Posted by rob on November 28, 2009 under Uncategorized | 
Acute myelogenous leukemia and acute leukemic appendicitis: A case report.
World J Gastroenterol. 2009 Nov 28;15(44):5624-5625
Authors: Hsiao PJ, Kuo SM, Chen JH, Lin HF, Chu PL, Lin SH, Ho CL
Acute myelogenous leukemia (AML) can involve the gastrointestinal tract but rarely involves the appendix. We report a male patient who had 1 year partial remission from AML and who presented with apparent acute appendicitis as the initial manifestation of leukemia relapse. Pathological findings of the appendix revealed transmural infiltrates of myeloblasts, which indicated a diagnosis of leukemia. Unfortunately, the patient died from progression of the disease on the 19th d after admission. Although leukemic cell infiltration of the appendix is uncommon, patients with leukemia relapse can present with symptoms mimicking acute appendicitis.
PMID: 19938205 [PubMed - as supplied by publisher]
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Intracardiac Chloroma.
J Pediatr Hematol Oncol. 2009 Nov 20;
Authors: Mignano JE, Chan MD, Rosenwald IB, Kimmelstiel CD, Wolfe LC
Chloromas are not frequently seen in patients with acute myelogenous leukemia and chloromas involving cardiac structures have only been rarely reported in the literature. We report a complete radiographic response to low-dose fractionated radiotherapy in a patient with an intracardiac chloroma.
PMID: 19935434 [PubMed - as supplied by publisher]
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Imatinib Mesylate Induces Cisplatin Hypersensitivity in Bcr-Abl+ Cells by Differential Modulation of p53 Transcriptional and Proapoptotic Activity.
Cancer Res. 2009 Nov 24;
Authors: Skorta I, Oren M, Markwardt C, Gutekunst M, Aulitzky WE, van der Kuip H
Imatinib is highly effective in inducing remission in chronic myelogenous leukemia (CML). However, complete eradication of the malignant clone by imatinib is rare. We investigated the efficacy of combining imatinib with cisplatin. Inhibition of Bcr-Abl by imatinib induced a hypersensitive phenotype both in Bcr-Abl(+) cell lines and in CD34(+) cells from CML patients. Importantly, cisplatin sensitivity of leukemic cells harboring an inactive Bcr-Abl greatly exceeded that of Bcr-Abl(-) parental cells. The cisplatin response of Bcr-Abl(+) cells treated with imatinib was characterized by an impaired G(2)-M arrest and by rapid induction of mitochondrial cell death after the first passage through G(2). Imatinib abrogated ATM activation on cisplatin selectively in Bcr-Abl(+) cells. As a consequence, phosphorylation of p53 on Ser(15) and its activity as a transcription factor was significantly diminished. Furthermore, p53 accumulated predominantly in the cytoplasm in Bcr-Abl(+) cells treated with imatinib and cisplatin. Silencing of p53 significantly reduced sensitivity to cisplatin in imatinib-treated Bcr-Abl(+) cells, indicating that p53 retains its proapoptotic activity. Simultaneous downregulation of Bcl-x(L) was an additional requirement for cisplatin hypersensitivity, as p53-dependent cell death could be antagonized by exogenous Bcl-x(L). We conclude that imatinib sensitizes Bcr-Abl(+) cells to cisplatin by simultaneous inhibition of p53 transactivation, induction of p53 accumulation predominantly in the cytoplasm, and reduction of Bcl-x(L). [Cancer Res 2009;69(24):OF1-9].
PMID: 19934315 [PubMed - as supplied by publisher]
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Acute myelogenous leukemia cells with the MLL-ELL translocation convert morphologically and functionally into adherent myofibroblasts.
Biochem Biophys Res Commun. 2009 Nov 20;
Authors: Tashiro H, Mizutani-Noguchi M, Shirasaki R, Shirafuji N
Bone marrow-myofibroblasts, a major component of bone marrow-stroma, are reported to originate from hematopoietic stem cells. We show in this paper that non-adherent leukemia blasts can change into myofibroblasts. When myeloblasts from two cases of acute myelogenous leukemia with a fusion product comprising mixed lineage leukemia and RNA polymerase II elongation factor, were cultured long term, their morphology changed to that of myofibroblasts with similar molecular characteristics to the parental myeloblasts. The original leukemia blasts, when cultured on the leukemia blast-derived myofibroblasts, grew extensively. Leukemia blasts can create their own microenvironment for proliferation.
PMID: 19932689 [PubMed - as supplied by publisher]
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Issues of imatinib and pregnancy outcome.
J Natl Compr Canc Netw. 2009 Nov;7(10):1050-8
Authors: Apperley J
The introduction of tyrosine kinase inhibitors into clinical practice now offers most patients with chronic myelogenous leukemia lengthy remissions and the possibility of normal life expectancies. These improved survivals have resulted in the need to address issues relating to quality of life, including fertility and procreation. Treatment may require lifelong daily therapy with drugs that might inhibit proteins essential to gonadal function, implantation, and embryogenesis. Animal data suggest that imatinib at standard dosages is unlikely to impair fertility in either adult male or female animals. However, human data remain limited, particularly in children and adolescents. Children born to men who are actively taking imatinib at conception seem healthy, and current advice is not to discontinue treatment. In contrast, data are less encouraging for children born to women exposed to imatinib during pregnancy. Although numbers are small, a disturbing cluster of rare congenital malformations has prevented imatinib from being recommended safely, particularly during the period of organogenesis. Alternative strategies for managing pregnancy in chronic myelogenous leukemia include one or both of regular leukapheresis and interferon-alpha. Pregnancy in advanced-phase disease presents particular problems.
PMID: 19930974 [PubMed - in process]
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Evolving strategies in the treatment of MDS and AML.
Clin Adv Hematol Oncol. 2009 Aug;7(8):1-14; quiz 2 p following 14
Authors: Stone R, Sekeres M, Garcia-Manero G
Myelodysplastic syndrome (MDS) is a clonal hematopoietic disorder characterized by a hyperproliferative bone marrow, cellular dysplasia, and ineffective hematopoiesis. This heterogeneous malignancy is composed of several subtypes, the classification of which has evolved over several years. The treatment of MDS involves improving patient survival and quality of life while decreasing the likelihood of progression to acute myelogenous leukemia (AML). In addition to supportive care with transfusions and hematopoietic growth factors as well as stem cell transplantation, three chemotherapeutic agents have been approved to treat MDS–lenalidomide, azacitidine, and decitabine. In addition, multiple agents and novel combinations are currently in development to treat both MDS AML. Several clinical studies which have investigated these therapeutic approaches, as well as the incorporation of new tools used in the diagnosis of MDS, have been published since the 2008 American Society of Hematology (ASH) Annual Meeting and Exposition, and are discussed here. By becoming familiar with these studies, the physician will be better able to provide the optimal treatment for their patients, as well as become aware of novel therapeutic strategies to offer their patients in ongoing clinical trials.
PMID: 19927982 [PubMed - in process]
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