top of Berlin’s Cathedral
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Europe’s tallest Christmas tree, located in a square outside the 16th century monastery of Jeronimos in Lisbon, reaches a height of 62 metres or 20 storeys, and is decorated with two million lights.
Posted by rob on November 24, 2004 under Uncategorized | 2 Comments to Read
Moount of Temptation : Dark clouds sit above the Mount of Temptation around the Dead Sea during sunset near the Israeli West Bank settlement of Maale Adumim.
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An airplane plane flies past the moon in the skies of the German southern town of Nuremberg.
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Researchers at the National Cancer Institute (NCI), part of the National Institutes of Health (NIH), have found that inhibition of the same protein produces different effects in mouse cell lines depending on whether those cell lines expressing normal or cancerous forms of Kit, a cell surface receptor. These findings, appearing in the journal Blood online on November 12, reveal a potential new target for treating certain blood cell disorders.
Kit is critical for the development of certain blood cells, and mutations in Kit are associated with several diseases in mast cells, a type of white blood cell involved in immune responses. Gleevec, a drug that inhibits Kit and other related proteins, has been useful in the treatment of diseases associated with these proteins, including gastrointestinal stromal cell tumors and chronic myeloid leukemia. However, an activating mutation in Kit commonly found in mast cell disease and some forms of acute myeloid leukemia is resistant to Gleevec. Therefore, one potential method of circumventing a drug-resistant form of Kit would be to target one or more of the proteins activated by it.
NCI researchers Diana Linnekin, Ph.D., and Tanya Jelacic, Ph.D., found that inhibition of one such Kit activated protein, PKCδ <PKCdelta> (a member of a family of protein kinases involved in cell signaling), reduced the growth of a mouse mast cell line expressing mutant Kit by approximately 40 percent, while the growth of normal mast cells was not inhibited. “This is the first demonstration of a function change in PKCδ <PKCdelta> resulting from an oncogenic mutation in a growth factor receptor,” said Linnekin.
These results suggest that PKCδ <PKCdelta> may be a therapeutic target for diseases associated with mutations in Kit, since anti-PKCδ <PKCdelta> drugs would specifically inhibit the growth of mutated cells and not affect normal ones. “This work is a promising study on cancer inhibition,” said Linnekin. “Dr. Jelacic and I believe that follow-up work with human cell lines, as well as work in mouse models of cancer, would be definitely worthwhile.”
For more information about cancer, visit the NCI Web site at http://www.cancer.gov or call NCI’s Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).
Editor’s Note: The original news release can be found here.
http://www.sciencedaily.com/releases/2004/11/041118112702.htm
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| MAUREEN ROUHI | |||||
Peptides immobilized on a surface plus mass spectrometry equals rapid and direct analysis of kinase activities, a new study shows [Angew. Chem. Int. Ed., 43, 5973 (2004)]. Developed by University of Chicago researchers Dal-Hee Min, Jing Su, and Milan Mrksich, the strategy avoids the complications of traditional kinase assays, including use of radioactive labels or antibody binding. Kinases mediate the phosphorylation of specific substrates. They have many regulatory functions, and assaying kinase activity is key in many research areas, including drug discovery. Using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, the Chicago team evaluates kinase activity from the spectra of peptides, immobilized on a gold substrate, before and after exposure to a kinase-mediated phosphorylation. In the after spectrum, the mass peak of the kinase’s substrate is replaced by that of the product. The team applied the method to six kinases. The kinase reaction yielded a mass change of 80, due to addition of a phosphate group to each substrate. Multiple kinase activities can be measured by exposing a peptide array sequentially to different kinases. The assay also can be used to measure kinase inhibition. Results for the inhibition of the kinase Ab1 by the anticancer drug Gleevec are within the range of values reported in the literature. “The most significant aspect of our work has been the development of surfaces that allow both quantitative assays of enzyme activity and readout by mass spectrometry,” Mrksich says. “These tailored substrates simplify the use of mass spectrometry for analyzing enzymatic activities and therefore move this technique closer to routine use in research laboratories.” |
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| Chemical & Engineering News ISSN 0009-2347 Copyright © 2004 |
