A Worldwide Support Network For Chronic Myelogenous Leukemia
Posted by rob on May 30, 2005 under Uncategorized | 
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A whale jumps in the air. Australian Environment Minister Ian Campbell set off on a diplomatic lobbying mission to Europe and the Pacific as part of a campaign to undermine Japan’s push to increase its whale cul
Posted by rob on May 29, 2005 under Uncategorized | Be the First to Comment
A group of geese swim in a river in Guanghan city, in China’s southwestern province of Sichuan.
Posted by rob on May 28, 2005 under Uncategorized | Be the First to Comment
The European Union on Friday cleared the creation of world’s largest generic medicine producer but told Swiss drug maker Novartis AG it must shed some products in EU member states.
Under the EU-approved deal, Novartis acquired German generic drug maker Hexal and 67.7 percent of the U.S. company Eon Labs Inc.
The deal must still win clearance from the U.S. Federal Trade Commission, which submitted a request to Novartis on April 6, asking for additional information about the transaction.
(Novartis has a manufacturing plant northeast of Lincoln.)
Novartis will sell off some drugs in Poland, Germany and Denmark. The Swiss drug company must sell to a competitor Cacihexal, used to treat osteoporosis, in Poland. It also must sell an anti-rheumatic drug called Diclac in Germany and two drugs, Apurin and Allopurnol, in Denmark.
In the specific markets concerned, combining Novartis and Hexal drugs would have led to a dominant position.
Novartis purchased the privately owned Hexal along with a majority stake in New York-based Eon Labs from the Struengmann family for $8.3 billion in cash.
Novartis offered to divest products in selected markets after the EU extended its investigation of the takeover an additional two weeks.
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Hot-air balloons fly above Debrecen, 226 kms east of Budapest, Hungary during the 14th European Hot-Air Balloon Championships organized by the Federation Aeronautic International (FAI).
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For all the wonders of modern medicine, experts say that some aspects of cancer care remain old-fashioned. Many diagnoses are still made with light microscopes — technology that’s hundreds of years old, says Michael Heinrich, a professor at Oregon Health & Science University in Portland. And doctors have relatively few ways to tailor chemotherapy for individuals. “We give them all the same poison and there’s no way to tell who is going to respond and who isn’t,” Heinrich says.
Thanks to a better understanding of genes, however, doctors are finding new ways to provide more personalized therapies.
At the annual meeting of the American Society of Clinical Oncology in Orlando last week, scientists described a way to tailor therapy for a rare cancer called neuroblastoma. The tumor, a malignancy of the sympathetic nervous system, is the most common cancer in infants, striking about 650 children a year, typically at 17 months.
Because treatments can harm such small children, doctors are looking for ways to determine which children need aggressive treatments and which might benefit from gentler regimens, says Edward Attiyeh, a hematology/oncology fellow at Children’s Hospital of Philadelphia.
Treatments match genetics
Attiyeh and his colleagues say they have found a clue. Children whose tumors are missing part of chromosome 11 are more likely to die than other young patients. A study of more than 900 children found that only 65% of patients with the genetic change survived three years, compared with 83% of the other kids. That tells doctors which children need aggressive care and which can scale back treatment and avoid some toxic side effects. He hopes to isolate the genes involved, which could help researchers develop even better therapies.
In some cases, genetic markers help identify which patients will respond to particular drugs. The experimental drug Revlimid, for example, appears especially promising for some patients with myelodysplastic syndromes, or MDS, a cancer in which the bone marrow fails to make enough functioning blood cells. The disease strikes up to 15,000 people a year.
MDS patients receive transfusions as often as once or twice a month to treat their anemia and fatigue, says Alan List, a professor at the H. Lee Moffitt Cancer Center in Tampa. But repeated transfusions can lead to a toxic buildup called “iron overload” that can damage the heart, liver and pancreas.
Early studies suggested that Revlimid produces dramatic recoveries in people whose cancers are missing a hunk of chromosome 5, or about 20% to 30% of patients.
Based on that study, List and his colleagues tested Revlimid in 148 patients with this genetic change in a study funded by the drug’s manufacturer, Celgene Corp.
Doctors had hoped the drug would treat the symptoms of MDS. In some cases, however, Revlimid treated the disease itself, List says. After treatment, 97 patients no longer needed transfusions. Even more impressive, the drug erased all signs of the cancer’s genetic cause in 51 patients, putting the cancer into remission. List says it’s too soon to say if these patients are cured.
Doctors don’t know how long remissions will last. Patients who take other targeted therapies, such as Gleevec, need to take the drugs indefinitely to prevent relapse. And even Gleevec will eventually stop working for some patients.
Serious risks involved
But unlike Gleevec, which causes few severe side effects, Revlimid can pose serious risks, such as suppressing infection-fighting white blood cells and platelets, which aid clotting. Two-thirds of Revlimid patients had to lower their dose because of those problems, according to the study. Fifteen patients in the trial died, including two deaths that doctors suspect were caused by the drug. Revlimid, which has not been approved by the Food and Drug Administration, is similar to thalidomide, which caused birth defects in the 1950s. Doctors today are testing thalidomide in a blood cancer called multiple myeloma.
Patients such as Lynn Nance already are benefiting from this new research. Nance, a turkey farmer from Monroe, N.C., was diagnosed with MDS in 2000. He needed transfusions as often as twice a month before beginning Revlimid about a year ago.
Nance has only required one transfusion since. Although the drug has lowered his white cells and platelets, Nance is again able to work full time.
“It’s given me my life back,” says Nance, 69. “Now, I can go all day.”
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Oregon Health & Science University in Portland
Story from REDNOVA NEWS:
http://www.rednova.com/news/display/?id=151802
Published: 2005/05/25 06:00:00 CDT
RedNova News – Health – Tailored Treatments Take Aim at Cancer
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Cornet AD, Issa AI, Loosdrecht AA, Ossenkoppele GJ, van Schijndel RJ, Johan Groeneveld AB
Eur J Haematol. 2005 Jun ; 74(6): 511-6
OBJECTIVES: Poor survival of patients with a haematological malignancy admitted to the intensive care unit (ICU) prompts for proper admission triage and prediction of ICU treatment failure and long-term mortality. We therefore tried to find predictors of the latter outcomes. METHODS: A retrospective analysis of charts and a prospective follow-up study were done, of haemato-oncological patients, admitted to our ICU in a 7-year period with a follow-up until 2 yr thereafter. Clinical parameters during the first four consecutive days were taken to calculate the simplified acute physiology (SAPS II) and the sequential organ failure assessment (SOFA) scores, of proven predictive value in general ICU populations. RESULTS: From a total of 58 patients (n = 47 with acute myelogenous leukaemia or non-Hodgkin lymphoma), admitted into ICU mostly because of respiratory insufficiency, sepsis, shock or combinations, 36 patients had died during their stay in the ICU. Of ICU survivors (n = 22), 20 patients died during follow-up so that the 1-year survival rate was only 12%. The SAPS II and particularly the SOFA scores were of high predictive value for ICU and long-term mortality. CONCLUSIONS: Patients with life-threatening complications of haematological malignancy admitted to ICU ran a high risk for death in the ICU and on the long-term, and the risk can be well predicted by SOFA. The latter may help us to decide on intensive care in individual cases, in order to avoid potentially futile care for patients with a SOFA score of 15 or higher.
Posted by rob on May 27, 2005 under Uncategorized | Be the First to Comment
A woman rests on a cow-shaped bench in Hanover during the 30th Church Day organized by the German Protestants.
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Decision Resources, Inc., one of the world’s leading research and advisory firms focusing on pharmaceutical and health care issues, finds that longer treatment durations and the launch of novel treatments will grow the drug market for chronic myelogenous leukemia almost 12% annually between 2004 and 2009. Novel agents such as those from Bristol-Myers Squibb and Novartis will increase patient drug consumption by offering a viable, and likely durable, second-line pharmacological approach to the treatment of chronic myelogenous leukemia.
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Mutations in the kinase domain (KD) of BCR-ABL are the leading cause of acquired imatinib resistance. In some cases, identical mutations were detected at relapse and in pre-therapeutic specimens, consistent with selection of resistant clones in the presence of drug. However, the incidence of KD mutations in imatinib-naive patients, irrespective of response to therapy, is unknown. We studied mutation frequency in 66 CML patients, using cDNA sequencing and allele specific oligonucleotide (ASO) – PCR assays for 8 common mutations. Thirteen patients were positive by ASO-PCR only, 1 by ASO-PCR and sequencing in 1 patient and 1 by sequencing only (overall frequency 22.7%). T315I was most frequent (12% of patients). Eleven of the 14 ASO-PCR-positive patients had follow-up samples available for sequencing. Wild type sequence was detected in 6/11, two different mutations in 1/11 and identical mutations in 4/11 patients, two of whom had achieved major cytogenetic response. In multivariate analysis mutation detection was associated with clonal cytogenetic evolution, exposure to 6-Thioguanine and a low platelet count, but not with response to imatinib, event-free and overall survival. KD mutants present at low levels do not invariably lead to relapse and additional factors are required to induce a fully drug resistant phenotype.
High sensitivity detection of BCR-ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic ev | CMLHope.Com
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Imashuku S, Kakazu N, Ueda I, Morimoto A, Harada H, Teramura T, Tamura S, Fukushima-Nakase Y, Kuroda H
Int J Hematol. 2005 May ; 81(4): 310-4
A 26-year-old man with idiopathic hypereosinophilic syndrome (HES) was treated with imatinib mesylate following a 5-year history of prednisolone therapy. The patient had hypereosinophilia (absolute eosinophil counts >1500/3L) occurring in cyclic oscillations as well as histologically diagnosed eosinophilic vasculitis, bursitis, and periodic soft-tissue swellings. Laboratory data revealed high levels of serum tryptase and increased numbers of mast cells in the bone marrow, but serum interleukin 5 levels were within the normal range. The disease initially responded well to 100 mg/day of imatinib mesylate but recurred 8 weeks later.Thereafter, a daily 200-mg dose was temporarily effective. Despite the response to imatinib, the FIP1L1-PDGFRA fusion gene was not detected by fluorescence in situ hybridization analysis. Additional molecular and cytogenetic studies showed neither translocations of platelet-derived growth factor receptor (PDGFR) genes nor mutations in the c-KIT or the PDGFR genes.Although imatinib mesylate is a choice of treatment for patients with HES, its precise molecular mechanism in individual cases remains to be clarified.
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Maki K, Yamagata T, Asai T, Yamazaki I, Oda H, Hirai H, Mitani K
Blood. 2005 May 24;
The AML1/Evi-1 chimeric gene is created by the t(3;21)(q26;q22) chromosomal translocation seen in patients with leukemic transformation of myelodysplastic syndrome or blastic crisis of chronic myelogenous leukemia. We knocked-in the AML1/Evi-1 chimeric gene into mouse AML1 genomic locus to explore its effect in developmental hematopoiesis in vivo. AML1/Evi-1/+ embryo showed defective hematopoiesis in the fetal liver, and died around E13.5 due to hemorrhage in the central nervous system. The peripheral blood had yolk sac-derived nucleated erythroblasts but lacked erythrocytes of the definitive origin. While E12.5 fetal liver contained progenitors for macrophage only, E13.5 fetal liver contained multi-lineage progenitors capable of differentiating into dysplastic myelocyte and megakaryocyte. No erythroid progenitor was detected in E12.5 or E13.5 fetal liver. Hematopoietic progenitor from E13.5 AML1/Evi-1/+ fetal liver was highly self-renewal compared to that from wild-type liver. Maintained expression of PU.1 gene and decreased expression of LMO2 and SCL genes may explain the aberrant hematopoiesis in AML1/Evi-1/+ fetal liver.
Dysplastic definitive hematopoiesis in AML1/Evi-1 knock-in embryos.
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Liu MJ, Yue PY, Wang Z, Wong RN
Cancer Lett. 2005 Jun 28; 224(2): 229-41
Methyl protodioscin is a furostanol bisglycoside with antitumor properties. The present study investigated its effects on human chronic myelogenous leukemia K562 cells. Cell cycle analysis showed that methyl protodioscin caused distinct G(2)/M arrest, with the appearance of polyploidy population. The levels of cyclin B1 decreased, whereas Cdc2 kept at a steady level. Subsequent apoptosis after G(2)/M blockage was demonstrated through DNA fragmentation and the annexin V staining assay. Methyl protodioscin induced a biphasic alteration (i.e. an early hyperpolarization, followed by depolarization) in mitochondrial membrane potential of K562 cells. The transient decline of intracellular Ca(2+) concentration was observed at early stage. The generation of reactive oxygen species was also detected. The anti-apoptotic Bcl-x(L) transiently increased and then decreased. And the pro-apoptotic Bax was markedly up-regulated. Taken together, these data demonstrated that methyl protodioscin inhibits K562 cell proliferation via G(2)/M arrest and apoptosis, with mitochondrial hyperpolarization and the disruption of Ca(2+) homeostasis playing important roles.
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Matsuda M, Morita Y, Shimada T, Miyatake J, Hirase C, Tanaka M, Tatsumi Y, Maeda Y, Kanamaru A
Int J Hematol. 2005 May ; 81(4): 307-9
We describe a patient with Philadelphia chromosome (Ph)-positive chronic myelogenous leukemia (CML) who developed an extramedullary blast crisis in the central nervous system (CNS) and then a subcutaneous tumor of the neck during treatment with imatinib mesylate.Administered 400 mg of imatinib mesylate after the diagnosis of chronic-phase CML, the patient achieved a complete cytogenetic remission 4 months later. However, he developed a mixed myeloid/B-cell blast crisis with additional karyotype abnormalities only in the CNS during a complete cytogenetic remission in the bone marrow. Several doses of intrathecal chemotherapy and whole-brain irradiation were effective in treating the blast crisis in the CNS. After 7 months of complete cytogenetic remission, the patient experienced a subcutaneous tumor in the right neck. A biopsy of the tumor revealed a mixed myeloid/T-cell blast crisis.The cytogenetic analysis showed that the blast crisis clone in the neck tumor was different from that of the CNS. An increased dose of imatinib mesylate was ineffective in treating the neck tumor. Irradiation to the right neck was therefore undertaken.This case suggests that the development of a clone resistant to imatinib mesylate is not always detected in the bone marrow and that multiple Ph-positive clones have the potential to become transformed into a blast crisis.
Posted by rob on May 26, 2005 under Uncategorized | Be the First to Comment
Turkish military cadets march prior performance at the begining of the UEFA Champions league football final AC Milan vs Liverpool at the Ataturk Stadium in Istanbul.
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A Russian couple enjoy the warm weather standing next to a fountain in Manezh Square in central Moscow.
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Paragliders are seen above the Swiss Alps during the Swiss Paragliding Championships near Lenk, western Switzerland.
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Lightening is seen in the sky over Istanbul on a rainy night as a cargo ship sails along the Bosphorous.
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Wild goats cross a road in Fuerteventura Island, one of the Spanish Canary islands.
Posted by rob on May 21, 2005 under Uncategorized | Be the First to Comment
We had a database failure of the CMLHope.Com site yesterday. We are trying to restore user accounts and archives from the backup.
We were in the process of adding live feeds of news and medical articles when the database crashed. We now have a live feed of the latest medical articles on CML along with other cancer and health news on the left side of the page. This will be automatically updated once each hour 24 hours a day.
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The pack rides through the countryside during the 12th stage of the 88th cycling Tour of Italy, between Alleghe and Roveretto.
