Learning The Language of CML Lab Tests
Posted by rob on September 16, 2004 under Uncategorized | 
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Pic Of The Day
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Waiting before the storm
Cytogenetic and Clinical analysis of -7/7q- Abnormalities in Acute Leukemia and Myelodysplastic Syndrome
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[Cytogenetic and Clinical analysis of -7/7q- Abnormalities in Acute Leukemia and Myelodysplastic Syndrome]
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2004 Aug ; 12(4): 460-3
The objective was to study the incidence and prognosis significance of -7/7q- abnormalities in acute leukemia and myelodysplastic syndrome. Conventional cytogenetic analysis of R-band was used to test -7/7q- chromosome abnormalities in 410 patients with acute leukemia (AL), in 71 cases of myelodysplastic syndrome (MDS) and in 36 cases of chronic myelogenous leukemia in accelerated phase (CML-AP). The results showed that the incidences of -7/7q- abnormalities in AL, MDS and CML-AP patients were 4.88%, 9.86% and 8.33% respectively. The -7/7q- abnormalities could be found in acute myeloblastic leukemia (AML) and acute lymphocytic leukemia (ALL), incidences of which were 4.70% and 6.25% (P > 0.05) respectively. 9 cases had -7 or 7q- as the sole chromosome abnormalities, 22 cases showed other additional chromosome abnormalities: -X, -5, +8, t(3; 3), t(11;16) and t(2;11). Monosomy -7 and 7q- abnormality clone was found in one patient with MDS-RAEB, and the number of cells with -7 abnormality was greater than that of 7q- abnormality cells. Four patients acquired CR among 7 patients with ALL after chemotherapy, but 2 out of 13 patients with AML achieved CR while 6 out of 7 patients with MDS transformed into AL. No patients with CML-AP achieved CR. In conclusion, -7/7q- is a frequent aberration in hematologic malignancies as well as AML and ALL. The monosomy -7 and 7q-abnormalities were detected in the same patient. The patients with -7/7q- abnormalities show poor prognosis.
http://www.hubmed.org/display.cgi?issn=10092137&uids=15363131
Eosinophilic gastroenteritis or eosinophilic chloroma?
Posted by rob on September 15, 2004 under Uncategorized | Be the First to Comment
Eosinophilic gastroenteritis or eosinophilic chloroma?
Acta Haematol. 2004; 112(3): 164-6
Granulocytic sarcoma of the small intestine preceding or as the presenting feature of acute myelogenous leukemia with chromosome 16 abnormalities has been observed in at least 4 patients. We report the case of a patient initially diagnosed with eosinophilic gastroenteritis, responding to corticosteroid treatment for 21 months and eventually transforming into an acute myelogenous leukemia with eosinophilia (M4Eo variant).
http://www.hubmed.org/display.cgi?issn=00015792&uids=15345900
Pic Of The Day
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I took pictures of some of the spiderlillies from the yard today while they still look good before we get the effects of Hurricane Ivan in the next several days.
Diagnosis and conservative treatment of gastrointestinal stromal tumors (GIST)
Posted by rob on September 14, 2004 under Uncategorized | Be the First to Comment
[Diagnosis and conservative treatment of gastrointestinal stromal tumors (GIST)]
Dtsch Med Wochenschr. 2004 Aug 20; 129(34-35): 1808-10
http://www.hubmed.org/display.cgi?issn=00120472&uids=15314745
Gastrointestinal stromal tumors (GIST)–current concepts of surgical management
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[Gastrointestinal stromal tumors (GIST)--current concepts of surgical management]
Dtsch Med Wochenschr. 2004 Aug 20; 129(34-35): 1817-20
http://www.hubmed.org/display.cgi?issn=00120472&uids=15314746
Presentation of extramedullary acute myelogenous leukemia as bilateral testicular masses
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Presentation of extramedullary acute myelogenous leukemia as bilateral testicular masses: response to non-myeloablative allogeneic transplantation.
Leuk Lymphoma. 2004 Jul ; 45(7): 1481-3
We present an unusual case of extramedullary acute myelogenous leukemia (AML) presenting as bilateral testicular masses. The patient subsequently developed diffuse skin lesions and bone marrow involvement. Although he had only a partial response to intensive chemotherapy, the patient obtained a complete remission after non-myeloablative allogeneic transplantation.
http://www.hubmed.org/display.cgi?issn=10428194&uids=15359653
Allogeneic hematopoietic stem cell transplantation with non-myeloablative conditioning
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Allogeneic hematopoietic stem cell transplantation with non-myeloablative conditioning in patients with acute myelogenous leukemia eligible for conventional allografting: a prospective study.
Ruiz-Argüelles GJ, Gómez-Almaguer D, David-Gomez-Rangel J, Vela-Ojeda J, Cantú-RodrÃguez OG, Jaime-Pérez JC, González-Llano O, Herrera-Garza JL
Leuk Lymphoma. 2004 Jun ; 45(6): 1191-5
Using a non-myeloablative stem cell trasplantation (NST) program, 25 allografts were prospectively given to 24 patients with acute myelogenous leukemia (AML) eligible for conventional allografting; 2 individuals had secondary forms of AML. The median age of the patients was 35 years, with a range of 12 to 56. All patients engrafted; median time to achieve an absolute neutrophil count > 0.5 x 10(9)/1 was 12 days (range 0-26), whereas the median time to a platelet count > 20 x 10(9)/1 was 13 days (range 0-26). Patients developed mixed chimerism 15 to 100 (median 30) days after the allograft. The follow-up periods range between 33 and 2670 days (median 450). The median post-transplant overall survival of the patients has not been reached and is above 89 months, whereas the 683 days both overall and progression-free survival is 66%. In 14 grafts (56%) acute GVHD ensued; in 12 cases grades I-II and in 2 cases grade IV which was fatal in both. In 9/19 patients (47%) limited chronic GVHD developed. In 22 cases (88%), the procedure could be completed fully on an outpatient basis. The 100-day and the transplant-related mortality were both 8%. NST appears to be an effective additional therapeutic option for patients with AML in remission and a matched donor available.
http://www.hubmed.org/display.cgi?issn=10428194&uids=15360000
Clinical impact of graft-versus-host disease against leukemias not in remission
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Clinical impact of graft-versus-host disease against leukemias not in remission at the time of allogeneic hematopoietic stem cell transplantation from related donors. The Japan Society for Hematopoietic Cell Transplantation Working Party.
Kataoka I, Kami M, Takahashi S, Kodera Y, Miyawaki S, Hirabayashi N, Okamoto S, Matsumoto N, Miyazaki Y, Morishita Y, Asai O, Maruta A, Yoshida T, Imamura M, Hamajima N, Matsuo K, Harada M, Mineishi S
Bone Marrow Transplant. 2004 Sep 13; ():
Summary:Acute graft-versus-host disease (GVHD) increases post-transplant mortality and morbidity, but exerts a potent graft-versus-leukemia (GVL) effect. To clarify the impact of GVHD on outcome after transplant in aggressive diseases, patients with acute myeloid or lymphoblastic leukemia (AML, n=366 or ALL, n=255) in nonremission states, or chronic myelogenous leukemia (CML, n=180) in accelerated phase (AP) or blastic crisis (BC), who received allogeneic hematopoietic stem cell transplantation (HSCT) from a related donor between 1991 and 2000, were analyzed. Significant improvement in overall and disease-free survival (DFS) was detected with grade I acute GVHD in AML (P=0.0002 for overall survival and 0.0009 for DFS, respectively) and in CML (P=0.0256 and 0.0366, respectively), while the trend towards improved survival was observed in ALL. Relapse rate was lower in grade I acute GVHD than in grade II in all three diseases, suggesting that treatment for grade II GVHD may compromise the GVL effect associated with GVHD. Chronic GVHD was found to suppress relapse in CML and ALL, but not in AML, although no improvement in survival was observed in any disease category. Our results suggest that treatment for grade II acute GVHD may need to be attenuated in transplant for refractory leukemias.Bone Marrow Transplantation advance online publication, 13 September 2004; doi:10.1038/sj.bmt.1704659
http://www.hubmed.org/display.cgi?issn=02683369&uids=15361916
Pic Of The Day
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A giant kite in the form of an Australian outback windmill floats above surfers at Bondi Beach in Sydney.
After chronic myelogenous leukemia: tyrosine kinase inhibitors in other hematologic malignancies.
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After chronic myelogenous leukemia: tyrosine kinase inhibitors in other hematologic malignancies.
Blood. 2004 Sep 9; ():
Tyrosine kinases phosphorylate proteins on tyrosine residues, producing a biological signal that influences many aspects of cellular function including cell growth, proliferation, differentiation and death. Constitutive or unregulated activity through mutation or over expression of these enzymes is a common pathologic feature in many acute and chronic leukemias. Inhibition of tyrosine kinases represents a strategy to disrupt signaling pathways that promote neoplastic growth and survival in hematologic malignancies, and likely in other neoplasias as well. This review will focus on tyrosine kinases that have been implicated in the pathogenesis of hematologic diseases other than chronic myelogenous leukemia (CML) and will discuss the evidence for the use of small molecules to target these kinases.
http://www.hubmed.org/display.cgi?issn=00064971&uids=15358622
Two Ph Chromosome positive chronic myelogenous leukemia patients with rare bcr/abl fusion gene
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[Two Ph Chromosome positive chronic myelogenous leukemia patients with rare bcr/abl fusion gene]
Zhonghua Xue Ye Xue Za Zhi. 2004 Jul ; 25(7): 409-12
OBJECTIVE: To investigate the unusual bcr/abl fusion gene structures of two Ph chromosome positive chronic myelogenous leukemia (CML) patients in chronic phase (CP). METHODS: By using general M- and micro -bcr/abl specific primers respectively, bcr/abl fusion transcripts were detected by reverse transcription-polymerase chain reaction (RT-PCR). The RT-PCR products sequencing was performed, the DNA sequences were analyzed in Genebank and the bcr and abl sequences at the fusion site were identified. DNA was amplified by PCR using a set of primers designed according to the sequencing result of RT-PCR products. RESULTS: Two patients showed typical manifestations of CML-CP. Their RT-PCR products were different from usual M- or micro -type; one was longer than M-bcr/abl but shorter than micro -bcr/abl, the other one was shorter than M-bcr/abl. The RT-PCR products sequencing showed that both products contained bcr and abl gene sequences. The first patient’s bcr gene was broken within exon 18, and fused to abl gene exon 2(a2), and a 40 bp of partial abl intron 1b fragment was inserted between them, resulting in a novel in-frame bcr/abl fusion transcript-e18-int-a2 which has not been reported in the literature so far. In the second patient, deletion of abl exon2(a2) led to exon 13(b2) of bcr gene fusing with abl exon 3(a3). CONCLUSION: Uncommon bcr/abl fusion gene may occur in typical Ph(+) CML patient.
http://www.hubmed.org/display.cgi?issn=02532727&uids=15355693
Prevalence and clinical significance of FLT3 internal tandem duplication mutation in acute leukemia
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[Prevalence and clinical significance of FLT3 internal tandem duplication mutation in acute leukemia]
Zhonghua Xue Ye Xue Za Zhi. 2004 Jul ; 25(7): 393-6
OBJECTIVE: To evaluate the prevalence of FLT3 mutation-internal tandem duplication in acute leukemia (AL) patients and its significance. METHODS: Genomic DNAs from 194 cases of AL were screened by polymerase chain reaction (PCR) and gel electrophoresis for FLT3-ITD mutations. RESULTS: FLT3-ITDs were found in 37 (25.9%) of 143 de novo acute myeoloid leukemia (AML) patients, including 10/53 of M(2), 15/40 of M(3), 4/20 of M(4) and 8/23 of M(5). Significantly more FLT3 aberrations were found in AML M(3) and M(5) (P < 0.05). No FLT3-ITD was found in 25 acute lympoid leukemia (ALL), 2 acute hybrid leukemia, 17 myelodysplastic syndromes and 7 chronic myelogenous leukemia in blast crisis. Sequence analysis of 5 cases with abnormal PCR electrophoretic patterns revealed that the ITDs were located within exon 14 from 21 bp to 60 bp, in 3 cases the ITD was a simple tandem duplication, and in 2 cases the ITD was tandem duplication with insertion, but all of the above ITD did not altered the FLT3 reading frame. FLT3-ITD was associated with a higher peripheral white cell count (P < 0.05) and a lower complete remission rate (P < 0.05), and was more prevalent in patients with normal karyotype (P < 0.05). CONCLUSION: FLT3-ITD mutation occurs with a significant percentage in AML M(3) and M(5) patients. Sequences of the mutants are in frame mutation. FLT3-ITD mutation was associated with a higher peripheral white cell count and a lower complete remission rate.
http://www.hubmed.org/display.cgi?issn=02532727&uids=15355689
A prototype antibody microarray platform to monitor changes in protein tyrosine phosphorylation.
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A prototype antibody microarray platform to monitor changes in protein tyrosine phosphorylation.
Mol Cell Proteomics. 2004 Sep 8; ():
Reversible protein phosphorylation is a key regulatory process in all living cells. Deregulation of modification control mechanisms, especially in the case of tyrosine, may lead to malignant transformation and disease. Phosphotyrosine (p-Tyr) accounts for only 0.05% of the total cellular phospho-amino acid content, yet plays an unusually prominent role in eukaryotic signaling, development, and growth. Tracking temporal and positional p-Tyr changes across the cellular proteome, i.e. tyrosine phosphoproteomics, is therefore tremendously valuable. Here, we describe and evaluate a prototype antibody (Ab) micro-array platform to monitor changes in protein Tyr phosphorylation. Availability permitting, a virtually unlimited number of Abs, each recognizing a specific cellular protein, may be arrayed on a chip, incubated with total cell or tissue extracts or with biological fluids, and then probed with a fluorescently labeled p-Tyr-specific monoclonal Ab, PY-KD1, specifically generated for this assay as part of the current study. The optimized protocol allowed detection of changes in the Tyr phosphorylation state of selected proteins using submicrogram to low nanogram of total protein extract, amounts that may conceivably be obtained from a thousand to a hundred thousand cells, or less, depending on the cell or tissue type. The assay platform was evaluated by assessing changes in a rationally selected subset of the Tyr phosphoproteome of Bcr-Abl-expressing cells treated with a specific inhibitor, Gleevec, and of EGF-treated HeLa cells. The results, ratiometric rather than strictly quantitative in nature, conformed with previous identifications of several Bcr-Abl and EGF receptor targets, and associated proteins, as detected by exhaustive mass spectrometric analyses. The Ab micro-array method described here offers advantages of low sample and reagent consumption, scalability, detection multiplexing, and potential compatibility with micro-fluidic devices and automation. The system may hold particular promise for dissecting signaling pathways, molecular classification of tumors and profiling of novel target-cancer drugs.
http://www.hubmed.org/display.cgi?issn=15359476&uids=15358805
Pic Of The Day
Posted by rob on September 10, 2004 under Uncategorized | Be the First to Comment
Hurricane Ivan is seen south of the Hispaniola and southeast of Jamaica
The Jab1/ COP9 signalosome subcomplex is a downstream mediator of Bcr-Abl kinase activity and facilitates cell cycle progression.
Posted by rob on September 9, 2004 under Uncategorized | Be the First to Comment
The Jab1/ COP9 signalosome subcomplex is a downstream mediator of Bcr-Abl kinase activity and facilitates cell cycle progression.
Blood. 2004 Sep 7; ():
Jab1 is a multifunctional protein associated with the signaling pathway, cell cycle regulation and development, and acts as a key subunit of COP9 signalosome (CSN). Jab1 promotes degradation of the cyclin-dependent kinase inhibitor p27(Kip1) by transportation from the nucleus to the cytoplasm. However, there has been no clear evidence for whether and how Jab1 contributes to malignant transformation in human cancers. Here we show that Bcr-Abl tyrosine kinase facilitates the downregulation of p27 by modulating complex formation of Jab1/CSN through the MAP kinase and PI3 kinase signaling pathways. Nearly half of the chronic myelogenous leukemia cell lines and the murine hematopoietic precursor cells expressing Bcr-Abl exhibited a marked increase in the small Jab1complex located in the cytoplasm. Inhibition of Bcr-Abl kinase by STI571 induced G1 arrest and caused a recovery of the p27 level with reduction of the small Jab1complex from the cytoplasm. Either blockade of the MAP kinase and PI3 kinase pathways by specific inhibitors or Jab1-knockdown by siRNA prevented p27 downregulation as well as formation of the small complex. Thus, regulation of p27 via modulation of the Jab1 subcomplex is a novel mechanism whereby Bcr-Abl oncogenic signals accelerate abnormal cell proliferation.
http://www.hubmed.org/display.cgi?issn=00064971&uids=15353483
The modulation of radiation-induced cell death by genistein in K562 cells: Activation of thymidine kinase 1.
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The modulation of radiation-induced cell death by genistein in K562 cells: Activation of thymidine kinase 1.
Ionizing radiation is one of the most effective tools in cancer therapy. In a previous study, we reported that protein tyrosine kinase (PTK) inhibitors modulate the radiation responses in the human chronic myelogenous leukemia (CML) cell line K562. The receptor tyrosine kinase inhibitor, genistein, delayed radiation-induced cell death, while non-recepter tyrosine kinase inhibitor, herbimycin A (HMA) enhances radiation-induced apoptosis. In this study, we focused on the modulation of radiation-induced cell death by genistein and performed PCR-select suppression subtractive hybridization (SSH) to understand its molecular mechanism. We identified human thymidine kinase 1 (TK1), which is cell cycle regulatory gene and confirmed expression of TK1 mRNA by Northern blot analysis. Expression of TK1 mRNA and TK 1 enzymatic activity were parallel in their increase and decrease. TK1 is involved in G1-S phase transition of cell cycle progression. In cell cycle analysis, we showed that radiation induced G2 arrest in K562 cells but it was not able to sustain. However, the addition of genistein to irradiated cells sustained a prolonged G2 arrest up to 120 h. In addition, the expression of cell cycle-related proteins, cyclin A and cyclin B1, provided the evidences of G1/S progression and G2-arrest, and their relationship with TK1 in cells treated with radiation and genistein. These results suggest that the activation of TK1 may be critical to modulate the radiation-induced cell death and cell cycle progression in irradiated K562 cells.
http://www.hubmed.org/display.cgi?issn=10010602&uids=15353126
Leukemia & Lymphoma Soc Educates Patients on Myelodysplastic Syndromes and Myeloproliferative Disorders
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Leukemia & Lymphoma Soc Educates Patients on Myelodysplastic Syndromes and Myeloproliferative Disorders
08 Sep 2004
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The Leukemia & Lymphoma Society, the leading source of information and support for patients battling leukemia, lymphoma and myeloma, in collaboration with CancerCare, is offering a free telephone workshop entitled, Myelodysplastic Syndrome and Other Myeloproliferative Disorders. The program is scheduled for Wednesday, Sept.15, 2004, 1 p.m. – 2 p.m. ET.
The program will feature leukemia expert Elihu Estey, M.D., professor of medicine, Department of Leukemia, The University of Texas M.D. Anderson Cancer Center in Houston. Dr. Estey will deliver an overview of myelodysplastic syndromes (MDS) and other myeloproliferative disorders, and discuss: treatment options; the role of clinical trials; symptom management; quality of life issues; and how to effectively communicate with your healthcare provider. A question-and-answer period will follow.
“The diagnosis of myelodysplastic syndrome may provoke a profound emotional response. A lack of understanding of what’s in store, and what’s next should be met by thoughtful, straight forward, and frequent discussions between physician, nurse, patient, and family,” explains Robin Kornhaber, M.S.W., the Society’s senior vice president of patient services. “We strongly encourage patients, caregivers and healthcare providers to participate in this comprehensive program.”
The program is approved for 0.1 Continuing Education Unit for social workers upon verification of completion. The program, supported by an unrestricted educational grant from the Celgene Corp. and sponsored by The Leukemia & Lymphoma Society, will be archived at http://www.lls.org/MDS.
Registration
Register online at http://www.lls.org/MDS or go to http://www.cancercare.org and click on “Teleconferences.” Registrants will receive a packet of information and dial-in instructions.
About Myelodysplastic Syndromes
MDS are a group of diseases that originate in an early blood-forming cell in the marrow. In patients with this disorder, the marrow produces too few red blood cells, white blood cells and, in many cases, platelets. In MDS, the maturing blood cells often die in the marrow before they reach full maturity and enter the blood, accounting for the low blood cell concentrations. There may also be an accumulation of very immature marrow cells, called leukemic blast cells. The severity of the marrow cell disturbance is varied and can range from mild to severe.
The disease may be indolent or chronic and be manifest primarily as mild anemia; it may have severe decreases in red and white blood cells and platelets and be more troublesome; or, it may have severe decreases in blood cells and have leukemic blast cells in the marrow and be even more threatening to the health of the patient. In addition, the disease can progress such that the leukemic blast cells take over the marrow and the disease evolves into acute myelogenous leukemia. The marked decrease in blood cell formation makes it difficult for patients to prevent or fight infection and it predisposes them to exaggerated bleeding.
The annual incidence of new cases of MDS in the United States is not known. There are about 10,000 cases of acute myelogenous leukemia each year and about 5,000 cases of unclassified leukemia. The annual incidence of MDS may be in the range of 4,000 to 6,000 cases per year.
About The Leukemia & Lymphoma Society
The Leukemia & Lymphoma Society, headquartered in White Plains, NY, is the world’s largest voluntary health organization dedicated to funding blood cancer research and providing education and patient services. The Society’s mission: Cure leukemia, lymphoma, Hodgkin’s disease and myeloma, and improve the quality of life of patients and their families. Since its founding in 1949, the Society has invested more than $360 million in research specifically targeting leukemia, lymphoma and myeloma. Last year alone, the Society made more than 812,000 contacts with patients, caregivers and healthcare professionals through services provided at its Home Office and by its 63 chapters nationwide.
For more information about blood cancer, visit http://www.lls.org or call the Society’s Information Resource Center (IRC), a call center staffed by master’s level social workers, nurses and health educators who provide information, support and resources to patients and their families and caregivers. IRC information specialists are available at (800) 955-4572 or Infocenter@lls.org, Monday through Friday, 9 a.m. to 6 p.m. ET.
Contact: Jon Garbo, garboj@lls.org, director, public relations, (914) 821-8969
Huge database of hospitals world wide .
http://www.medicalnewstoday.com/medicalnews.php?newsid=13072
Pic Of The Day
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Floodwaters surround an overturned vehicle in the heart of Biltmore Village, North Carolina