scholarly journals Coexistent Tuberculosis of Spine and Chronic Myeloid Leukemia: Resolving the Diagnostic Dilemma and Management

2015 ◽  
Vol 49 (2) ◽  
pp. 85-87
Author(s):  
Arvind Jayaswal ◽  
Sanjay Yadav ◽  
Ankur Goswami ◽  
G Vijayraghavan
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Management Strategies ◽  
Poor Response ◽  
Diagnostic Methods ◽  
Current Standard ◽  
Diagnostic Challenge ◽  
Diagnostic Dilemma ◽  
Ct Guided ◽  
Tuberculosis Of Spine

ABSTRACT Tuberculosis (TB) and association with hematological malignancy is well described in literature. Lymphoid malignancies like non-Hodgkin lymphoma and chronic lymphocytic lymphoma (CLL) are documented but chronic myeloid leukemia (CML) is uncommon. The association of TB and malignancy can be sequential, concurrent or masquerading. We encountered a case posing diagnostic challenge between CML and tuberculosis. The objective to report such a clinical situation is to be aware of such rare possibilities, to analyze the diagnostic methods and subsequent management strategies. Though tuberculosis is usually the first differential diagnosis in endemic areas, it can be overstressed upon and other concurrent pathologies may be missed. Such possibilities should be kept in consideration in cases with poor response or clinical deterioration on antitubercular treatment (ATT). The importance of tissue diagnosis by CT-guided core biopsy as current standard of care is reiterated even in prevalent regions. Multidisciplinary approach is must for optimum outcome. How to cite this article Yadav S, Jayaswal A, Vijayraghavan G, Goswami A. Coexistent Tuberculosis of Spine and Chronic Myeloid Leukemia: Resolving the Diagnostic Dilemma and Management. J Postgrad Med Edu Res 2015;49(2):85-87.

scholarly journals How I treat atypical chronic myeloid leukemia

Blood ◽  
2017 ◽  
Vol 129 (7) ◽  
pp. 838-845 ◽  
Author(s):  
Jason Gotlib
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Myeloproliferative Neoplasm ◽  
Treatment Strategies ◽  
Standard Of Care ◽  
High Rate ◽  
Current Standard ◽  
Hematopoietic Stem ◽  
Genetic Features ◽  
Atypical Chronic Myeloid Leukemia

Abstract Atypical chronic myeloid leukemia, BCR-ABL1 negative (aCML) is a rare myelodysplastic syndrome (MDS)/myeloproliferative neoplasm (MPN) for which no current standard of care exists. The challenges of aCML relate to its heterogeneous clinical and genetic features, high rate of transformation to acute myeloid leukemia, and historically poor survival. Therefore, allogeneic hematopoietic stem cell transplantation should always be an initial consideration for eligible patients with a suitable donor. Nontransplant approaches for treating aCML have otherwise largely relied on adopting treatment strategies used for MDS and MPN. However, such therapies, including hypomethylating agents, are based on a paucity of data. With an eye toward making a more meaningful impact on response rates and modification of the natural history of the disease, progress will rely on enrollment of patients into clinical trials and molecular profiling of individuals so that opportunities for targeted therapy can be exploited.

scholarly journals MYC in Chronic Myeloid Leukemia: Induction of Aberrant DNA Synthesis and Association with Poor Response to Imatinib

2011 ◽  
Vol 9 (5) ◽  
pp. 564-576 ◽  
Author(s):  
Marta Albajar ◽  
M. Teresa Gómez-Casares ◽  
Javier Llorca ◽  
Itsaso Mauleon ◽  
Jose P. Vaqué ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Dna Synthesis ◽  
Myeloid Leukemia ◽  
Poor Response

scholarly journals Atypical Chronic Myeloid Leukemia

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5455-5455
Author(s):  
Chandralekha Ashangari ◽  
Praveen K. Tumula
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Peripheral Blood ◽  
Myeloid Leukemia ◽  
Conflicts Of Interest ◽  
Philadelphia Chromosome ◽  
Myeloproliferative Neoplasm ◽  
Peripheral Blood Flow ◽  
Current Standard ◽  
Atypical Chronic Myeloid Leukemia ◽  
Wbc Count

Abstract Introduction: Atypical chronic myeloid leukemia (aCML), BCR-ABL1 negative is a rare myelodysplastic syndromes (MDS)/myeloproliferative neoplasm (MPN) for which no current standard of care exists. We present one of the rare presentations of aCML in an elderly patient. Case: A 76 year old male presented to the Hematology clinic for consultation after discharge from local hospital for elevated WBC count. Past medical history was significant for COPD, acid reflux, peripheral arterial disease and hypertension. Physical exam was unremarkable. Initial labs were significant for leukocytosis of 30 k/cu mm, anemia with Hb 10 gm/dl, thrombocytosis 695,000 with neutrophilia of ANC 25,200. Peripheral blood was negative for JAK2 V617F and BCR-ABL. Peripheral blood flow cytometry showed granulocytic left shift with 1.5% myeloblasts. Bone marrow biopsy suggestive of hypercellular marrow (100%) with myeloid predominance, atypical megakaryocytes, increased ring sideroblasts (49% of NRBC), increased blasts (5%) and dysgranulopoeisis over all suggestive of Myelodyplastic Syndrome/Chronic Myeloproliferative Disorder (MDS/MPD). Cytogenetics were positive for U2AF1 positive, CSF3R T6181, CSF3R Q776 pathognomonicof atypical CML and negative for BCR-ABL, FLT3. He was considered transplant ineligible. He was started on Azacitadine and is currently receiving 2nd cycle therapy. He is also receiving darbepoeitin periodically to avoid frequent transfusions. He is currently transfusion independent. Discussion: Increased WBC count (e.g., cutoffs of >40×109/L or 50×109/L), increased percentage of peripheral blood myeloid precursors, female sex, and older age are adverse prognostic factors for overall survival or leukemia-free survival in aCML. aCML cases lack in Philadelphia chromosome. Overall 50-65% of patients show cytogenetic abnormalities. The most frequent is +8 (25%). Other changes such as -7 and del(12p) have also been recurrently observed. Patients with aCML have an estimated median survival between 14 and 30 months. aCML tends to exhibit a more aggressive clinical course than other MDS/MPN subtypes. Figure. Figure. Disclosures No relevant conflicts of interest to declare.

Chronic Myeloid Leukemia (CML) Patients With Atypical e1a2 P190 BCR-ABL Translocation Show a Poor Response To Therapy With Tyrosine Kinase Inhibitors (TKI)

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 5193-5193
Author(s):  
Carme Montoriol-Sabaté ◽  
Carolina Martínez-Laperche ◽  
P Jiménez-Gámiz ◽  
Rosa Collado ◽  
Alfredo Minguela-Puras ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Molecular Biology ◽  
Myeloid Leukemia ◽  
Kinase Inhibitors ◽  
Poor Response ◽  
Response To Therapy ◽  
Molecular Response ◽  
Spanish Society ◽  
Biology Group

Abstract Introduction P210 BCR-ABL translocation resulting from rearrangements within the major breakpoint cluster region (M-BCR), either e13a2 or e14a2, is the molecular hallmark of chronic myeloid leukemia (CML). However, some CML patients may harbor atypical BCR-ABL rearrangements such e1a2 P190 BCR-ABL which involves the minor breakpoint cluster region (m-BCR). Response to therapy with tyrosine kinase inhibitors (TKI) and outcome of such atypical patients is not well defined. Objective To evaluate response to TKI therapy of CML patients with the atypical e1a2 P190 BCR-ABL translocation. Patients and Methods Since 2009, 4 patients with CML in chronic phase and with atypical e1a2 P190 BCR-ABL rearrangement have been recruited in various institutions belonging to the Hematological Molecular Biology Group (GBMH) of the Spanish Society of Hematology (SEHH). Patient characteristics, treatments administered and response to therapy for the 4 patients is shown in Table 1. BCR-ABL transcripts were revealed at diagnosis by quantitative PCR followed by conventional agarose electrophoresis of PCR products. Molecular follow-up of BCR-ABL transcripts throughout treatment was performed by quantitative PCR following the guidelines of the European Leukemia Net. Results One patient received treatment (HU and INF+araC) prior to TKI (Pat. 1; Table 1). All 4 patients received Imatinib as initial TKI treatment. Two of the patients treated with Imatinib (Pat. 1,2) obtained a complete molecular response (CMR) and the other 2 (Pat. 3,4) only achieved a complete hematological response (CHR) as best response (Table 1). All patients had to switch to a second generation TKI (3 Nilotinib and 1 Dasatinib) due to intolerance to Imatinib (n=1; Pat. 1) or resistance (n=3; Pat. 2-4). The patient who received Dasatinib as second line TKI (Pat. 3) only achieved a partial hematologic response (PHR) and was changed to Nilotinib as third line TKI, achieving CHR after which the patient entered in blast crisis and died 36 months after diagnosis (Table 1). Overall, only 1 (Pat. 1) out of the 4 patients included in the present study achieved a sustained molecular response with Imatinib. At last follow-up, among the 4 patients included in the study, all 4 had needed a change of TKI, 1 had died due to disease progression (Pat. 3) and only 2 of them retained a molecular response (Pat. 1,2). Conclusion CML patients harboring atypical e1a2 P190 BCR-ABL transcripts show a poor response and short-lived responses to TKI therapy and therefore should be identified as high-risk patients at diagnosis. These patients must be closely monitored during therapy with TKI and should be treated upfront with a second generation TKI or even be considered for allogeneic SCT in the early phase of the disease. Paper presented on behalf of the Hematological Molecular Biology Group (GBMH) of the Spanish Society of Hematology (SEHH). AJ-V and IB contributed equally to this work. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Loss of the Y chromosome in Philadelphia-positive cells predicts a poor response of chronic myeloid leukemia patients to imatinib mesylate therapy

Haematologica ◽  
2010 ◽  
Vol 95 (9) ◽  
pp. 1604-1607 ◽  
Author(s):  
E. Lippert ◽  
G. Etienne ◽  
M.-J. Mozziconacci ◽  
S. Laibe ◽  
C. Gervais ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Imatinib Mesylate ◽  
Y Chromosome ◽  
Myeloid Leukemia ◽  
Poor Response

Síndrome Mieloproliferativa Crônica Inclassificável: Relato de Caso/Nondescript Chronicles Myeloproliferative Syndrome: Case Report

1970 ◽  
Vol 4 (2) ◽  
pp. 96-107
Author(s):  
Vanessa Parducci Brandão ◽  
Vitória Santos De Souza ◽  
Mônica de Macedo E Silva
Keyword(s):  
Case Report ◽  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Myeloproliferative Neoplasms ◽  
Diagnostic Methods ◽  
World Health ◽  
Rt Pcr ◽  
Myeloproliferative Syndrome ◽  
Disease Case ◽  
Leucemia Mieloide Crónica

Introdução: As neoplasias mieloproliferativas são patologias que se originam de células tronco totipotentes e se caracterizam por multiplicação acelerada de uma ou mais séries sanguíneas, sem relevante displasia. São classificadas em diversos subtipos entre eles: Leucemia Mielóide Crônica, Leucemia Neutrofílica Crônica,Mielofribrose Primária e Doença Mieloproliferativa Crônica Inclassificável. Essa classificação justifica-se por mutações genéticas que definem a evolução e a fisiopatologia de cada doença. Casuística: Apresentamos o caso de uma paciente, sexo feminino, 58 anos, com queixas inespecíficas, que por achado laboratorial suspeitou-se de leucemia. Foi submetida à investigação clínica, laboratorial,radiológica, e realizada a biópsia de MO, sendo diagnosticada com Síndrome Mieloproliferativa Crônica Inclassificável. Foi orientada a fazer uso de hidroxiureiapara controle hematimétrico, porém sem melhora, iniciou citarabina. Paciente encontra-se na fase blástica da doença e devido à ausência de remissão da patologia,foi encaminhada para lista de transplante. Discussão: o caso foi bem conduzido quanto aos métodos diagnósticos utilizados na investigação da mesma, sendo fundamental o RT-PCR para identificação do cromossomo Philadelphia. O tratamento foi semelhante à literatura em relação aos medicamentos usados, porém algumas posologias não foram as mesmas. A condução do caso levou a paciente paraa fila de transplante, visto que não houve resposta terapêutica. Conclusão: este relato de caso trata-se, portanto, de uma Neoplasia Mieloproliferativa Crônica do tipo inclassificável, pois não preenche os critérios diagnósticos preconizados pela Organização Mundial de Saúde, visto que foi classificada como Leucemia Mielóide Crônica atípica BCR/ABL negativa, para fins terapêuticos.Palavras-chave: Neoplasias mieloproliferativas, Leucemia mielóide crônica,transplante de medula óssea. Introduction: Myeloproliferative diseases are neoplasms that originate from to tipotent stem cell, and is characterized by rapid proliferation of one or more bloodseries without significant dysplasia. They are classified into several subtypes including: Chronic Myeloid Leukemia, Chronic Neutrophilic Leukemia,Polycythemia Vera, Primary Mielofribrose and Unclassifiable chronic myeloproliferative syndrome. This classification is justified by genetic mutations that define the evolution and pathophysiology of each disease. Case report: We present a case of a female, 58, with nonspecific complaints, which in laboratoryfinding was suspected leukemia. Underwent clinical, laboratory, radiological,underwent bone marrow biopsy, was diagnosed with Unclassifiable chronic myeloproliferative syndrome.She was oriented to make use of hydroxyurea forerythrocyte control, but without improvement, started cytarabine. The patient lies onthe blast phase of the disease. Due to lack of remission of the disease, the patient wasreferred to the transplant list. Discussion: the case was properly conducted as to the diagnostic methods used in the investigation, the RT-PCR was fundamental for identification of Philadelphia chromosome. The medications used in the treatmentwas similar to the literature, however some doses, according to the survey were notthe same. The patient was refered to transplant, because there was no therapeutic response. Conclusion: This case report is a Nondescript Chronicles Myeloproliferative Syndrome, since it does not satisfy the standard diagnostic recommended by the World Health Organization, as it was classified as Atypical Chronic Myeloid Leukemia BCR / ABL negative for purposes therapeutic.Keywords: myeloproliferative neoplasms, chronic leukemia, myeloid bone marrowtransplantation.

Current Therapies for Chronic Myeloid Leukemia

2008 ◽  
Vol 21 (2) ◽  
pp. 116-125
Author(s):  
Laureen K. Kenealy ◽  
Courtney B. Christenson ◽  
Casey B. Williams
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Kinase Inhibitors ◽  
Management Strategies ◽  
Treatment Strategies ◽  
Chronic Phase ◽  
Initial Therapy ◽  
Molecular Monitoring ◽  
Hematopoietic Stem ◽  
Current Therapies

Management strategies for patients with chronic-phase chronic myeloid leukemia (CML) have changed dramatically since the introduction of imatinib into clinical trials in 1998. Imatinib is generally accepted, at present, to be the most appropriate initial therapy for newly diagnosed chronic-phase CML; however, a proportion of patients will not respond adequately. Many of these patients may benefit from alternative treatment strategies, including second- and third-generation BCR-ABL kinase inhibitors and allogeneic hematopoietic stem cell transplantation (HSCT). Additionally, with continued improvements in molecular monitoring, it is much more clinically routine to measure ongoing treatment efficacy or characterize pending disease relapse via molecular analysis. The challenge is to now combine molecular monitoring information with timely treatment decisions to achieve the best possible outcomes. Additionally, unanswered questions about HSCT remain, and include (1) What is the role of allogeneic HSCT in CML? (2) What type of transplant, reduced-intensity or myeloablative, should be performed? The goal of this article is to provide an overview of where we stand in the treatment of CML in 2008.

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