A myelodysplastic/myeloproliferative disorder characterized by myelodysplasia associated with bone marrow and peripheral blood patterns similar to CHRONIC MYELOID LEUKEMIA, but cytogenetically lacking a PHILADELPHIA CHROMOSOME or bcr/abl fusion gene (GENES, ABL).
A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)
Retrovirus-associated DNA sequences (abl) originally isolated from the Abelson murine leukemia virus (Ab-MuLV). The proto-oncogene abl (c-abl) codes for a protein that is a member of the tyrosine kinase family. The human c-abl gene is located at 9q34.1 on the long arm of chromosome 9. It is activated by translocation to bcr on chromosome 22 in chronic myelogenous leukemia.
Translation products of a fusion gene derived from CHROMOSOMAL TRANSLOCATION of C-ABL GENES to the genetic locus of the breakpoint cluster region gene on chromosome 22. Several different variants of the bcr-abl fusion proteins occur depending upon the precise location of the chromosomal breakpoint. These variants can be associated with distinct subtypes of leukemias such as PRECURSOR CELL LYMPHOBLASTIC LEUKEMIA-LYMPHOMA; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; and NEUTROPHILIC LEUKEMIA, CHRONIC.
Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.
Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.
A chronic leukemia characterized by abnormal B-lymphocytes and often generalized lymphadenopathy. In patients presenting predominately with blood and bone marrow involvement it is called chronic lymphocytic leukemia (CLL); in those predominately with enlarged lymph nodes it is called small lymphocytic lymphoma. These terms represent spectrums of the same disease.
Proto-oncogene protein bcr is a serine-threonine kinase that functions as a negative regulator of CELL PROLIFERATION and NEOPLASTIC CELL TRANSFORMATION. It is commonly fused with cellular abl protein to form BCR-ABL FUSION PROTEINS in PHILADELPHIA CHROMOSOME positive LEUKEMIA patients.
Leukemia induced experimentally in animals by exposure to leukemogenic agents, such as VIRUSES; RADIATION; or by TRANSPLANTATION of leukemic tissues.
Leukemia associated with HYPERPLASIA of the lymphoid tissues and increased numbers of circulating malignant LYMPHOCYTES and lymphoblasts.
Non-receptor tyrosine kinases encoded by the C-ABL GENES. They are distributed in both the cytoplasm and the nucleus. c-Abl plays a role in normal HEMATOPOIESIS especially of the myeloid lineage. Oncogenic transformation of c-abl arises when specific N-terminal amino acids are deleted, releasing the kinase from negative regulation.
A neoplasm characterized by abnormalities of the lymphoid cell precursors leading to excessive lymphoblasts in the marrow and other organs. It is the most common cancer in children and accounts for the vast majority of all childhood leukemias.
BENZOIC ACID amides.
An ERYTHROLEUKEMIA cell line derived from a CHRONIC MYELOID LEUKEMIA patient in BLAST CRISIS.
Species of GAMMARETROVIRUS, containing many well-defined strains, producing leukemia in mice. Disease is commonly induced by injecting filtrates of propagable tumors into newborn mice.
A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (CYTOSINE; THYMINE; and URACIL) and form the basic structure of the barbiturates.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in leukemia.
An aberrant form of human CHROMOSOME 22 characterized by translocation of the distal end of chromosome 9 from 9q34, to the long arm of chromosome 22 at 22q11. It is present in the bone marrow cells of 80 to 90 per cent of patients with chronic myelocytic leukemia (LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE).
A system of categories to which morbid entries are assigned according to established criteria. Included is the entire range of conditions in a manageable number of categories, grouped to facilitate mortality reporting. It is produced by the World Health Organization (From ICD-10, p1). The Clinical Modifications, produced by the UNITED STATES DEPT. OF HEALTH AND HUMAN SERVICES, are larger extensions used for morbidity and general epidemiological purposes, primarily in the U.S.
Extensive collections, reputedly complete, of facts and data garnered from material of a specialized subject area and made available for analysis and application. The collection can be automated by various contemporary methods for retrieval. The concept should be differentiated from DATABASES, BIBLIOGRAPHIC which is restricted to collections of bibliographic references.
Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (MYELOID PROGENITOR CELLS) in the bone marrow and other sites.
An adenosine monophosphate analog in which ribose is replaced by an arabinose moiety. It is the monophosphate ester of VIDARABINE with antiviral and possibly antineoplastic properties.
A myelodysplastic-myeloproliferative disease characterized by monocytosis, increased monocytes in the bone marrow, variable degrees of dysplasia, but an absence of immature granulocytes in the blood.
A severe sometimes chronic anemia, usually macrocytic in type, that does not respond to ordinary antianemic therapy.
Transfer of HEMATOPOIETIC STEM CELLS from BONE MARROW or BLOOD between individuals within the same species (TRANSPLANTATION, HOMOLOGOUS) or transfer within the same individual (TRANSPLANTATION, AUTOLOGOUS). Hematopoietic stem cell transplantation has been used as an alternative to BONE MARROW TRANSPLANTATION in the treatment of a variety of neoplasms.
Preparative treatment of transplant recipient with various conditioning regimens including radiation, immune sera, chemotherapy, and/or immunosuppressive agents, prior to transplantation. Transplantation conditioning is very common before bone marrow transplantation.
Irradiation of the whole body with ionizing or non-ionizing radiation. It is applicable to humans or animals but not to microorganisms.
A nucleoside antibiotic isolated from Streptomyces antibioticus. It has some antineoplastic properties and has broad spectrum activity against DNA viruses in cell cultures and significant antiviral activity against infections caused by a variety of viruses such as the herpes viruses, the VACCINIA VIRUS and varicella zoster virus.
Tumor necrosis factor receptor family members that are widely expressed and play a role in regulation of peripheral immune responses and APOPTOSIS. The receptors are specific for TNF-RELATED APOPTOSIS-INDUCING LIGAND and signal via conserved death domains that associate with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
A transmembrane-protein belonging to the TNF family of intercellular signaling proteins. It is a widely expressed ligand that activates APOPTOSIS by binding to TNF-RELATED APOPTOSIS-INDUCING LIGAND RECEPTORS. The membrane-bound form of the protein can be cleaved by specific CYSTEINE ENDOPEPTIDASES to form a soluble ligand form.
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
A pyrimidine nucleoside analog that is used mainly in the treatment of leukemia, especially acute non-lymphoblastic leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle. It also has antiviral and immunosuppressant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p472)
Clonal hematopoietic stem cell disorders characterized by dysplasia in one or more hematopoietic cell lineages. They predominantly affect patients over 60, are considered preleukemic conditions, and have high probability of transformation into ACUTE MYELOID LEUKEMIA.
The circulation or wide dispersal of information.
Countries in the process of change with economic growth, that is, an increase in production, per capita consumption, and income. The process of economic growth involves better utilization of natural and human resources, which results in a change in the social, political, and economic structures.
Chemically synthesized structures which functionally resemble natural cells.
A heterogeneous group of immunocompetent cells that mediate the cellular immune response by processing and presenting antigens to the T-cells. Traditional antigen-presenting cells include MACROPHAGES; DENDRITIC CELLS; LANGERHANS CELLS; and B-LYMPHOCYTES. FOLLICULAR DENDRITIC CELLS are not traditional antigen-presenting cells, but because they hold antigen on their cell surface in the form of IMMUNE COMPLEXES for B-cell recognition they are considered so by some authors.
Countries that have reached a level of economic achievement through an increase of production, per capita income and consumption, and utilization of natural and human resources.
The science that investigates the principles governing correct or reliable inference and deals with the canons and criteria of validity in thought and demonstration. This system of reasoning is applicable to any branch of knowledge or study. (Random House Unabridged Dictionary, 2d ed & Sippl, Computer Dictionary, 4th ed)
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
Any woven or knit material of open texture used in surgery for the repair, reconstruction, or substitution of tissue. The mesh is usually a synthetic fabric made of various polymers. It is occasionally made of metal.
The terms, expressions, designations, or symbols used in a particular science, discipline, or specialized subject area.
Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.
The transfer of STEM CELLS from one individual to another within the same species (TRANSPLANTATION, HOMOLOGOUS) or between species (XENOTRANSPLANTATION), or transfer within the same individual (TRANSPLANTATION, AUTOLOGOUS). The source and location of the stem cells determines their potency or pluripotency to differentiate into various cell types.
Transplantation between individuals of the same species. Usually refers to genetically disparate individuals in contradistinction to isogeneic transplantation for genetically identical individuals.
Computer-based information systems used to integrate clinical and patient information and provide support for decision-making in patient care.
Transplantation of an individual's own tissue from one site to another site.
Progenitor cells from which all blood cells derive.
A large group of diseases which are characterized by a low prevalence in the population. They frequently are associated with problems in diagnosis and treatment.
Tomography using x-ray transmission and a computer algorithm to reconstruct the image.
The proximal portion of the respiratory passages on either side of the NASAL SEPTUM. Nasal cavities, extending from the nares to the NASOPHARYNX, are lined with ciliated NASAL MUCOSA.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
Process that is gone through in order for a drug to receive approval by a government regulatory agency. This includes any required pre-clinical or clinical testing, review, submission, and evaluation of the applications and test results, and post-marketing surveillance of the drug.
An agency of the PUBLIC HEALTH SERVICE concerned with the overall planning, promoting, and administering of programs pertaining to maintaining standards of quality of foods, drugs, therapeutic devices, etc.

Analysis of Philadelphia chromosome-negative BCR-ABL-positive chronic myelogenous leukemia by hypermetaphase fluorescence in situ hybridization. (1/42)

BACKGROUND: In 5%-10% of patients with of chronic myelogenous leukemia (CML), the Philadelphia chromosome (Ph) is not identified, despite the presence of the associated BCR-ABL molecular abnormality (Ph-negative, BCR-ABL-positive CML) because of sub-microscopic rearrangements. PATIENTS AND METHODS: Six patients with Ph-negative, BCR-ABL-positive CML were investigated. The Ph chromosome detection via fluorescence in situ hybridization after 24-hour mitotic arrest of bone marrow cultures resulting in several hundreds of metaphases (hypermetaphase FISH or HMF) was useful in explaining the nature of the six cases. RESULTS: Four patients had a low frequency of Ph-positive cells by HMF (5.7%, 4.8%, 3.9%, 0.2%), i.e., a typical Ph translocation. However, two cases involved a 9q34 inserted into chromosome 22q11 (74.2% and 92%), without a deletion from chromosome 22 and reciprocal translocation onto 9, i.e., not a typical Ph translocation. The pattern of UBCR gene rearrangement was characterized by the same genomic recombination of 5-BCR and c-ABL, both in the four cases of typical translocation (9;22) and in the two cases of insertion of 9q34 into chromosome 22q11. CONCLUSIONS: The HMF identified two different bases for Ph-negative, BCR-ABL-positive cells in CML-presence of low frequency of cells with typical Ph translocations or presence of cells with ABL insertions into the BCR gene on chromosome 22.  (+info)

Cytogenetic status pre-transplant as a predictor of outcome post bone marrow transplantation for chronic myelogenous leukaemia. (2/42)

We have analysed pre-transplant cytogenetic findings in 418 patients with CML in pre-blastic phase who underwent allogeneic BMT between February 1981 and January 1998. Five different patient groups were identified: A = Philadelphia (Ph)+; B = Ph-, BCR-ABL+; C = variant Ph (VPh); D = Ph chromosome plus at least one of: trisomy 8, +Ph, chromosome 17 abnormalities and E = other abnormalities in addition to the Ph chromosome. There were two principal conclusions. Firstly, Ph- patients showed a better outcome, and VPh patients a worse outcome, than those with a standard Ph, both in terms of leukaemia-free survival (LFS) (76.9%, 22.1% and 31.9%) and the risk of treatment failure relative to those with a standard Ph (relative risks of 0.49 and 1.92, respectively). One contributing factor may be relapse: no Ph- patients relapsed, whereas all other groups showed similar probabilities of relapse at 5 years (range 33.0-44. 0%). Secondly, those with the additional changes of +8, +Ph and i(17q) did not show a worse outcome than those with no additional changes (5 year survival of 44.7% vs 51.8%; 5 year LFS of 40.6% vs 31.9%), whereas those with other additional changes may fare worst of all (40.4% and 16.0%, respectively). Bone Marrow Transplantation (2000) 25, 143-146.  (+info)

Collection of Ph-negative progenitor cells from interferon responsive patients with chronic myeloid leukemia: effect of granulocyte-colony-stimulating factor mobilization. (3/42)

BACKGROUND AND OBJECTIVE: The observation that patients with chronic myeloid leukemia (CML) may relapse following stem cell transplantation because of Philadelphia positive cells contaminating the graft have led to a variety of strategies to reduce this contamination. This study investigate the feasibility of collective, Ph-re cells from patients with CML in chronic phase. DESIGN AND METHODS: A total of 18 patients with chronic myeloid leukemia in chronic phase who had responded to varying degrees to treatment with interferon-a (IFN) were subjected to mobilization with granulocyte colony-stimulating factors and peripheral blood progenitor cell collection. Nine patients were in complete cytogenetic remission (CCR) and nine were partial responders. IFN was stopped 2 to 4 weeks before the procedure. G-CSF was given by subcutaneous injection once daily at a dose of 10 microg/kg. RESULTS: Five patients underwent one collection procedure only, 10 underwent two procedures and 3 patients had three collections. The median number of nucleated cells (NC) per patient collected was 10.2 x 10(8)/kg (4.4-19.7) and the median number of CD34(+) cells was 2.5 x 10(6)/kg (0.4-9.4). Analyzable cytogenetic data were available for 26/34 (76%) leukapheresis procedures. The median percentage of Ph- negative metaphases for patients in CCR was 100% (73-100). Patients not in CCR had a higher level of Ph-positive cells in their collections (median 23%, range 0-79%, p=0.01). Of the nine patients in CCR, 8 had at least one apheresis from which progenitor cells were 100% Ph-negative; conversely, patients not in CCR had detectable Ph-positive cells in every collection. Four patients have undergone autologous stem cell transplantation. INTERPRETATION AND CONCLUSIONS: It was possible to collect sufficient Ph negative progenitor cells from patients in CCR but collections from other patients contained significant numbers of Ph-positive cells.  (+info)

Characteristics and outcome of patients with Philadelphia chromosome negative, bcr/abl negative chronic myelogenous leukemia. (4/42)

BACKGROUND: Up to 5% of patients with chronic myelogenous leukemia (CML) do not have the Philadelphia (Ph) translocation t(9;22)(q34;q11) or a bcr/abl molecular rearrangement. Although the diagnostic criteria of this entity are still under debate, there is general agreement that patients with Ph negative, bcr/abl negative CML have a severe clinical course that is not affected significantly by current treatment options. METHODS: A population of 76 patients with bcr/abl negative CML who had received minimal or no previous therapy was characterized carefully with the intent of investigating clinical and hematologic variables and their association with survival by univariate, correlation, and multivariate analyses. A group of 73 patients with Ph negative CML who were not tested for the bcr/abl rearrangement (bcr/abl unknown) was analyzed separately and used for extension of the analysis. RESULTS: In the bcr/abl negative patient population, the median overall survival was 24 months. At the time of the analysis, 38 patients (50%) had died, and blastic transformation preceded death in 31%. Chromosomal abnormalities were found in 30% of the 76 patients, with trisomy 8 the most common abnormality. Complex chromosomal abnormalities were rare, and monosomy 7 was not observed. Survival was not affected significantly by treatment. Multivariate analysis identified older age (> 65 years), anemia (hemoglobin < 10 g/dL), and severe leukocytosis (white blood cells > 50 x 10(9)/L) as variables with independent prognostic significance for poor survival. A prognostic scoring system stratified patients into a low-risk group (53%) and a high-risk group (47%), with median survivals of 38 months and 9 months, respectively. CONCLUSIONS: Bcr/abl negative CML is a distinct clinical entity associated with very poor prognosis. Two risk categories are identifiable using a simple scoring system based on age, hemoglobin level, and leukocyte number.  (+info)

Autologous stem cell transplantation for patients with chronic myeloid leukemia. The Argentine Group of Bone Marrow Transplantation (GATMO) experience. (5/42)

BACKGROUND: The objective of this analysis was to evaluate the role of autologous stem cell transplantation (ASCT) in prolonging disease free survival (DFS) and overall survival (OS) in patients with chronic myeloid leukemia (CML) who received autografts of Philadelphia chromosome (Ph) positive or Ph negative cell harvests. METHODS: Over a 4-year period (1994-1999), 53 patients who underwent ASCT for CML were reported to the Argentine Group of Bone Marrow Transplantation (GATMO) Registry. RESULTS: Ph negative cell products were harvested in only 18 patients (34%). Comparison of disease status at the time of autograft, duration of neutropenia, thrombocytopenia, days of antibiotics, and transfusional requirements of red blood cells and platelets did not reveal statistical significant differences between the Ph positive group and the Ph negative group. Only days of hospitalization were increased significantly in patients who received Ph positive autografts. Although DFS at 36 months was significantly longer after infusion of Ph negative cell products (54% vs. 14%; P +info)

Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment. (6/42)

The BCR/ABL tyrosine kinase inhibitor imatinib mesylate (Gleevec, STI571; Novartis, Basel, Switzerland) has shown remarkable efficacy in the treatment of chronic myelogenous leukemia (CML), with a high proportion of patients achieving complete cytogenetic responses (CCRs). However, it is not clear whether remissions will be durable and whether imatinib mesylate can eliminate the malignant primitive progenitors in which the disease arises. We investigated whether residual BCR/ABL+ hematopoietic progenitors were present in patients who achieved CCRs with imatinib mesylate treatment. CD34+ progenitor cells were selected from bone marrow mononuclear cells (MNCs) and analyzed for the presence of the BCR/ABL fusion gene by fluorescence in situ hybridization (FISH). CD34+ cells were also plated in committed progenitor (colony-forming cell, or CFC) and primitive progenitor (long-term bone marrow culture-initiating cell, or LTCIC) cultures and resulting colonies analyzed for the presence of BCR/ABL+ cells by FISH. Using these assays, residual BCR/ABL+ progenitors were detected in all patients studied. Quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) analysis demonstrated increased levels of BCR/ABL mRNA in CD34+ cells compared with total MNCs. Evaluation of samples collected at different time points demonstrated persistence of BCR/ABL+ progenitors despite continued treatment with imatinib mesylate. Our results indicate that inhibition of BCR/ABL tyrosine kinase activity by imatinib mesylate does not eliminate malignant primitive progenitors in CML patients. Patients in CCR with imatinib mesylate treatment need to be followed carefully to assess for risk of relapse.  (+info)

Beyond chronic myelogenous leukemia: potential role for imatinib in Philadelphia-negative myeloproliferative disorders. (7/42)

The myeloproliferative disorders (MPDs) are chronic malignant conditions originating from the clonal expansion of a multipotential hematopoietic stem cell. These diseases include polycythemia vera (PV), essential thrombocythenia, atypical chronic myeloid leukemia, idiopathic hypereosinophilic syndrome (HES), agnogenic myeloid metaplasia with myelofibrosis, and others. Receptor tyrosine kinases-the platelet-derived growth factor receptors (PDGFRs) and c-Kit-and their respective ligands have been implicated in the pathogenesis of MPDs. For example, a constitutively activated PDGFR fusion tyrosine kinase (FIP1L1-PDGFRA) was identified in some patients with HES, a disease characterized by sustained overproduction of eosinophils that has been classified by the World Health Organization as a chronic subtype of the MPDs. Imatinib is a selective inhibitor of PDGFRs, c-Kit, Abl and Arg protein-tyrosine kinases, as well as Bcr-Abl, the oncogenic tyrosine kinase that causes chronic myeloid leukemia. The efficacy of imatinib in treating HES, systemic mast cell disease, chronic myelomonocytic leukemia associated with PDGFRbeta fusion genes, and (to a lesser extent) PV and idiopathic myelofibrosis was reviewed from institutional experience and a review of the literature. In 3 studies that involved 11 patients with PV, 10 patients had reductions in phlebotomy with imatinib. Eight studies of 42 patients with HES indicated that 70% achieved complete hematologic remissions with imatinib. Four studies of 6 patients with MPD indicated responses with imatinib in 5 patients. Insight into the molecular pathogenesis of MPDs will improve the definitions of different disease categories and suggests that signal transduction inhibition is likely to be an increasingly important treatment option in the future.  (+info)

Sensitivity to imatinib therapy may be predicted by testing Wilms tumor gene expression and colony growth after a short in vitro incubation. (8/42)

BACKGROUND: The objective of the current study was to verify the ability to predict response to imatinib therapy using in vitro assays to evaluate the inhibition of Wilms tumor gene (WT1) expression and colony growth after samples obtained from patients with chronic myelogenous leukemia (CML) before the start of treatment were subjected to short-term incubation with imatinib. METHODS: WT1 transcript levels and colony growth in bone marrow (BM) samples from 23 patients with CML that was later identified as being responsive to imatinib and from 13 patients with CML that was later identified as not being responsive to imatinib were evaluated after incubation of these samples with imatinib at a concentration of 1 microM for 18 hours. In addition, real-time quantitative polymerase chain reaction (RQ-PCR) analysis of WT1 expression was performed during follow-up, and the results were analyzed for associations with cytogenetic response and with BCR/ABL transcript levels as determined using RQ-PCR analysis. RESULTS: Before treatment, it was found that WT1 expression was elevated in BM samples obtained from all patients with CML. WT1 expression and colony growth were reduced significantly after an 18-hour incubation with imatinib in samples obtained from patients who were later identified as responders to treatment, but not in samples obtained from patients who did not experience responses to treatment. Inhibition of WT1 expression in vitro was associated with inhibition of imatinib-induced BCR-ABL tyrosine kinase activity, a finding that also has been made in studies involving certain Philadelphia chromosome (Ph)-positive and Ph-negative cell lines. CONCLUSIONS: Inhibition of WT1 transcript levels after a short period of in vitro exposure of pretherapy BM samples to imatinib was correlated with inhibition of colony growth and may represent the basis for an easy test that is capable of predicting the sensitivity of CML to treatment with imatinib for individual patients.  (+info)

TY - JOUR. T1 - Preferential sequestration in vitro of BCR/ABL negative hematopoietic progenitor cells among cytokine nonresponsive CML marrow CD34+ cells. AU - Veena, P.. AU - Cornetta, K.. AU - Davidson, A.. AU - Agüero, B.. AU - McMahel, J.. AU - Traycoff, C. M.. AU - Srour, E. F.. PY - 1997/6/2. Y1 - 1997/6/2. N2 - It is believed that long-term cultures of CML marrow cells favor the outgrowth of BCR/ABL negative hematopoietic progenitor cells (HPC) and that this phenomenon may be enhanced with negative hematopoietic regulators which can maintain primitive HPC in a quiescent state. Proliferation of CML marrow CD34+ cells in primary short-term cultures, maintained in the presence or absence of macrophage inhibitory protein-1 alpha (MIP-1α), was tracked with the membrane dye PKH2. After 7 to 10 days it was possible to distinguish between cytokine responsive (CR) CD34+ cells (cells which had divided thus becoming PKH2(dim)) and cytokine nonresponsive (CNR) CD34+ cells (cells which had not ...
TY - JOUR. T1 - Characteristics and survival of BCR/ABL negative chronic myeloid leukemia. T2 - A retrospective analysis of the Surveillance, Epidemiology and End Results database. AU - Giri, Smith. AU - Pathak, Ranjan. AU - Martin, Mike G.. AU - Bhatt, Vijaya Raj. PY - 2015/12. Y1 - 2015/12. UR - http://www.scopus.com/inward/record.url?scp=84993736220&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=84993736220&partnerID=8YFLogxK. U2 - 10.1177/2040620715607416. DO - 10.1177/2040620715607416. M3 - Letter. C2 - 26622999. AN - SCOPUS:84993736220. VL - 6. SP - 308. EP - 312. JO - Therapeutic Advances in Hematology. JF - Therapeutic Advances in Hematology. SN - 2040-6207. IS - 6. ER - ...
Free, official coding info for 2021 ICD-10-CM C92.2 - includes detailed rules, notes, synonyms, ICD-9-CM conversion, index and annotation crosswalks, DRG grouping and more.
TY - JOUR. T1 - DETECTION OF REARRANGEMENT WITHIN THE BREAKPOINT CLUSTER REGION OF CHROMOSOME 22 IN THE DIAGNOSIS OF CHRONIC MYELOID LEUKEMIA. AU - HUTCHINS, C.. AU - CASEY, G.. AU - White, Deborah. AU - MOORE, S.. AU - RUDZKI, Z.. AU - KIMBER, R.. PY - 1989/1/1. Y1 - 1989/1/1. N2 - Chronic myeloid leukemia (CML) is characterised by the presence of a Philadelphia (Ph) chromosome in approximately 95% of patients. Molecular analysis has shown that the Ph chromosome translocation breakpoints are clustered within 5.8kb on chromosome 22 (breakpoint cluster region or bcr). This has facilitated the diagnosis of CML by nucleic acid hybridisation using probes specific for the bcr to detect DNA rearrangement in this region. Forty patients diagnosed with CML, including four with variant Ph chromosome translocations and three with normal karyotypes were analysed for rearrangement within the bcr. All except one patient with Ph negative CML had rearrangement within the bcr. In contrast, none of the patients ...
Description: The protein encoded by this gene is a component of centriolar satellites, which are electron dense granules scattered around centrosomes. Inhibition studies show that this protein is essential for the correct localization of several centrosomal proteins, and for anchoring microtubules to the centrosome. Chromosomal aberrations involving this gene are associated with papillary thyroid carcinomas and a variety of hematological malignancies, including atypical chronic myeloid leukemia and T-cell lymphoma. Multiple transcript variants encoding different isoforms have been found for this gene ...
The protein encoded by this gene is a component of centriolar satellites, which are electron dense granules scattered around centrosomes. Inhibition studies show that this protein is essential for the correct localization of several centrosomal proteins, and for anchoring microtubules to the centrosome. Chromosomal aberrations involving this gene are associated with papillary thyroid carcinomas and a variety of hematological malignancies, including atypical chronic myeloid leukemia and T-cell lymphoma.
The official nomenclature in this field has gone through many changes over the years and the MeSH tree structure in this area had not been revised, in toto, for a long time. The main authority source used in this revision was the International Classification of Diseases for Oncology (ICD-O), 3d edition, supplemented by recent papers and texts1. Members of some working groups who are advising on the upcoming 4th edition were also consulted.. Many of the leukemia terms have undergone name changes as immunophenotypic and molecular biological techniques have made diagnosis more precise. For instance the old descriptor LEUKEMIA, MYELOID, CHRONIC is now called LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE. The old descriptor LEUKEMIA, MYELOID, PHILADELPHIA-NEGATIVE is now LEUKEMIA, MYELOID, CHRONIC, ATYPICAL, BCR-ABL NEGATIVE.. The old classification system for lymphomas, was discarded for a simpler model. Many old names are now obsolete, though some have been retained as entry terms. This includes ...
To characterize the pharmacokinetics of vincristine in two patient cohorts: Bcr-Abl positive ALL patients treated with the standard protocol with imatinib and Bcr-Abl negative ALL patients treated with the same protocol but without imatinib ...
The FAB group has recently published guidelines for distinguishing chronic granulocytic leukaemia (CGL) from chronic myelomonocytic leukaemia (CMML) and atypical chronic myeloid leukaemia (aCML). Whereas CGL is generally recognized to be a distinct entity, there is debate as to whether CMML and aCML are separate disorders or part of a spectrum of myeloproliferative disorders with dysplastic features. Data are presented on 10 cases who developed features of a CML during the course of their disease but who presented with a normal or a low leucocyte count without a monocytosis and were diagnosed as refractory anaemia. This suggests that, at least in some cases, aCML represents an unusual evolution of MDS, and even though these patients have a uniformly poor prognosis it may be premature to regard aCML as a distinct clinical entity ...
TY - JOUR. T1 - Prognostic impact of pretreatment cytogenetics in adult Philadelphia chromosome-negative acute lymphoblastic leukemia in the era of minimal residual disease. AU - Issa, Ghayas C.. AU - Kantarjian, Hagop M.. AU - Yin, C. Cameron. AU - Qiao, Wei. AU - Ravandi, Farhad. AU - Thomas, Deborah. AU - Short, Nicholas J.. AU - Sasaki, Koji. AU - Garcia-Manero, Guillermo. AU - Kadia, Tapan M.. AU - Cortes, Jorge E.. AU - Daver, Naval. AU - Borthakur, Gautam. AU - Jain, Nitin. AU - Konopleva, Marina. AU - Khouri, Issa. AU - Kebriaei, Partow. AU - Champlin, Richard E.. AU - Pierce, Sherry. AU - OBrien, Susan M.. AU - Jabbour, Elias. PY - 2017/2/1. Y1 - 2017/2/1. N2 - BACKGROUND: The introduction of novel prognostic factors such as minimal residual disease (MRD) and genomic profiling has led to the reevaluation of the role of cytogenetics and other conventional factors in risk stratification for acute lymphoblastic leukemia (ALL). METHODS: This study assessed the impact of baseline ...
Outcomes of acute lymphoblastic leukemia (ALL) in older adults treated with chemotherapy are poor. The CD19/CD3 bispecific T-cell engager (BiTE) antibody blinatumomab is approved for refractory, relapsed or minimal/measurable residual disease (MRD)-positive B-cell ALL, but there is little experience in the upfront setting, including in older patients. We retrospectively analyzed outcomes of blinatumomab monotherapy in five newly diagnosed Philadelphia chromosome-negative B-cell ALL patients over 70 years. Three had cytokine release syndrome, treated with dexamethasone and/or tocilizumab, and four patients had neurotoxicity, treated with dexamethasone, without blinatumomab interruption. All five achieved complete remission (CR) after cycle one, three with undetectable MRD. All five were alive at 8 to 15 months. Three remained in MRD-negative CR. Two relapsed after cycle 3, one with extramedullary disease. In our small cohort of patients over 70 years, blinatumomab was safe initial therapy and ...
Philadelphia chromosome-negative ALL in the older adult (age ≥40 y): Standard multiagent chemotherapy regimen (eg, CALGB 8811 [daunorubicin, vincristine, prednisone, pegaspargase, cyclophosp... more
1 Schinzel A, Giedion A. A syndrome of severe midface retraction, multiple skull anomalies, clubfeet, and cardiac and renal malformations in sibs. Am J Med Genet 1978; 1: 361-375. 2 Piazza R, Valletta S, Winkelmann N, Redaelli S, Spinelli R, Pirola A et al. Recurrent SETBP1 mutations in atypical chronic myeloid leukemia. Nat Genet 2012; 45: 18-24. 3 Makishima H, Yoshida K, Nguyen N, Sanada M, Okuno Y, Ng KP et al. Somatic mutations in Schinzel-Giedion Syndrome gene SETBP1 determine progression in myeloid malignancies. Blood 2012; 120: 2 (abstract). 4 Damm F, Itzykson R, Kosmider O, Droin N, Renneville A, Chesnais V et al. SETBP1 mutations in 658 patients with myelodysplastic syndromes, chronic myelomonocytic leukemia and secondary acute myeloid leukemias. Leukemia 2013; 27: 1401-1403. 5 Laborde RR, Patnaik MM, Lasho TL, Finke CM, Hanson CA, Knudson RA et al. SETBP1 mutations in 415 patients with primary myelofibrosis or chronic myelomonocytic leukemia (CMML): independent prognostic impact in CMML.
Wang SA, Hasserjian RP, Fox PS, Rogers HJ, Geyer JT, Chabot-Richards D, Weinzierl E, Hatem J, Jaso J, Kanagal-Shamanna R, Stingo FC, Patel KP, Mehrotra M, Bueso-Ramos C, Young KH, Dinardo CD, Verstovsek S, Tiu RV, Bagg A, Hsi ED, Arber DA, Foucar K, Luthra R, Orazi A. Atypical chronic myeloid leukemia is clinically distinct from unclassifiable myelodysplastic/myeloproliferative neoplasms. Blood. 2014 Apr 24; 123(17):2645-51 ...
2.1.2 If superiority of blinatumomab in the MRD positive group is shown, to compare the OS of blinatumomab in conjunction with chemotherapy to chemotherapy alone in patients with BCR-ABL-negative B cell precursor ALL who are MRD negative after induction and intensification chemotherapy, based on MFC assessment of residual blasts ...
The high toxicity of current Anti-Retroviral Therapy (ART) regimens has driven a number of studies investigating therapeutic approaches aimed at reducing drug exposure while maintaining the beneficial effects of immune reconstitution. Preliminary observations in HCV/HIV co-infected individuals already support an antiviral effect by Pegylated Interferon-Alpha-2A (Peg-IFN-Alpha-2A:Pegasys®) on HIV-1 replication; however, the ability of Peg-IFN-Alpha-2A (as a single agent) to maintain long-term suppression of HIV-1 replication in patients who interrupt ART after having achieved immune reconstitution remains undetermined. The rationale for addressing two doses of Peg-IFN-Alpha-2A (180 and 90 ug/week) is based on the antiviral activity reported with both doses and the lower incidence of adverse events associated with doses lower than that approved for HCV therapy (90 versus 180ug/week).. The long-range goal of this proposal is to determine if Peg-IFN-Alpha-2A monotherapy can sustain HIV-1 ...
PRIMARY OBJECTIVES: I. To evaluate the 3-year survival rate in elderly patients with newly diagnosed Philadelphia (Ph)-negative acute
Vincristine Liposome is an anti-cancer chemotherapy drug used in the treatment of Philadelphia chromosome-negative acute lymphoblastic leukemia.
PRIMARY OBJECTIVES:I. To compare the overall survival (OS) of blinatumomab in conjunction with chemotherapy to chemotherapy alone in patients with
Sigma-Aldrich offers abstracts and full-text articles by [Nicholas A Vitanza, Wafik Zaky, Roy Blum, Julia A Meyer, Jinhua Wang, Teena Bhatla, Debra J Morrison, Elizabeth A Raetz, William L Carroll].
Based on assessments of ropeginterferon alpha-2b in a real-world setting, researchers highlighted the safety, tolerance, and efficacy of the treatment in Philadelphia-negative myeloproliferative neoplasm (MPNs).
TY - JOUR. T1 - Monosomal karyotype in Philadelphia chromosome-negative acute lymphoblastic leukemia. AU - Kenderian, S. S.. AU - Al-Kali, A.. AU - Gangat, N.. AU - Letendre, L.. AU - Hogan, W. J.. AU - Litzow, M. R.. AU - Patnaik, M. M.. N1 - Copyright: Copyright 2013 Elsevier B.V., All rights reserved.. PY - 2013/7. Y1 - 2013/7. UR - http://www.scopus.com/inward/record.url?scp=84880877717&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=84880877717&partnerID=8YFLogxK. U2 - 10.1038/bcj.2013.21. DO - 10.1038/bcj.2013.21. M3 - Letter. C2 - 23832069. AN - SCOPUS:84880877717. VL - 3. JO - Blood Cancer Journal. JF - Blood Cancer Journal. SN - 2044-5385. IS - 7. ER - ...
On December 3, 2014, blinatumomab (Blincyto) was granted accelerated approval for use in treating Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL).1,2. Supporting Trial. Approval was based on results of a single-arm trial in 185 patients showing achievement of durable complete remission/complete remission with partial hematologic recovery. Blinatumomab was administered by continuous infusion for 4 weeks of a 6-week cycle. In the first cycle, the initial dose was 9 µg/d for week 1, then 28 µg/d for the remaining 3 weeks. The target dose of 28 µg/d was administered in cycle 2 and subsequent cycles starting on day 1 of each cycle.. Among treated patients, the median age was 39 years (range, 18-79 years), 34% had undergone hematopoietic stem cell transplantation prior to receiving blinatumomab, and 17% had received more than two prior salvage therapies.. Complete remission/complete remission with partial hematologic recovery within two ...
TY - JOUR. T1 - Philadelphia chromosome‐negative chronic myelogenous leukemia with rearrangement of the breakpoint cluster region. Long term follow‐up results. AU - Cortes, Jorge E.. AU - Talpaz, Moshe. AU - Beran, Miloslav. AU - OBrien, Susan M.. AU - Rios, Mary B.. AU - Stass, Sanford. AU - Kantarjian, Hagop M.. PY - 1995/1/15. Y1 - 1995/1/15. N2 - Background. Five to 10% of patients with chronic myelogenous leukemia (CML) do not have the Philadelphia chromosome (Ph), but one‐third of them have rearrangements of the breakpoint cluster region (BCR‐positive). Methods. The authors analyzed the characteristics, treatment response, and prognosis of 23 patients with BCR‐positive, Ph‐negative CML, and compared them with patients with Ph‐positive CML, Ph‐negative BCR‐negative CML and chronic myelomonocytic leukemia (CMML) treated during the same period. Results. Seventeen patients had early chronic phase CML, 3 had late chronic phase, 2 had accelerated phase, and 1 had blastic ...
TY - JOUR. T1 - The colony-Stimulating factor 3 receptor T640N mutation is oncogenic, sensitive toJAKInhibition, and mimics T618i. AU - Maxson, Julia. AU - Luty, Samuel B.. AU - MacManiman, Jason D.. AU - Paik, Jason C.. AU - Gotlib, Jason. AU - Greenberg, Peter. AU - Bahamadi, Swaleh. AU - Savage, Samantha L.. AU - Abel, Melissa L.. AU - Eide, Christopher A.. AU - Loriaux, Marc. AU - Stevens, Emily A.. AU - Tyner, Jeffrey. PY - 2016/2/1. Y1 - 2016/2/1. N2 - Purpose: Colony-stimulating factor 3 receptor (CSF3R) mutations have been identified in the majority of chronic neutrophilic leukemia (CNL) and a smaller percentage of atypical chronic myeloid leukemia (aCML) cases. Although CSF3R point mutations (e.g., T618I) are emerging as key players in CNL/aCML, the significance of rarer CSF3R mutations is unknown. In this study, we assess the importance of the CSF3R T640N mutation as a marker of CNL/aCML and potential therapeutic target. Experimental Design: Sanger sequencing of leukemia samples was ...
TY - JOUR. T1 - Clonal cytogenetic abnormalities and BCL2 rearrangementin interdigitating dendritic cell sarcoma [3]. AU - Nayer, Hassan. AU - Murphy, Kathleen M.. AU - Hawkins, Anita L.. AU - Long, Patricia P.. AU - Gillison, Maura. AU - Borowitz, Michael. AU - Griffin, Constance A.. PY - 2006/12/1. Y1 - 2006/12/1. UR - http://www.scopus.com/inward/record.url?scp=33845572651&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=33845572651&partnerID=8YFLogxK. U2 - 10.1080/10428190600879896. DO - 10.1080/10428190600879896. M3 - Letter. C2 - 17169812. AN - SCOPUS:33845572651. VL - 47. SP - 2651. EP - 2654. JO - Leukemia and Lymphoma. JF - Leukemia and Lymphoma. SN - 1042-8194. IS - 12. ER - ...
TY - JOUR. T1 - Unbiased pro-thrombotic features at diagnosis in 977 thrombocythemic patients with Philadelphia-negative chronic myeloproliferative neoplasms. AU - Gugliotta, Luigi. AU - Iurlo, Alessandra. AU - Gugliotta, Gabriele. AU - Tieghi, Alessia. AU - Specchia, Giorgina. AU - Gaidano, Gianluca. AU - Scalzulli, Potito Rosario. AU - Rumi, Elisa. AU - Dragani, A.. AU - Martinelli, Vincenzo. AU - Santoro, Cristina. AU - Randi, M. L.. AU - Tagariello, G.. AU - Candoni, Anna. AU - Cattaneo, Daniele. AU - Ricco, Alessandra. AU - Palmieri, Raffaele. AU - Liberati, M.. AU - Langella, Maria. AU - Rago, Angela. AU - Bergamaschi, Micaela. AU - Monari, Paola. AU - Miglio, Rossella. AU - Santoro, Umberto. AU - Cacciola, Rossella R.. AU - Rupoli, Serena. AU - Mastrullo, Lucia. AU - Musto, Pellegrino. AU - Mazzucconi, M. G.. AU - Vignetti, Marco. AU - Cortelezzi, Agostino. AU - Vianelli, Nicola. AU - Martino, Bruno. AU - De Stefano, Valerio. AU - Passamonti, Francesco. AU - Vannucchi, Alessandro ...
Julia E. Maxson, Jason Gotlib, Daniel A. Pollyea, Angela G. Fleischman, Anupriya Agarwal, Christopher A. Eide, Daniel Bottomly, Beth Wilmot, Shannon K. McWeeney, Cristina E. Tognon, J. Blake Pond, Robert H. Collins, Basem Goueli, T. Oh Stephen, W. Deininger Michael, Bill H. Chang, Marc M. Loriaux, Brian J. Druker, Jeffrey W. Tyner ...
Abstract: The major complications of Philadelphia‐negative (Ph‐Negative) myeloproliferative neoplasms (MPNs) are thrombosis, haemorrhage and leukemic transformation. As systemic and haematological diseases, MPNs have the potential to affect many tissues and organs. Some complications lead to the diagnosis of MPNs, but other signs and symptoms are often misdiagnosed or neglected as a sign of MPN disease. […]. ...
SILVER SPRING, Md. - The Food and Drug Administration has approved a new drug for treating a rare type of leukemia, the agency said Thursday.. The FDA approved South San Francisco, Calif.-based Talon Therapeutics Marqibo (vincristine sulfate liposome), an injectable drug for Philadelphia chromosome-negative acute lymphoblasic leukemia, or Ph-negative ALL. The drug, which consists of the widely used anti-cancer drug vincristine encased within a liposome - a drug delivery system made of a material similar to cell membranes - is approved for patients whose leukemia has returned twice or more or has progressed after two or more regimens of therapy.. According to the National Cancer Institute, part of the National Institutes of Health, more than 6,000 people will be diagnosed with ALL this year, and 1,440 will die from it. The disease is a rapidly progressing form of blood and bone marrow cancer more common in children than adults.. ...
Persistence or recurrence of minimal residual disease (MRD) after chemotherapy results in clinical relapse in patients with acute lymphoblastic leukemia (ALL). In a phase 2 trial of B-lineage ALL patients with persistent or relapsed MRD, a T cell-engaging bispecific Ab construct induced an 80% MRD response rate. In the present study, we show that after a median follow-up of 33 months, the hematologic relapse-free survival of the entire evaluable study cohort of 20 patients was 61% (Kaplan-Meier estimate). The hema-tologic relapse-free survival rate of a subgroup of 9 patients who received allogeneic hematopoietic stem cell transplantation after blinatumomab treatment was 65% (Kaplan-Meier estimate). Of the subgroup of 6 Philadelphia chromosome-negative MRD responders with no further therapy after blinatumomab, 4 are in ongoing hematologic and molecular remission. We conclude that blinatumomab can induce long-lasting complete remission in B-lineage ALL patients with persistent or recurrent MRD. The
Learn more about Marqibo® (vinCRIStine sulfate LIPOSOME injection) at MARQIBO.com. Marqibo® is for the treatment of adult patients with Philadelphia chromosome-negative (Ph‒) acute lymphoblastic leukemia (ALL) in second or greater relapse or whose disease has progressed following 2 or more anti-leukemia therapies. This indication is based on overall response rate. Clinical benefit such as improvement in overall survival has not been verified.
Mutations in JAK2, MPL and CALR are highly relevant to the Philadelphia chromosome (Ph)-negative myeloproliferative neoplasms (MPNs). We performed high resolution melting analysis and Sanger sequencing together with T-A cloning to elucidate the unique mutation profile of these genes, in Chinese patients with MPNs. Peripheral blood DNA samples were obtained from 80 patients with polycythemia vera (PV), 80 patients with essential thrombocytosis (ET) and 50 patients with primary myelofibrosis (PMF). Ten PV patients were identified with diverse JAK2 exon 12 mutations. Five novel JAK2 Exon 12 mutation patterns (M532V/E543G, N533D, M535I/H538Y/K549I, E543G and D544N) were described. JAK2 V617F was detected in 140 samples (66 PV, 45 ET and 29 PMF). JAK2 Exon 12 mutations were prevalent (13%) and variable in the Chinese patients. Compared with PV patients with JAK2 V617F mutations, PV patients with JAK2 exon 12 mutations had an earlier median onset of disease (P = 0.0013). MPL W515L/K mutations were ...
We have followed one patient with Philadelphia (Ph)-negative chronic myelogenous leukemia and identified an additional four patients from the literature who showed the rearrangement in the breakpoint cluster region (bcr) on chromosome 22 characteristic of Ph-positive chronic myelogenous leukemia. The clinical course of these five patients was similar to that of Ph-positive patients, with easily controlled leukocyte counts, a prolonged benign phase, and prolonged survival. Furthermore, we have shown, for the first time, that bcr rearrangement in Ph-negative chronic myelogenous leukemia can result in expression of the aberrant 210-kilodalton bcr-abl fusion protein, which has been strongly implicated in Ph-positive leukemogenesis. Research data pertaining to possible cytogenetic mechanisms leading to production of p210bcr-abl in the absence of the Ph chromosome are reviewed. Molecular analysis provides an important tool for classifying and predicting prognosis of some patients with Ph-negative ...
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Imatinib mesylate (Gleevec; Novartis) has been successfully employed in the treatment of Philadelphia-positive chronic myeloid leukaemia (Ph+ CML) (Deininger et al, 2005). Although imatinib restores a polyclonal haemopoiesis in over 90% of patients, development of clonal chromosome abnormalities in Ph-negative cells (Ph) clonal evolution) occurs in about 15% of cases with a complete cytogenetic remission (CCR). This phenomenon has been very rarely observed in patients treated with interferon-a and/or cytotoxic agents. As the biological and clinical significance of these clones are still unclear, we investigated two cases of CML in chronic phase, not previously treated with genotoxic agents or drugs, in which imatinib therapy lead to the emergence of Ph) clones characterised by an abnormality initially disclosed in the Ph+ cells, a picture found only in two other cases in the literature (Gozzetti et al, 2003; Royer-Pokora et al, 2003). In patient 1, all metaphases at diagnosis carried both the Ph ...
The FDA approved South San Francisco, Calif.-based Talon Therapeutics Marqibo (vincristine sulfate liposome), an injectable drug for Philadelphia chromosome-negative acute lymphoblasic leukemia, or Ph-negative ALL. The drug, which consists of the widely used anti-cancer drug vincristine encased within a liposome - a drug delivery system made of a material similar to cell membranes - is approved for patients whose leukemia has returned twice or more or has progressed after two or more regimens of therapy.. According to the National Cancer Institute, part of the National Institutes of Health, more than 6,000 people will be diagnosed with ALL this year, and 1,440 will die from it. The disease is a rapidly progressing form of blood and bone marrow cancer more common in children than adults.. ...
Patients With Relapsed or Refractory ALL - INO-VATE ALL. The safety and efficacy of BESPONSA were evaluated in INO-VATE ALL (NCT01564784) a randomized (1:1), open-label, international, multicenter study in patients with relapsed or refractory ALL. Patients were stratified at randomization based on duration of first remission (, 12 months or ≥ 12 months, salvage treatment (Salvage 1 or 2) and patient age at randomization (, 55 or ≥ 55 years). Eligible patients were ≥ 18 years of age with Philadelphia chromosome-negative or Philadelphia chromosome-positive relapsed or refractory B-cell precursor ALL. All patients were required to have ≥ 5% bone marrow blasts and to have received 1 or 2 previous induction chemotherapy regimens for ALL. Patients with Philadelphia chromosome-positive B-cell precursor ALL were required to have disease that failed treatment with at least 1 tyrosine kinase inhibitor and standard chemotherapy. Table 1 shows the dosing regimen used to treat patients.. Among all ...
Class: Biological Therapy. Generic Name: Blinatumomab. Trade Name: Blincyto®. For which conditions is this drug approved? Blincyto is approved for treatment of a certain type of acute lymphoblastic leukemia (ALL): Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute ALL.. What is the mechanism of action? Blincyto is a type of drug known as a monoclonal antibody. Monoclonal antibodies target and attach to cancer cells, which tells the immune system to destroy the cancer. Specifically, Blincyto targets a protein called CD19 thats found on the surface of B-cell leukemia cells. Another protein, CD3, thats found on the surface of T-cell lymphocytes (part of the immune system), then connects with CD19 to destroy the cancer cells.. How is Blincyto typically given (administered)? Blincyto is given by intravenous (IV) infusion into your vein using an infusion pump. One treatment cycle includes a continuous IV infusion for four weeks, followed by a two-week break during which ...
DEERFIELD, Ill., January 15, 2015 - Walgreens today announced that, effective immediately, Walgreens Infusion Services will serve as a limited network home infusion provider for BLINCYTO™ (blinatumomab), a therapy for the treatment of patients with Philadelphia chromosome-negative (Ph-) relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). BLINCYTO™ can now be obtained through and administered by Walgreens Infusion Services.. Through our nationwide, community-based infusion services, we deliver comprehensive and collaborative patient care for those with complex conditions and were pleased to be able to provide home infusion services to appropriate patients requiring immunotherapy to treat this rare form of ALL, said Paul Mastrapa, president, Walgreens Infusion Services.. Walgreens Infusion Services specially trained infusion nurses and pharmacists treat patients with a wide range of acute, chronic and rare conditions. As the nations largest provider of home and ...
Background. Prognosis of acute lymphoblastic leukemia in elderly is poor. The GRAALL-SA1 phase II trial randomly compared the efficacy and toxicity of pegylated liposomal doxorubicin versus continuous-infusion doxorubicin in patients ≥55 years with Philadelphia chromosome-negative ALL. Design and Methods. Sixty patients received either continuous infusion-Doxorubicin (12 mg/m²/d) and continuous infusion-vincristine (0.4 mg/day) on day1-4 or liposomal-Doxorubicin (40 mg/m2;) and standard vincristine (2 mg) on day1, accompanied by dexamethasone, followed at day 28 by a second cycle, reinforced by cyclophosphamide. Endpoints were safety, outcome and prognostic factors. Results. Myelosupression was reduced in the Peg-Dox arm with shorter severe neutropenia (P=0.05), shorter severe thrombocytopenia (P=0.03), and less erythrocytes transfusions (P=0.04). Grade 3/4 infections and gram-negative bacteremia were reduced in the Peg-Dox arm (P=0.04 and 0.02, respectively). There was a trend toward less ...
Background: The discovery of somatic acquired mutations of JAK2 (V617F) in Philadelphia-negative myeloproliferative neoplasms (Ph-negative MPNs) including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) has not only improved rational disease classification and prognostication but also brings new understanding insight into the pathogenesis of diseases. Dosage effects of the JAK2 (V617F) allelic burden in Ph-negative MPNs may partially influence clinical presentation, disease progression, and treatment outcome. Material and Methods: Pyrosequencing was performed to detect JAK2 (V617F) and MPL (W515K/L) and capillary electrophoresis to identify CALR exon 9.0 mutations in 100.0 samples of Ph-negative MPNs (38.0 PV, 55 ET, 4 PMF, and 3 MPN-U). Results: The results showed somatic mutations of JAK2 (V617F) in 94.7% of PV, 74.5% of ET, 25.0% of PMF, and all MPN-U. A high proportion of JAK2 (V617F) mutant allele burden (mutational load | 50.0%) was predominantly observed
Class: Biological Therapy. Generic Name: Blinatumomab. Trade Name: Blincyto®. For which conditions is this drug approved? Blincyto is approved for treatment of a certain type of acute lymphoblastic leukemia (ALL): Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute ALL.. What is the mechanism of action? Blincyto is a type of drug known as a monoclonal antibody. Monoclonal antibodies target and attach to cancer cells, which tells the immune system to destroy the cancer. Specifically, Blincyto targets a protein called CD19 thats found on the surface of B-cell leukemia cells. Another protein, CD3, thats found on the surface of T-cell lymphocytes (part of the immune system), then connects with CD19 to destroy the cancer cells.. How is Blincyto typically given (administered)? Blincyto is given by intravenous (IV) infusion into your vein using an infusion pump. One treatment cycle includes a continuous IV infusion for four weeks, followed by a two-week break during which ...
Epigallocatechin-3-gallate induces apoptosis and cell cycle arrest in Human T-Cell Lymphotrophic Virus type 1 -positive and negative leukemia cells.
The cytokine BAFF is produced by a number of cell types, including monocytes, neutrophils, macrophages, dendritic cells, and some subsets of T cells (17). Receptors for BAFF, however, were initially thought to be restricted to more differentiated B-lineage cells. Therefore, the expression of BAFF receptors on transformed B-lineage lymphocytes in CLL was not entirely unexpected. In contrast, based on BAFF-null and BAFF-R-null mutants as well as other studies, it has been generally accepted that precursor B-lineage cells do not express this receptor. Our studies confirm that there is no expression of this receptor in normal bone marrow pre-B cells. Interestingly, Rodig and colleagues (35) also performed FACS on two pre-B ALL samples and reported that these were negative for expression of BAFF-R. Therefore, the prominent expression of the BAFF-R that we detected on both Ph-positive and Ph-negative ALL samples was unanticipated. In fact, all 12 samples that were tested by us, including original ALL ...
Background: This study was conducted to evaluate the frequency of JAK2, CALR and MPL mutations in with BCR-ABL myeloproliferative neoplasms and their association with demographic data and hematologic parameters in a referral center, in the Middle East. Methods: Seventy-one patients with BCR-ABL negative myeloproliferative neoplasms were evaluated for JAK2 V617F, CALR type 1, type 2, and MPL by allele-specific PCR and conventional PCR from 2018 to 2019. Results: Twenty three patients were categorized as polycythemia vera and demonstrated JAK2 V617F in 91.3 % of these cases. Thirty-eight patients were classified as essential thrombocythemia and showed JAK2 V617F in 52.6%, CALR type 1 in 18.4%, CALR type 2 in 7.9% and no mutation in 21.1%. Seven patients were recognized as primary myelofibrosis and exhibited JAK2 V617F mutation in 57.1%, CALR type 1 in 14.3 %, CALR type 2 in 14.3% and no mutation in 14.3%. Three patients were diagnosed as MPN, unclassifiable and revealed JAK2 V617F mutation in 33.3% and
Human leukocyte antigen (HLA) haploidentical stem cell transplantation (haplo-SCT) as a postremission treatment for standard risk Philadelphia chromosome-negative acute lymphoblastic leukemia (SR Ph-ALL) in the first complete remission (CR1) has not been defined. In this multicenter, phase 3 study (NCT02042690), of the 131 consecutive Ph-ALL young adult patients (YA, aged 18-39 years) without high-risk features who achieved CR1, 114 patients without HLA-matched donors received consolidation with an adult chemotherapy regimen (n = 55) or haplo-SCT (n = 59). In the landmark analysis, haplo-SCT resulted in a lower 2-year cumulative incidence of relapse (CIR, 12.8% vs 46.7%, P = 0.0017) and superior 2-year leukemia-free survival (LFS, 80.9% vs 51.1%, P = 0.0116) and 2-year overall survival (OS, 91.2% vs 75.7 [64.8-93.2] %, P = 0.0408) than chemotherapy. In the time-dependent multivariate analysis with propensity score adjustment, postremission treatment (haplo-SCT vs chemotherapy) was an independent risk
In this issue of the Hematology, Transfusion and Cell Therapy Journal, Cacemiro et al. evaluated the plasma cytokine profile of 47 patients with Ph-negative myeloproliferative neoplasms (MPN) [essential thrombocythemia (ET), primary myelofibrosis (PMF), and polycythemia vera (PV)] and of healthy subjects.1 They demonstrated increased levels of pro-inflammatory cytokines in MPN patients and higher levels of interferon (IFN)-γ-induced protein 10 (IP-10) in PMF patients with the JAK2 V617F mutation. They found differences in the cytokine profile among the three MPN disorders, including increased levels of IL-12p70, IL-17A, and RANTES in PMF, showing that MPN, in particular PMF, have altered inflammatory profiles. However, their sample population did not make clinical and prognostic implications of their findings possible.. What is the clinical relevance of the altered cytokine levels in MPN? Are they related to constitutional symptoms, transformation or evolution to fibrosis? Do they have an ...
Key words. Myelofibrosis (MF), including primary myelofibrosis (PMF) and MF secondary to essential thrombocythemia (ET) or polycythemia vera (PV), is a chronic Philadelphia chromosome-negative myeloproliferative neoplasm associated with progressive bone marrow fibrosis.1 Many patients with MF experience new or worsening anemia during disease progression. Varying from study to study, 35% to 54% of patients with PMF have been reported to have anemia (i.e., hemoglobin ,10 g/dL) at the time of diagnosis.2-5 Anemia adversely affects overall survival (OS), and is included as a key negative prognostic factor in validated prognostic scoring systems for patients with PMF, which were developed before the introduction of Janus kinase (JAK) inhibitor therapy.2,3,5 Ruxolitinib, a JAK1/JAK2 inhibitor, improved OS compared with placebo and best available therapy in patients with intermediate-2 or high-risk MF5 in the phase 3 COntrolled MyeloFibrosis Study With ORal JAK Inhibitor Treatment (COMFORT) ...
The classical Philadelphia chromosome-negative myeloproliferative neoplasms (MPN), which include essential thrombocythemia, polycythemia vera, and myelofibrosis (MF), are in a new era of molecular diagnosis, ushered in by the identification of the JAK2 V617F and cMPL mutations in 2005 and 2006, respectively, and the CALR mutations in 2013. Coupled with increased knowledge of disease pathogenesis and refined diagnostic criteria and prognostic scoring systems, a more nuanced appreciation has emerged of the burden of MPN in the United States, including the prevalence, symptom burden, and impact on quality of life. Biological advances in MPN have translated into the rapid development of novel therapeutics, culminating in the approval of the first treatment for MF, the JAK1/JAK2 inhibitor ruxolitinib. However, certain practical aspects of care, such as those regarding diagnosis, prevention of vascular events, choice of cytoreductive agent, and planning for therapies, present challenges for ...
BACKGROUND: The classical Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs), consisting of polycythemia vera, essential thrombocythemia, and primary myelofibrosis, are a heterogeneous group of neoplasms that harbor driver mutations in the JAK2, CALR, and MPL genes. The detection of these mutations has been incorporated into the recent World Health Organization (WHO) diagnostic criteria for MPN. Given a pressing clinical need to screen for these mutations in a routine diagnostic setting, a targeted next-generation sequencing (NGS) assay for the detection of MPN-associated mutations located in JAK2 exon 14, JAK2 exon 12, CALR exon 9, and MPL exon 10 was developed to provide a single platform alternative to reflexive, stepwise diagnostic algorithms ...
Conclusions:. Essential thrombocythemia, primary myelofibrosis, and polycythemia vera patients exhibited different patterns of cytokine production, as revealed by cytokine network correlations. Together, these findings suggest that augmented cytokine levels are associated with the physiopathology of myeloproliferative neoplasms. ...
Expert-reviewed information summary about the treatment of myelodysplastic/myeloproliferative neoplasms including chronic/juvenile myelomonocytic leukemias and atypical CML.
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At its peak in the early 1950s, Philadelphias manufacturing workforce totaled 365,000 people. As we all know, the citys domination declined long ago. Yet manufacturing survives and now manufacturers of all kinds are springing up.
Mayor Nutter said Monday evening that there were no specific threats or threat incidents in Philadelphia. - $author, Philadelphia Daily News
Brian Patrick Smith MD is a Critical Care Specialist who practices in Philadelphia, PA. Get a full report about this doctors background by clicking here.
Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med 344, 1031- ... BCR rearrangement-negative chronic myelogenous leukemia revisited. J Clin Oncol. 19, 2915-26 (2001). Druker, B.J. et al. ... Atypical chronic myeloid leukemia (aCML) is a type of leukemia. It is a heterogeneous disorder belonging to the group of ... Recurrent SETBP1 mutations in atypical chronic myeloid leukemia. Nat Genet. 2013 Jan;45(1):18-24. doi: 10.1038/ng.2495. Epub ...
M9876/3 Atypical chronic myelogenous leukemia BCR/ABL negative Atypical chronic myeloid leukemia (BCR/ABL negative)/(Ph1 ... Chronic lymphocytic leukemia Chronic lymphoid leukemia Chronic lymphatic leukemia M9826/3 Burkitt cell Leukemia (see also M9687 ... M9874/3 Acute myeloid leukemia, with maturation (FAB M2), NOS M9875/3 Chronic myelogenous leukemia BCR/ABL positive ... leukemia Acute granulocytic leukemia Acute myelogenous leukemia Acute myelocytic leukemia M9863/3 Chronic myeloid leukemia, NOS ...
JAK2 Myelodysplastic/myeloproliferative neoplasms Chronic myelomonocytic leukaemia Atypical chronic myeloid leukaemia, BCR-ABL1 ... Lymphomas, lymphocytic leukemias, and myeloma are from the lymphoid line, while acute and chronic myelogenous leukemia, ... BCR-ABL 1―like B-lymphoblastic leukaemia/lymphoma with iAMP21 T-lymphoblastic leukaemia/lymphoma Early T-cell precursor ... ALK-negative Breast implant-associated anaplastic large cell lymphoma Hodgkin lymphomas Nodular lymphocyte predominant Hodgkin ...
Myeloid. *Philadelphia chromosome t(9 ABL; 22 BCR). *Acute myeloblastic leukemia with maturation t(8 RUNX1T1;21 RUNX1) ... The effect of chronic exposure to carbon monoxide can depend on the stage of pregnancy in which the mother is exposed. Exposure ... Tetracycline, an antibiotic, should never be prescribed to women of reproductive age or to children, because of its negative ... cerebral calcifications means certain areas of the brain have atypical calcium deposits,[50] and meningoencephalitis is the ...
Myeloid. *Philadelphia chromosome t(9 ABL; 22 BCR). *Acute myeloblastic leukemia with maturation t(8 RUNX1T1;21 RUNX1) ... Treatment of chronic kidney failure is dependent on the type of kidney failure and may involve dialysis. ... Atypical plasma cell infiltrate with both Russell (cytoplasmic) and Dutcher (nuclear) bodies (H&E, 50x) ... and CD45 negative.[15] Flow cytometry is often used to establish the clonal nature of the plasma cells, which will generally ...
Atypical chronic myeloid leukemia, BCR/ABL-negative. 2016 2017 2018 2019 2020 2021 Non-Billable/Non-Specific Code *C92.2 should ... atypical chronic myeloid leukemia BCR/ABL-negative (C92.2-). *chronic myeloid leukemia BCR/ABL-positive (C92.1-) ... Chronic myeloid leukemia, BCR/ABL-positive. 2016 2017 2018 2019 2020 2021 Non-Billable/Non-Specific Code Applicable To*Chronic ... Chronic myeloid leukemia, BCR/ABL-positive. 2016 2017 2018 2019 2020 2021 Non-Billable/Non-Specific Code Applicable To*Chronic ...
Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative*Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative ... BCR-ABL Negative" by people in this website by year, and whether "Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative" was a ... "Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative" is a descriptor in the National Library of Medicines controlled ... Below are the most recent publications written about "Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative" by people in ...
Myeloid, Chronic, Atypical, BCR-ABL Negative; Atypical Chronic Myeloid Leukemia; Chronic Myeloid Leukemia, Atypical; Leukemia, ... Myeloid, Philadelphia-Negative; Myeloid Leukemia, Philadelphia-Negative. On-line free medical diagnosis assistant. Ranked list ... Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative (Atypical Chronic Myeloid Leukemia; Chronic Myeloid Leukemia, Atypical; ... Chronic, Atypical, BCR-ABL Negative"Drugs, active principles and "Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative" ...
Chronic myeloid leukemia (CML) is a cancer of the white blood cells. It usually affects older adults. Learn about symptoms, ... BCR-ABL Positive (National Institutes of Health) * ClinicalTrials.gov: Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative ( ... What is chronic myeloid leukemia (CML)? Chronic myeloid leukemia (CML) is a type of chronic leukemia. "Chronic" means that the ... Chronic Myeloid Leukemia Also called: Chronic granulocytic leukemia, Chronic myelogenous leukemia, CML ...
Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative. Hemoglobinuria. Hemoglobinuria, Paroxysmal. Disease. Pathologic ... Atypical Chronic Myeloid Leukemia, BCR-ABL1 Negative Chronic Myelomonocytic Leukemia de Novo Myelodysplastic Syndrome Essential ... Atypical chronic myeloid leukemia (CML): Philadelphia chromosome-negative patients with a diagnosis of atypical CML ... Leukemia, Myelogenous, Chronic, BCR-ABL Positive. Leukemia, Myelomonocytic, Chronic. Anemia, Refractory. Polycythemia. ...
Leukemia, Monocytic, Acute. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative. Hypereosinophilic Syndrome. Leukemia, ... Atypical Chronic Myeloid Leukemia, BCR-ABL1 Negative Blastic Phase Chronic Myelogenous Leukemia Chronic Eosinophilic Leukemia ... Chronic, BCR-ABL Positive. Primary Myelofibrosis. Leukemia, Myelomonocytic, Acute. Leukemia, Myelomonocytic, Chronic. Leukemia ... Recurrent Adult Acute Myeloid Leukemia Relapsing Chronic Myelogenous Leukemia Secondary Acute Myeloid Leukemia Secondary ...
Translation: Atypical chronic myeloid leukemia, BCR/ABL-negative.. Before we can realize the benefits of an "international ...
Exposures to DNA-damaging drugs and ionizing radiations increase risks of acute myeloid leukemia (AML) and myelodysplastic ... Leukemia, Myeloid, Chronic, Atypical, Bcr-abl Negative. A myelodysplastic/myeloproliferative disorder characterized by ... Vaccine Therapy Plus Immune Adjuvant in Treating Patients With Chronic Myeloid Leukemia, Acute Myeloid Leukemia, or ... Leukemia, Myelomonocytic, Acute. A pediatric acute myeloid leukemia involving both myeloid and monocytoid precursors. At least ...
The old descriptor LEUKEMIA, MYELOID, PHILADELPHIA-NEGATIVE is now LEUKEMIA, MYELOID, CHRONIC, ATYPICAL, BCR-ABL NEGATIVE. ... For instance the old descriptor LEUKEMIA, MYELOID, CHRONIC is now called LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE. ... Leukemia - Lymphoma Changes. The official nomenclature in this field has gone through many changes over the years and the MeSH ... Many of the leukemia terms have undergone name changes as immunophenotypic and molecular biological techniques have made ...
accelerated phase chronic myelogenous leukemia. *atypical chronic myeloid leukemia, BCR-ABL negative ... Chronic Myeloproliferative Disorders, Leukemia, Lymphoma, Myelodysplastic Syndromes, Myelodysplastic/Myeloproliferative ... blastic phase chronic myelogenous leukemia. *childhood acute lymphoblastic leukemia in remission. *childhood acute myeloid ... recurrent childhood acute lymphoblastic leukemia. *recurrent childhood acute myeloid leukemia. *relapsing chronic myelogenous ...
Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative. *Neoplasms, Glandular and Epithelial. *Ovarian Neoplasms ... Adult Acute Myeloid Leukemia With t(8;21)(q22;q22), Atypical Chronic Myeloid Leukemia, BCR-ABL1 Negative, Myelodysplastic/ ... Adult Acute Myeloid Leukemia With Inv(16)(p13;q22), Adult Acute Myeloid Leukemia With t(15;17)(q22;q12), Adult Acute Myeloid ... Adult Acute Myeloid Leukemia With t(8;21)(q22;q22). *Atypical Chronic Myeloid Leukemia, BCR-ABL1 Negative ...
Leukemia, Myeloid, Chronic, Atypical, Bcr-abl Negative. A myelodysplastic/myeloproliferative disorder characterized by ... Clofarabine and Cyclophosphamide in Treating Patients With Relapsed or Refractory Acute Leukemia, Chronic Myelogenous Leukemia ... but cytogenetically lacking a PHILADELPHIA CHROMOSOME or bcr/abl fusion gene (GENES, ABL). ... myelodysplasia associated with bone marrow and peripheral blood patterns similar to CHRONIC MYELOID LEUKEMIA, ...
Atypical chronic myeloid leukemia BCR-ABL 1 negative: A case report and literature review - Open access 2019 ... A case of chronic eosinophilic leukemia with secondary transformation to acute myeloid leukemia - Open access 2018 ... Effects of nilotinib on platelet function in patients with chronic myeloid leukemia in chronic phase - Open access 2019 ... Myodesopsia is a symptom of central nervous system blast crisis in chronic myeloid leukemia - Open access 2019 ...
Atypical Chronic Myeloid Leukemia BCR-ABL 1 negative: A case report and literature review ... Mohamed ChakourAbstractAtypical chronic myeloid leukemia (aCML), BCR-ABL1 negative is a rare myelodysplastic syndrome / ... chronic << (leukemia,leukaemia) here the word chronic must come somewhere before either the work leukemia or leukaemia.. ... Source: Leukemia Research Reports - May 26, 2019. Category: Hematology Source Type: research ...
C92.2 Atypical chronic myeloid leukemia, BCR/ABL-negative C92.20 …… not having achieved remission ... it is called acute myeloid leukemia. When the proliferating myeloid cells are neutrophils, it is called chronic myelogenous ... Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (myeloid progenitor ... Myeloid leukemia. 2016 2017 2018 2019 Non-Billable/Non-Specific Code *C92 should not be used for reimbursement purposes as ...
Chronic myeloid leukemia (CML) should be ruled out by screening for BCR-ABL gene fusion. In addition, atypical Philadelphia ... chromosome negative (Ph-) CML needs to be excluded. Cases of MDS/MPN with eosinophilia associated with t(5;12) (q31-33;p12)/ ... Clinical Trial: Genetic Study of Chronic Lymphocytic Leukemia Families. *TKIs Appear Safe in Patients With Chronic Myeloid ... Chronic myelomonocytic leukemia. What every physician needs to know:. Chronic myelomonocytic leukemia (CMML) is a clonal stem- ...
Atypical Chronic Myeloid Leukemia BCR-ABL 1 negative: A case report and literature review ... Mohamed ChakourAbstractAtypical chronic myeloid leukemia (aCML), BCR-ABL1 negative is a rare myelodysplastic syndrome / ... chronic << (leukemia,leukaemia) here the word chronic must come somewhere before either the work leukemia or leukaemia.. ... kinase inhibitors are considered as highly effective and relatively safe drugs for the treatment of chronic myeloid leukemia. ...
T lymphoblastic lymphoma with BCR-ABL negative chronic myeloid leukaemia: a novel association Mahwish Faizan1, Saadia Anwar1, ... 16. Crisa E, Nicolosi M, and Ferri V, et al (2020) Atypical chronic myeloid leukemia: where are we now? Int J Mol Sci 21(18) ... Chronic myeloid leukaemia (CML) constitutes 2%-3% of leukaemia in children. Atypical CML (BCR-ABL negative) is a challenging ... T lymphoblastic lymphoma with BCR-ABL negative chronic myeloid leukaemia: a novel association. Mahwish Faizan1, Saadia Anwar1, ...
Chronic myeloid leukemia (CML) should be ruled out by screening for BCR-ABL gene fusion. In addition, atypical Philadelphia ... chromosome negative (Ph-) CML needs to be excluded. Cases of MDS/MPN with eosinophilia associated with t(5;12) (q31-33;p12)/ ... Chronic myelomonocytic leukemia. What every physician needs to know:. Chronic myelomonocytic leukemia (CMML) is a clonal stem- ... Beware of other conditions that can mimic chronic myelomonocytic leukemia: * Which individuals are most at risk for developing ...
Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med 344, 1031- ... BCR rearrangement-negative chronic myelogenous leukemia revisited. J Clin Oncol. 19, 2915-26 (2001). Druker, B.J. et al. ... Atypical chronic myeloid leukemia (aCML) is a type of leukemia. It is a heterogeneous disorder belonging to the group of ... Recurrent SETBP1 mutations in atypical chronic myeloid leukemia. Nat Genet. 2013 Jan;45(1):18-24. doi: 10.1038/ng.2495. Epub ...
BCR-ABL is only present in hematopoietic cells, but it has been found using very sensitive PCR methods in the hematopoietic ... The remaining cases, collectively referred to as true Ph-negative CML or atypical CML, are a heterogeneous group of disorders ... "Chapter 4. Chronic Myeloid Leukemia." The MD Anderson Manual of Medical Oncology, 2e Kantarjian HM, Wolff RA, Koller CA. ... Chronic myeloid leukemia (CML) is a pluripotent hematopoietic stem cell disorder leading to myeloproliferation and its ...
Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative Mutation Survival Erythrocyte Transfusion Myelodysplastic Syndromes ... N2 - Atypical chronic myeloid leukemia (aCML) is an aggressive myeloid neoplasm with overlapping features of myelodysplastic ... AB - Atypical chronic myeloid leukemia (aCML) is an aggressive myeloid neoplasm with overlapping features of myelodysplastic ... Atypical chronic myeloid leukemia (aCML) is an aggressive myeloid neoplasm with overlapping features of myelodysplastic ...
Chronic Myelomonocytic leukemia. 2. Atypical chronic myeloid leukemia BCR/ABL negative. 1. HISTIOCYTIC AND DENDRITIC CELL ... Precursor B/T lymphoblastic leukemia/lymphoma (and Burkitt leukemia/lymphoma). 2. T cutaneous lymphoma (Sezary syn, Mycosis ...
Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative Leukemia, Neutrophilic, Chronic Mutation Janus Kinases ... and a smaller percentage of atypical chronic myeloid leukemia (aCML) cases. Although CSF3R point mutations (e.g., T618I) are ... and a smaller percentage of atypical chronic myeloid leukemia (aCML) cases. Although CSF3R point mutations (e.g., T618I) are ... and a smaller percentage of atypical chronic myeloid leukemia (aCML) cases. Although CSF3R point mutations (e.g., T618I) are ...
Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative Leukemia, Neutrophilic, Chronic Mutation Phosphotransferases ... Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity. Corbin, A. S., ... Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity (Journal of ... Threshold levels of ABL tyrosine kinase inhibitors retained in chronic myeloid leukemia cells determine their commitment to ...
Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative * Intrahepatic Cholestasis * Philadelphia Chromosome * Leukemia, ... Onset of Philadelphia chromosome negative chronic myeloid leukemia with symptoms of intrahepatic cholestasis. ... The case of a chronic myelogenous leukemia (CML) starting in an unusual form in a young woman is reported. Rapidly progressing ... abstract = "The case of a chronic myelogenous leukemia (CML) starting in an unusual form in a young woman is reported. Rapidly ...
Atypical chronic myeloid leukemia, BCR/ABL negative Current Synonym true false 474604011 Atypical chronic myeloid leukaemia, ... BCR/ABL negative (morphologic abnormality). Code System Preferred Concept Name. Atypical chronic myeloid leukemia, BCR/ABL ... BCR/ABL negative Current Synonym true false 474605012 Atypical chronic myeloid leukaemia, Philadelphia chromosome (Ph1) ... Atypical chronic myeloid leukemia, Philadelphia chromosome (Ph1) negative Current Synonym true false ...
... it is categorized as a variant of atypical chronic myeloid leukemia (aCML) or Ph-negative CML. Most of the cases reported in ... literature have been negative for the Ph chromosome or the BCR-ABL gene. Till date, Ph positivity has been demonstrated in just ... Abnormal chromatin clumping in leucocytes of Ph positive Chronic Myeloid Leukemia cases - extending the morphological spectrum ... Coombs negative autoimmune hemolytic anemia: A diagnostic dilemma for the hematologist. Ruchika Gupta, Deepak Kumar Singh, ...
A chronic myeloid leukemia patient with atypical karyotype and BCR-ABL e13a3 transcript ... ... in a patient with Philadelphia-negative chronic myeloid leukemia (CML). Using reverse 4,6-diamidino-2-phenylindole banding on ... by characterizing genomic breakpoints in chronic myeloid leukemia (CML) and BCR-ABL-positive acute lymphoblastic leukemia (ALL ... Molecular pathogenesis of Philadelphia-positive chronic myeloid leukemia - is it all BCR-ABL? ...
Full text: Available Index: LILACS (Americas) Main subject: Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative Type of ... Full text: Available Index: LILACS (Americas) Main subject: Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative Type of ... Humans , Male , Female , Adult , Middle Aged , Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative/genetics , Cuba ... To describe the behavior of two patients with chronic myeloid leukemia who have an atypical BCR-ABL transcript. Clinical cases ...
  • Escalated daunorubicin dosing as an induction treatment for Philadelphia-negative adult acute lymphoblastic leukemia. (sickkids.ca)
  • This phase I trial is studying the side effects and best dose of vorinostat when given together with cytarabine and etoposide in treating patients with relapsed or refractory acute leukemia or myelodysplastic syndromes or myeloproliferative disorders. (clinicaltrials.gov)
  • I. Determine the feasibility, tolerability, and toxicities, in terms of the maximum tolerated dose (MTD), of the sequential combination of vorinostat (SAHA) followed by cytarabine and etoposide in patients with relapsed and/or refractory acute leukemia or transforming myelodysplastic syndromes or myeloproliferative disorders. (clinicaltrials.gov)
  • Risk of acute myeloid leukemia and myelodysplastic syndrome after autotransplants for lymphomas and plasma cell myeloma. (bioportfolio.com)
  • Exposures to DNA-damaging drugs and ionizing radiations increase risks of acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). (bioportfolio.com)
  • Addition of histone deacetylase inhibitors does not improve prognosis in patients with myelodysplastic syndrome and acute myeloid leukemia compared with hypomethylating agents alone: A systematic review and meta-analysis of seven prospective cohort studies. (bioportfolio.com)
  • To compare the efficacy and safety between hypomethylating agent (HMA) alone and the combination of HMA and histone deacetylase inhibitor (HDACi) in myelodysplastic syndrome (MDS) or acute myeloid leu. (bioportfolio.com)
  • Implications of Mutation Profiling in Myeloid Malignancies-PART 1: Myelodysplastic Syndromes and Acute Myeloid Leukemia. (bioportfolio.com)
  • Therapy-related acute myeloid leukemia and myelodysplastic syndrome among refractory germ cell tumor patients. (bioportfolio.com)
  • To analyze cases of therapy-related acute myeloid leukemia and myelodysplastic syndrome diagnosed after chemotherapy for refractory testicular and extragonadal germ cell tumor in our experience. (bioportfolio.com)
  • Systematic review of azacitidine regimens in myelodysplastic syndrome and acute myeloid leukemia. (bioportfolio.com)
  • Long-term survivors of Ewing sarcoma (ES) and osteosarcoma may be at risk for therapy-related acute leukemia or myelodysplastic syndrome (t-AL/MDS). (bioportfolio.com)
  • The purpose of this study is to determine the activity of SY-1425 in patients with relapsed/refractory acute myeloid leukemia (AML) or high-risk myelodysplastic syndrome (MDS) who are posi. (bioportfolio.com)
  • This phase I trial studies the side effects and best dose of ipilimumab in treating patients with high-risk myelodysplastic syndrome or acute myeloid leukemia that has come back or no long. (bioportfolio.com)
  • This phase II trial studies how well cytarabine and idarubicin or decitabine work in treating patients with acute myeloid leukemia or high-risk myelodysplastic syndrome. (bioportfolio.com)
  • A pediatric acute myeloid leukemia involving both myeloid and monocytoid precursors. (bioportfolio.com)
  • I. To determine the safety of MDX-CTLA-4 in patients previously and not previously vaccinated with GM-CSF-based vaccines using lethally irradiated, autologous melanoma, ovarian cancer, acute myelogenous leukemia/myelodysplasia or lung cancer cells. (knowcancer.com)
  • When the proliferating cells are immature myeloid cells and myeloblasts, it is called acute myeloid leukemia. (icd10data.com)
  • These include acute and chronic infections (tuberculosis, herpes viruses), chronic inflammatory conditions (sarcoid), and other malignant conditions such as Hodgkin's lymphoma. (oncologynurseadvisor.com)
  • The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes. (wikipedia.org)
  • Acute lymphoblastic leukemia in adults and children that is Philadelphia chromosome positive. (icr.ac.uk)
  • Acute lymphoblastic leukemia in children and young adults aged 1 month to 21 years. (icr.ac.uk)
  • Acute lymphoblastic leukemia that is Philadelphia chromosome negative. (icr.ac.uk)
  • Acute lymphoblastic leukemia that is Philadelphia chromosome positive. (icr.ac.uk)
  • Acute myeloid leukemia (AML) that has relapsed (come back) or is refractory (does not respond to treatment). (icr.ac.uk)
  • Acute myeloid leukemia (AML) that is newly diagnosed. (icr.ac.uk)
  • Tumor protein 53 (TP53) mutations are uncommon in adult patients with acute lymphoblastic leukemia (ALL) and predict a poor outcome. (cdc.gov)
  • This BCR-JAK2 fusion gene has so far been found in only five patients in the whole world, with three clinical presentations: myeloproliferative neoplasm, acute lymphoblastic leukemia and acute myeloid leukemia. (bvsalud.org)
  • In some patients, CCA/Ph-negative status was associated with myelodysplasia or acute myeloid leukemia. (nih.gov)
  • Myelodysplastic/myeloproliferative diseases may progress to acute leukemia. (diseaseinfosearch.org)
  • To assess the incidence of grade II-IV acute graft-vs-host disease (GVHD) and chronic extensive GVHD. (clinicaltrials.gov)
  • Leukemia, Myeloid, Acute" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
  • This graph shows the total number of publications written about "Leukemia, Myeloid, Acute" by people in Harvard Catalyst Profiles by year, and whether "Leukemia, Myeloid, Acute" was a major or minor topic of these publication. (harvard.edu)
  • Below are the most recent publications written about "Leukemia, Myeloid, Acute" by people in Profiles. (harvard.edu)
  • Trends and outcomes of venous thromboembolism in adult hospitalizations with acute myeloid leukemia: analysis of nationwide inpatient sample from 2010 to 2014. (harvard.edu)
  • Outcomes of therapy with venetoclax combined with a hypomethylating agent in favorable-risk acute myeloid leukemia. (harvard.edu)
  • Does patient fitness play a role in determining first-line treatment of acute myeloid leukemia? (harvard.edu)
  • Blast/acute phase - is similar to acute leukemia (ALL) or acute myeloid leukemia (AML). (neurologyadvisor.com)
  • 3q26.2/EVI1 rearrangements resulting in EVI1 overexpression play an important role in leukemogenesis and are associated with treatment resistance and a poorer prognosis in patients with acute myeloid leukemia, myelodysplastic syndrome, chronic myeloid leukemia and BCR-ABL negative myeloproliferative neoplasms. (readbyqxmd.com)
  • All three BCR-ABL-negative MPNs have variable risk for progression towards more aggressive disease, including acute myeloid leukemia and blast-phase disease ( 12, 13 ). (aacrjournals.org)
  • This prognostic scoring system tells your physician how severe your illness is and how probably it is that your MDS would possibly become acute myeloid leukemia (AML). (xn--12cas5dua1c1a3fd6a7rpb.net)
  • Myelodysplastic syndromes (MDS) are characterized by ineffective hematopoiesis presenting with peripheral cytopenias in combination with a hyperplastic bone marrow and an increased risk of evolution to acute myeloid leukemia. (springer.com)
  • Genetic alterations of JAK2 occur in the majority of patients with myeloproliferative neoplasms and occur in a subset of patients with acute leukemias. (aacrjournals.org)
  • Childhood acute myeloid leukemia (AML) is a type of cancer in which the bone marrow makes a large number of abnormal blood cells. (rexhealth.com)
  • Childhood acute myeloid leukemia (AML) is a cancer of the blood and bone marrow. (rexhealth.com)
  • AML is also called acute myelogenous leukemia, acute myeloblastic leukemia, acute granulocytic leukemia, and acute nonlymphocytic leukemia. (rexhealth.com)
  • Importantly, allele burden was significantly associated with progression to myelofibrosis, but not with evolution to acute myeloid leukemia or thrombosis risk. (cancernetwork.com)
  • Gerbing RB, Alonzo TA, Sung L, Gamis AS, Meshinchi S, Plon SE, Bertuch AA, Gramatges MM. Shorter Remission Telomere Length Predicts Delayed Neutrophil Recovery After Acute Myeloid Leukemia Therapy: A Report From the Children's Oncology Group. (sickkids.ca)
  • A genome-wide single-nucleotide polymorphism-array can improve the prognostic stratification of the core binding factor acute myeloid leukemia. (sickkids.ca)
  • Abdelhaleem M, Shago M, Beimnet K, Sayeh E, Bartakke S, Weitzman S. Childhood acute myeloid leukemia with hemophagocytosis by the blasts and inv(8)(p11q13) with MOZ-TIF2 fusion transcripts. (sickkids.ca)
  • Abdelhaleem M. Frequent but nonrandom expression of lymphoid markers on de novo childhood acute myeloid leukemia. (sickkids.ca)
  • Granulocytic sarcoma usually occurs with or follows the onset of ACUTE MYELOID LEUKEMIA. (childrensmercy.org)
  • The initiation and evolution of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) are driven by genomic events that disrupt multiple genes controlling hematopoiesis. (jci.org)
  • Neben K, Giesecke C, Schweizer S, Ho AD, Krämer A: Centrosome aberrations in acute myeloid leukemia are correlated with cytogenetic risk profile. (uni-heidelberg.de)
  • The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia recognizes a distinct class of myeloid and lymphoid tumors with eosinophilia-related proliferations associated with specific gene rearrangements, one of which involves rearrangements of platelet-derived growth factor receptor B (PDGFRB) gene. (biomedcentral.com)
  • FLT3 Internal Tandem Duplication Mutations Associated with Human Acute Myeloid Leukemias Induce Myeloproliferative Disease in a Murine Bone Marrow Transplant Model Blood. (jove.com)
  • Activating mutations in FLT3 have been identified in approximately 30% of patients with acute myelogenous leukemia, making it one of the most common mutations observed in this disease. (jove.com)
  • When the proliferating myeloid cells are neutrophils, it is called chronic myelogenous leukemia. (icd10data.com)
  • In aCML many clinical features (splenomegaly, myeloid predominance in the bone marrow with some dysplastic features but without a differentiation block) and laboratory abnormalities (myeloid proliferation, low leukocyte alkaline phosphatase values) suggest the diagnosis of chronic myelogenous leukemia (CML). (wikipedia.org)
  • BCR rearrangement-negative chronic myelogenous leukemia revisited. (wikipedia.org)
  • The case of a chronic myelogenous leukemia (CML) starting in an unusual form in a young woman is reported. (elsevier.com)
  • Because of the presence of neutrophilic leukocytosis, aCML may resemble chronic myelogenous leukemia (CML). (bvsalud.org)
  • Characteristics and outcome of patients with Philadelphia chromosome negative, bcr/abl negative chronic myelogenous leukemia. (cancer.gov)
  • Philadelphia chromosome-negative chronic myelogenous leukemia with rearrangement of the breakpoint cluster region. (cancer.gov)
  • In the 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms, MPNs include chronic myelogenous leukemia (CML), chronic neutrophilic leukemia, polycythemia vera (PV), primary myelofibrosis (PMF), essential thrombocythemia (ET), chronic eosinophilic leukemia, mastocytosis, and unclassifiable MPNs. (clevelandclinicmeded.com)
  • Chronic myelogenous leukemia is the only MPN that is characterized by the presence of the BCR-ABL fusion gene, which is formed by translocation of the ABL gene from chromosome 9 joining to the BCR gene on chromosome 22. (clevelandclinicmeded.com)
  • Chronic myelogenous leukemia and chronic myelomonocytic leukemia are discussed in the Chronic Leukemia section. (clevelandclinicmeded.com)
  • and atypical chronic myelogenous leukemia (aCML). (diseaseinfosearch.org)
  • Since 1994, our MPD-SUPPORT web site and free support email list offers interesting information on chronic myelogenous leukemia, polycythemia vera, essential thrombocythemia, agnogenic myeloid metaplasia, myelodysplasia, and myelofibrosis. (diseaseinfosearch.org)
  • Atypical chronic myelogenous leukemia (aCML) is a leukemic disorder that exhibits both myelodysplastic and myeloproliferative features at the time of diagnosis. (cancertreatmenttoday.org)
  • Current World Health Organization classification separates BCR-ABL-negative MPNs: polycythemia vera (PV), essential thrombocytopenia (ET), and primary myelofibrosis (PMF), from BCR-ABL-positive chronic myelogenous leukemia (CML). (aacrjournals.org)
  • 20% in patients with MDS-Refractory anemia (RA)-(ringed sideroblasts [RS])/MPD and in patients with chronic myelomonocytic leukemia (CMML)/refractory anemia with excess blasts (RAEB). (clinicaltrials.gov)
  • Chronic myelomonocytic leukemia (CMML) is a clonal stem-cell disorder that has features of both a myelodysplastic syndrome (MDS) and a myeloproliferative neoplasm (MPN) and is thus classified by World Health Organization (WHO) as a mixed MDS/MPN disorder. (oncologynurseadvisor.com)
  • Are you sure your patient has chronic myelomonocytic leukemia? (oncologynurseadvisor.com)
  • BACKGROUND: In adults, the 2 main types of myelodysplastic/myeloproliferative neoplasms (MDS/MPN) are chronic myelomonocytic leukemia (CMML) and atypical chronic myeloid leukemia (aCML). (bvsalud.org)
  • however, patients who are BCR/ABL -negative by RT-PCR have a clinical course more consistent with chronic myelomonocytic leukemia, which is a distinct clinical entity related to myelodysplastic syndrome. (cancer.gov)
  • Martiat P, Michaux JL, Rodhain J: Philadelphia-negative (Ph-) chronic myeloid leukemia (CML): comparison with Ph+ CML and chronic myelomonocytic leukemia. (cancer.gov)
  • These include chronic myelomonocytic leukemia, atypical CML, juvenile myelomonocytic leukemia, and unclassifiable MDS/MPN. (clevelandclinicmeded.com)
  • Here, we report that knockout of the histone demethylase Utx in mice causes a chronic myelomonocytic leukemia (CMML)-like disease with splenomegaly, monocytosis, and extramedullary hematopoiesis. (readbyqxmd.com)
  • High-dose chemotherapy with allogeneic hematopoietic stem cell transplantation (allo-HSCT) can produce long-term remission in patients with higher-risk myelodysplastic syndromes (HR-MDS) and chronic myelomonocytic leukemia (CMML). (readbyqxmd.com)
  • According to WHO recommendations, diagnosis of chronic myelomonocytic leukemia (CMML) beforehand requires microscopic examination of peripheral blood to identify dysplasia and/or blasts when monocytes are greater or equal to 1.0 × 109/L and 10% of leucocytes. (readbyqxmd.com)
  • Chronic myelomonocytic leukemia with central nervous system involvement. (readbyqxmd.com)
  • Chronic myelomonocytic leukemia (CMML) is a clonal hematopoietic stem cell disorder that typically associates with mutations in epigenetic, splicing, and signaling genes. (readbyqxmd.com)
  • Specific disorders include chronic myelomonocytic leukemia (CMML), juvenile myelomonocytic leukemia (JMML), BCR-ABL negative atypical chronic myeloid leukemia (aCML) and unclassifiable MDS/MPN (MPN/MDS-U). Recurrent gene mutations in these conditions have been described. (biomedcentral.com)
  • In the 2008 WHO classification, chronic myeloid malignancies that share both myelodysplastic and myeloproliferative features define the myelodysplastic/myeloproliferative group, which includes chronic myelomonocytic leukemia, juvenile myelomonocytic leukemia, atypical chronic myeloid leukemia, refractory anemia with ring sideroblasts and thrombocytosis, and myelodysplastic/myeloproliferative unclassified. (elsevier.com)
  • Clonal or primary eosinophilia is generally associated with chronic myeloproliferative disorders (Eos-MPD), including atypical chronic myeloid leukemia (aCML), myeloproliferative variant of HES (M-HES), chronic myelomonocytic leukemia (CMML), unclassifiable overlap syndromes of myelodysplastic syndrome/myeloproliferative disorders (MDS/MPD) and systemic mastocytosis (SM). (haematologica.org)
  • The advent of high-throughput gene sequencing has revolutionized our understanding of the genetic mutations that drive myeloid malignancies. (bioportfolio.com)
  • In order to confirm the diagnosis of CMML, other myeloid malignancies must be ruled out. (oncologynurseadvisor.com)
  • Are chronic myeloid leukemia patients more at risk for second malignancies? (wikipedia.org)
  • Mutational analysis of patient data indicated that UTX mutations occur simultaneously with TP53 mutations in myeloid malignancies, and combined inactivation of Utx and Trp53 accelerated the development of CMML in a cell-autonomous manner. (readbyqxmd.com)
  • MPNs are chronic hematologic malignancies that are initiated in the hematopoietic stem cell (HSC) compartment. (aacrjournals.org)
  • Although these agents show clinical activity, the ability of these JAK inhibitors to induce clinical/molecular remissions in hematologic malignancies seems limited and resistance upon chronic drug exposure is seen. (aacrjournals.org)
  • Myeloid malignancies arise from the acquisition of somatic mutations among various genes implicated in essential functioning of hematopoietic stem cells and progenitor cells. (cancernetwork.com)
  • As demonstrated in Table 1, mutations are highly recurrent across myeloid malignancies. (cancernetwork.com)
  • and other myeloid malignancies associated with prominent blood eosinophilia. (mdnxs.com)
  • Characteristics and predictors for secondary leukemia and myelodysplastic syndrome in Ewing and osteosarcoma survivors. (bioportfolio.com)
  • Publication date: Available online 25 May 2019Source: Leukemia Research ReportsAuthor(s): Jihane Belkhair, Abderahim Raissi, Hicham Elyahyaoui, Mustapha Ait Ameur, Mohamed ChakourAbstractAtypical chronic myeloid leukemia (aCML), BCR-ABL1 negative is a rare myelodysplastic syndrome /myeloproliferative neoplasm for which no current standard of care exists. (medworm.com)
  • Oscier DG: Atypical chronic myeloid leukaemia, a distinct clinical entity related to the myelodysplastic syndrome? (cancer.gov)
  • Chronic myelomonocytic leukaemia (CMML) is a clonal haematopoietic disorder with features of both a myeloproliferative neoplasm and myelodysplastic syndrome (MDS). (readbyqxmd.com)
  • Lymphoblastic lymphoma and chronic myeloid leukaemia (CML) are two distinct neoplasms with different pathogenesis and clinical presentation. (ecancer.org)
  • Chronic myeloid leukaemia (CML) constitutes 2%-3% of leukaemia in children. (ecancer.org)
  • Intrahepatikus cholostasis tüneteivel kezdödö Philadelphia chromosoma negatív chronikus myeloid leukaemia. (elsevier.com)
  • A typical chronic myeloid leukaemia (aCML), which shows both myeloproliferative and myelodysplastic features, is a type of myeloproliferative/myelodysplastic disease as defined by the World Health Organisation (WHO) classification of the myeloid neoplasms. (bvsalud.org)
  • Apperley J (2007) Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia. (springer.com)
  • Cannistra SA (1990) Chronic myelogenous leukaemia as a model for a genetic basis of cancer. (springer.com)
  • Atypical chronic myeloid leukemia (aCML) is an aggressive myeloid neoplasm with overlapping features of myelodysplastic syndromes (prominent granulocytic dysplasia) and myeloproliferative neoplasms (neutrophilic leukocytosis). (elsevier.com)
  • To investigate the value of myeloproliferative neoplasms Symptom Assessment Form total symptom score (MPN-SAF-TSS)in assessing constitutional symptoms among Ph/BCR- ABL negative myeloproliferative neoplasm (MPN)patients. (bvsalud.org)
  • Chronic myeloid leukemia (CML) is a type of myeloproliferative neoplasm (MPN). (neurologyadvisor.com)
  • In 2013, two seminal studies identified gain-of-function mutations in the Calreticulin ( CALR ) gene in a subset of JAK2 / MPL -negative myeloproliferative neoplasm (MPN) patients. (aacrjournals.org)
  • Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasm arising from neoplastic transformation of a pluripotent stem cell. (biomedsearch.com)
  • According to the World Health Organization consensus criteria, the diagnosis of HES requires the absence of clonal cytogenetic or molecular markers of an underlying myeloid or lymphoid neoplasm. (mdnxs.com)
  • We report a case of a rare PDGFRB rearrangement with SPTNB1 (spectrin beta, nonerythrocytic 1) that presented as atypical myeloproliferative neoplasm. (biomedcentral.com)
  • Atypical chronic myeloid leukemia (aCML) is a type of leukemia. (wikipedia.org)
  • Purpose: Colony-stimulating factor 3 receptor (CSF3R) mutations have been identified in the majority of chronic neutrophilic leukemia (CNL) and a smaller percentage of atypical chronic myeloid leukemia (aCML) cases. (elsevier.com)
  • Experimental Design: Sanger sequencing of leukemia samples was performed to identifyCSF3Rmutations inCNLand aCML. (elsevier.com)
  • The optimal treatment of aCML is uncertain because of the rare incidence of this chronic leukemic disorder. (cancertreatmenttoday.org)
  • The diagnosis of both myeloid and lymphoid neoplasms in a single patient, whether simultaneous or sequential, is extremely rare, with an overall incidence of less than 1% [ 1 ]. (ecancer.org)
  • Myeloid/Lymphoid Neoplasms Associated With Eosinophilia and Rearrangements of PDGFRA, PDGFRB, or FGFR1 or With PCM1-JAK2. (harvard.edu)
  • A blood stem cell may become a myeloid stem cell or a lymphoid stem cell. (rexhealth.com)
  • Pubmed ID: 11756186 FLT3 receptor tyrosine kinase is expressed on lymphoid and myeloid progenitors in the hematopoietic system. (jove.com)
  • The neoplastic cells do not have a philadelphia chromosome or the bcr/abl fusion gene. (icd10data.com)
  • A myelodysplastic/myeloproliferative disorder characterized by myelodysplasia associated with bone marrow and peripheral blood patterns similar to chronic myeloid leukemia, but cytogenetically lacking a philadelphia chromosome or bcr/abl fusion gene (genes, abl). (icd10data.com)
  • In addition, atypical Philadelphia chromosome negative (Ph-) CML needs to be excluded. (oncologynurseadvisor.com)
  • However the lack of the pathognomonic Philadelphia chromosome and of the resulting BCR-ABL1 fusion point to a different pathogenetic process. (wikipedia.org)
  • Detailed hematological examinations confirmed Philadelphia chromosome (Ph1) negative CML. (elsevier.com)
  • Molecular pathogenesis of Philadelphia-positive chronic myeloid leukemia - is it all BCR-ABL? (biomedsearch.com)
  • CML is characterized by the presence of the Philadelphia chromosome, which is the product of a reciprocal translocation between chromosomes 9 and 22 that results in the formation of BCR-ABL1. (biomedsearch.com)
  • In Philadelphia chromosome negative myeloproliferative neoplasms (Ph(neg)MPN's), telomere dynamics during clonal evolution of these diseases have not yet been fully elucidated. (biomedsearch.com)
  • Chronic myeloid leukemia is a malignant clonal disorder of pluripotent hematopoietic stem cells and characterized by the presence of the Philadelphia chromosome , which is the product of a reciprocal translocation between the long arms of chromosomes 9 and 22. (bvsalud.org)
  • We report a chronic myeloid leukemia patient without evidence of a Philadelphia (Ph) chromosome in whom RT-PCR analysis performed in blast crisis demonstrated the existence of both common b3a2 and b2a2 BCR/ABL fusion transcripts. (unl.pt)
  • Philadelphia-negative classical myeloproliferative neoplasms: critical concepts and management recommendations from European LeukemiaNet. (nih.gov)
  • We present a review of critical concepts and produce recommendations on the management of Philadelphia-negative classical myeloproliferative neoplasms, including monitoring, response definition, first- and second-line therapy, and therapy for special issues. (nih.gov)
  • Interferon alfa in the treatment of Philadelphia-negative chronic myeloproliferative neoplasms. (nih.gov)
  • The prognosis for patients with chronic myeloid leukemia who have clonal cytogenetic abnormalities in philadelphia chromosome-negative cells. (nih.gov)
  • Clonal cytogenetic abnormalities (CCA) were detected in Philadelphia chromosome (Ph)-negative cells in some patients with chronic myeloid leukemia (CML) who attained a cytogenetic response to imatinib mesylate. (nih.gov)
  • The most commonly recognized mutation in the remainder of the Philadelphia chromosome-negative MPNs is Janus kinase 2 ( JAK2 ) V617F, which is present in more than 90% of patients with PV and approximately half of those with PMF or ET ( Table 1 ). (clevelandclinicmeded.com)
  • Clinical and biological aspects of Philadelphia-negative/BCR-negative chronic myeloid leukemia. (cancertreatmenttoday.org)
  • Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder resulting from an acquired genetic aberration t(9;22)(q34;q11) (Philadelphia chromosome) in stem cells. (springer.com)
  • At diagnosis, about 5% of Chronic Myeloid Leukemia (CML) patients lacks Philadelphia chromosome (Ph), despite the presence of the BCR/ABL rearrangement. (oncotarget.com)
  • Chronic Myeloid Leukemia (CML) is a myelopro- liferative disorder characterized by the presence of the Philadelphia (Ph) chromosome, produced by the reciprocal translocation t(9;22)(q34;q11) [ 1 , 2 ]. (oncotarget.com)
  • The classic MPNs include the Philadelphia chromosome ( BCR - ABL1 )-negative MPNs (polycythemia vera, essential thrombocythemia, primary myelofibrosis) and BCR-ABL1 -positive chronic myeloid leukemia (CML). (cancernetwork.com)
  • Variant Philadelphia translocations with different breakpoints in six chronic myeloid leukemia patients / Alti kronik miyeloid losemi olgusunda farkli kirik noktali varyant Philadelphia translokasyonlari. (biomedsearch.com)
  • Objective: The Philadelphia (Ph) chromosome, consisting of the t(9;22)(q34;q11) translocation, is observed in--90% of patients with chronic myeloid leukemia (CML). (biomedsearch.com)
  • Chronic neutrophilic leukemia - patients could present with hepatosplenomegaly due to granulocytic infiltration. (neurologyadvisor.com)
  • CALR mutations also occur in patients with chronic neutrophilic leukemia, refractory anemia with ringed sideroblasts and thrombocytosis, and in a small subset of patients with atypical CML ( 6, 15 ). (aacrjournals.org)
  • Mutations in CSF3R are frequently found in chronic neutrophilic leukemia,[5,6] and they are now incorporated into the latest WHO criteria for diagnosis. (cancernetwork.com)
  • A minute Chromosome in Human Chronic Granulocytic Leukemia. (wikipedia.org)
  • Sometimes leukemia cells form a solid tumor called a granulocytic sarcoma or chloroma. (rexhealth.com)
  • Nonetheless, roughly 10% of patients with ET or PMF lack JAK2 , CALR , or MPL gene mutations and have been referred to as being "triple-negative. (clevelandclinicmeded.com)
  • SETBP1 mutations in MDS/MPN overlap syndrome is associated with accelerated transformation to leukemia and poor prognosis. (biomedcentral.com)
  • Somatic mutations of SETBP1 were associated with −7/del(7q) and poor prognosis, possibly due to its gain-of-function which promotes myeloid leukemic transformation in patients with myelodysplastic syndromes (MDS) and CMML. (biomedcentral.com)
  • Recurrent SETBP1 mutations in atypical chronic myeloid leukemia. (semanticscholar.org)
  • A clonal proliferation of myeloid cells and their precursors in the bone marrow, peripheral blood, and spleen. (icd10data.com)
  • Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. (harvard.edu)
  • MPNs are stem cell-derived clonal disorders with proliferation of one or more of the components of myeloid lineage. (neurologyadvisor.com)
  • The three main chronic myeloproliferative disorders are polycythemia vera (PV), essential thrombocythemia (ET) and idiopathic myelofibrosis (IMF). (bioportfolio.com)
  • Pulmonary hypertension in patients with chronic myeloproliferative disorders. (mdnxs.com)
  • Network of tyrosine kinase fusion genes in eosinophilia-associated chronic myeloproliferative disorders. (haematologica.org)
  • Clinical, hematological and cytogenetic characteristics of atypical chronic myeloid leukemia. (cancertreatmenttoday.org)
  • Even if the number patient is inevitably low, we can confirm that the rare Ph-negative CML patients do not constitute a "warning" category, meanwhile the presence of further cytogenetic abnormalities remains an adverse prognostic factor even in TKI era. (oncotarget.com)
  • Fluorescence in situ hybridization (FISH) with whole-chromosome paints and BCR-ABL 1D probes were used to confirm and/or complement the findings, and identify rearrangements beyond the resolution of conventional cytogenetic methods. (biomedsearch.com)
  • Hypereosinophilic syndrome (HES), chronic eosinophilic leukemia (CEL), and mast cell disease (MCD) are all considered myeloproliferative neoplasms, and diagnosis in each instance requires bone marrow examination with cytogenetic and molecular studies. (mdnxs.com)
  • Chronic eosinophilic leukemia (CEL) is diagnosed in the presence of increased numbers of blasts and/or proof of clonality through cytogenetic or molecular analyses. (haematologica.org)
  • Cases of MDS/MPN with eosinophilia associated with t(5;12) (q31-33;p12)/ ETV6-PDGFRB which were previously included in CMML category are now assigned to a separate group of myeloid neoplasms associated with eosinophilia, and abnormalities of PDGFRA, PDGFRB , or FGFR1 (fibroblast growth factor receptor 1).This group of myeloid neoplasms is usually sensitive to imatinib treatment. (oncologynurseadvisor.com)
  • This sharply contrasts with the outcome for CML, for which the prognosis was dramatically improved by the development of imatinib as a specific inhibitor of the BCR-ABL protein and in particular for CML. (wikipedia.org)
  • The overall prognosis for patients who had CML with CCA/Ph-negative status was good and was driven by the CML response to imatinib mesylate. (nih.gov)
  • Six Ph-negative patients treated with tyrosine kinase inhibitors (TKIs) were characterized, in order to study the mechanisms leading to the rearrangement and the eventual correlation with prognosis in treatment with TKIs. (oncotarget.com)
  • In this second part of our two-part review, we discuss the use of mutation profiling in the diagnosis, prognosis, and treatment of patients with myeloproliferative neoplasms and other myeloid diseases. (cancernetwork.com)
  • Chronic myeloid leukemia (CML) is a pluripotent hematopoietic stem cell disorder leading to myeloproliferation and its attendant consequences. (mhmedical.com)
  • BCR-ABL is only present in hematopoietic cells, but it has been found using very sensitive PCR methods in the hematopoietic cells of 25 to 30% of healthy normal volunteers ( 3 , 4 ). (mhmedical.com)
  • As a result the BCR/ABL fusion gene is formed which encodes a specific mRNA, translated into BCR/ABL proteins with an abnormally high tyrosine kinase activity, playing a crucial role in leukemic transformation and neoplastic proliferation of hematopoietic stem cells. (springer.com)
  • FLT3-ITD mutants were cloned from primary human leukemia samples and assayed for transformation of primary hematopoietic cells using a murine bone marrow transplantation assay. (jove.com)
  • A small subset of patients have BCR/ABL rearrangement detectable only by reverse transcriptase-polymerase chain reaction (RT-PCR), which is the most sensitive technique currently available. (cancer.gov)
  • The BCR-ABL rearrangement, the pathognomonic molecular abnormality in CML, imparts a proliferative and survival advantage to the malignant clone leading to accumulation of leukemic cells. (mhmedical.com)
  • Among the remaining 5 to 10%, the molecular rearrangement characteristic of CML (BCR-ABL) can be identified in 30 to 50% by sensitive methods of detection. (mhmedical.com)
  • 5 ] Ph1-negative patients who have BCR/ABL gene rearrangement detectable by Southern blot analysis, however, have prognoses equivalent to Ph1-positive patients. (cancer.gov)
  • In our cases, the BCR/ABL rearrangement mapped more frequently on 9q34 region than on 22q11 region, in contrast to previous reports. (oncotarget.com)
  • Therapy resistance was observed in one patient with duplication of BCR/ABL rearrangement and in another one with high risk. (oncotarget.com)
  • A small amount of patients (about 5%), displaying typical features of CML, lacks the Ph chromosome by chromosome banding analysis (CBA), meanwhile shows BCR/ABL rearrangement. (oncotarget.com)
  • BCR-ABL rearrangement was not detected by fluorescence in situ hybridization (FISH) of PB. (biomedcentral.com)
  • Leukemia starts in blood-forming tissues such as the bone marrow. (medlineplus.gov)
  • When you have leukemia, your bone marrow makes large numbers of abnormal cells. (medlineplus.gov)
  • Chronic phase, where less than 10% of cells in the blood and bone marrow are blast cells (leukemia cells). (medlineplus.gov)
  • Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (myeloid progenitor cells) in the bone marrow and other sites. (icd10data.com)
  • Leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors in the bone marrow and other sites. (icd10data.com)
  • He was diagnosed as having novel association of concurrent T-lymphoblastic lymphoma diagnosed on cervical lymph node biopsy with BCR-ABL negative CML on bone marrow aspirate. (ecancer.org)
  • Patients may present with characteristic clinical findings caused by large numbers of circulating and bone marrow myeloid cells, such as splenomegaly, leukocytosis, or even isolated thrombocytosis. (mhmedical.com)
  • 6 , 8 , 9 ] Fluorescence in situ hybridization of the BCR/ABL translocation can be performed on the bone marrow aspirate or on the peripheral blood of patients with CML. (cancer.gov)
  • Bone marrow core biopsy in 508 consecutive patients with chronic myeloid leukemia: Assessment of potential value. (cancer.gov)
  • In leukemia, the bone marrow produces abnormal white blood cells. (icdlist.com)
  • Leukemia and other diseases of the blood and bone marrow may affect red blood cells, white blood cells, and platelets. (rexhealth.com)
  • The leukemia cells can build up in the blood and bone marrow so there is less room for healthy white blood cells, red blood cells, and platelets. (rexhealth.com)
  • Other myeloid diseases can affect the blood and bone marrow. (rexhealth.com)
  • Seggewiss R, Ho AD, Krämer A: Remarkable response to rituximab in a patient with atypical CD20++ B-cell chronic lymphocytic leukemia of the bone marrow leading to severe pancytopenia. (uni-heidelberg.de)
  • In the chronic and accelerated phase clinical symptoms developing as a consequence of hepatic organic manifestation were dominating. (elsevier.com)
  • 536 drugs have a clinical trial registered for Leukemia. (icr.ac.uk)
  • There are 4957 clinical trials for Leukemia, 3473 of which have one or more drug interventions, 1484 with no drug intervention. (icr.ac.uk)
  • Clinical cases In a qualitative molecular study of polymerase chain reaction carried out with two patients , a BCR-ABL fusion gene breakpoint was observed, which corresponded to the e14a3 (b3a3) transcript. (bvsalud.org)
  • MPN- SAF- TSS was effective in evaluating the symptomatic burden among Ph/BCRABL negative MPN patients and could be used for serial assessment in this clinical setting. (bvsalud.org)
  • Early recognition of clinical intolerance to BCR-ABL inhibitors used for chronic myeloid leukemia (CML) is important for maximizing patient benefit. (ons.org)
  • Many of the leukemia terms have undergone name changes as immunophenotypic and molecular biological techniques have made diagnosis more precise. (nih.gov)
  • Jabbour E, Kantarjian H: Chronic myeloid leukemia: 2020 update on diagnosis, therapy and monitoring. (cancer.gov)
  • Chronic phase - 85% of patients present with this phase at the time of diagnosis. (neurologyadvisor.com)
  • In situ hybridization studies with BCR- and ABL-specific probes showed location of the BCR/ABL fusion gene on chromosome 9, band q34, instead of at chromosome 22q11, and that it resulted from an insertion of the 5' side of BCR within the ABL gene on chromosome 9. (unl.pt)
  • The vast majority of cells showed a BCR/ABL fusion gene on both chromosomes 9, which is equivalent to a double Ph chromosome, thus reinforcing the notion that the critical event in CML is the formation of a functional BCR/ABL fusion gene. (unl.pt)
  • 3 ] This translocation results in the transfer of the ABL oncogene on chromosome 9 to an area of chromosome 22 termed the breakpoint cluster region (within the BCR gene). (cancer.gov)
  • Liu TX, Becker MW, Jelinek J et al (2007) Chromosome 5q deletion and epigenetic suppression of the gene encoding alpha-catenin (CTNNA1) in myeloid cell transformation. (springer.com)
  • The translocation leads to fusion of the proto-oncogene Abelson (ABL) and a particular DNA sequence known as breakpoint cluster region (BCR), thereby giving rise to 2 new chimeric genes 5' ABL-3' BCR on the derivative chromosome 9 and 5' BCR-3' ABL on the derivative chromosome 22. (biomedsearch.com)
  • Bose S, Deininger M, Gora-Tybor J, Goldman JM, Melo JV (1998) The presence of typical and atypical BCR-ABL fusion genes in leukocytes of normal individuals: biologic significance and implications for the assessment of minimal residual disease. (springer.com)
  • We report here on a rare case of BCR-ABL1-negative atypical chronic myeloid leukemia with a t(9;22)(p24;q11.2)translocation and a BCR-JAK2 fusion gene, with resistance to the tyrosine kinase inhibitors imatinib and dasatinib.At two years of follow-up, the patient showed no hematologic response and was submitted to an allogeneic bonemarrow transplantation. (bvsalud.org)
  • Leukemia is a term for cancers of the blood cells. (medlineplus.gov)
  • This protein allows the leukemia cells to grow out of control. (medlineplus.gov)
  • Determine the effects of SAHA on induction of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-death receptors DR4 and DR5 and other pro-apoptotic mediators in patient-derived cancer cells (leukemia blast cells) and somatic cells (buccal mucosa cells, using pre-SAHA and on SAHA treatment samples). (clinicaltrials.gov)
  • Determine the ability of SAHA to block leukemia blast cells in the G1 phase of the cell cycle (leukemia blast cells, using pre-SAHA and on SAHA treatment samples). (clinicaltrials.gov)
  • V. Determine the effects of SAHA on the expression of P-glycoprotein/MDR1/ABCB1, and the breast cancer resistance protein (BCRP/ABCG2), using functional and mRNA/protein assays for these transporters (leukemia blast cells, using pre-SAHA and on SAHA treatment samples). (clinicaltrials.gov)
  • RATIONALE: Vaccines made from peptides that are found on leukemia cells may make the body build an immune response and kill cancer cells. (bioportfolio.com)
  • The objective of the current study was to determine the prognostic impact of CCA/Ph-negative cells. (nih.gov)
  • No significant differences in pretherapeutic risk factors were detected between patients who attained an MCR with and without CCA/Ph-negative cells, except that exposure to alkylating agents was more frequent in patients with CCA/Ph-negative cells, and overall and progression-free survival were identical. (nih.gov)
  • Isolated CCA/Ph-negative cells in the absence of morphologic evidence of MDS do not justify a change in therapy. (nih.gov)
  • Leukemia is cancer of the white blood cells. (icdlist.com)
  • Biernaux C, Loos M, Sels A, Huez G, Stryckmans P (1995) Detection of major BCR-ABL gene expression at a very low level in blood cells of some healthy individuals. (springer.com)
  • In AML, the myeloid stem cells usually become a type of immature white blood cell called myeloblasts (or myeloid blasts). (rexhealth.com)
  • The myeloblasts, or leukemia cells, in AML are abnormal and do not become healthy white blood cells. (rexhealth.com)
  • The leukemia cells can spread outside the blood to other parts of the body, including the central nervous system (brain and spinal cord), skin, and gums. (rexhealth.com)
  • A proteomic chronology of gene expression through the cell cycle in human myeloid leukemia cells. (sickkids.ca)
  • Functional differences between myeloid leukemia-initiating and transient leukemia cells in Down's syndrome. (sickkids.ca)
  • An extramedullary tumor of immature MYELOID CELLS or MYELOBLASTS. (childrensmercy.org)
  • In this phase, people often have symptoms and standard treatment may not be as effective as in the chronic phase. (medlineplus.gov)
  • In the authors's case the moderate leukocytosis, initial thrombocytopenia, absence of splenomegaly, early blast-phase and short survival were atypical, characteristic of Ph1 negative CML. (elsevier.com)
  • A typical patient with CML is a male in his fourth and fifth decade of life (median age of 50) that usually presents in the chronic phase of the disease. (neurologyadvisor.com)
  • During the chronic phase, symptomatic patients complain of non-specific symptoms such as loss of energy, left upper quadrant pain, early satiety and decreased exercise tolerance. (neurologyadvisor.com)
  • Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. (wikipedia.org)
  • 3 ] This, in turn, results in a fused BCR/ABL gene and in the production of an abnormal tyrosine kinase protein that causes the disordered myelopoiesis found in CML. (cancer.gov)
  • The resulting chimeric BCR/ABL fusion gene encodes for constitutively active tyrosine kinase protein [ 3 ]. (oncotarget.com)
  • Acquired constitutive activation of protein tyrosine kinases is a central feature in the pathogenesis of chronic MPD. (haematologica.org)
  • In some cases the distinctions between leukemias and lymphomas are now considered artificial, and so the nomenclature contains new descriptors such as PRECURSOR CELL LYMPHOBLASTIC LEUKEMIA-LYMPHOMA. (nih.gov)
  • Our reported case has concurrent T lymphoblastic lymphoma and BCR-ABL negative CML, which have never been reported in the literature before. (ecancer.org)
  • Hypereosinophilic syndrome, chronic eosinophilic leukemia, and mast cell disease. (mdnxs.com)
  • The results showed that blood smears of both groups were negative for rickettsiales after therapy, with no morulae in peripheral blood samples. (medworm.com)
  • 1 In contrast to myelodysplastic syndromes (MDS) , MPNs demonstrate terminal myeloid cell expansion into the peripheral blood. (clevelandclinicmeded.com)
  • anemia and/or organomegaly, in patients with myelofibrosis with myeloid metaplasia. (bioportfolio.com)
  • Deininger MW, Goldman JM, Melo JV: The molecular biology of chronic myeloid leukemia. (cancer.gov)
  • Pathologic features of BCR-ABL-negative MPNs include erythrocytosis and myeloid hyperplasia in PV, thrombocytosis in ET, and collagen fibrosis in PMF. (aacrjournals.org)
  • 90%). Regardless of the driver mutation, resultant hyperactivity of JAK-STAT signaling is observed in these patients and is the central pathogenic theme of BCR-ABL1 -negative MPNs. (cancernetwork.com)
  • Publication date: Available online 25 May 2019Source: Leukemia Research ReportsAuthor(s): Jeanne Hersant, Martine Gardembas, Georges Leftheriotis, Patrick Vandeputte, Pierre Abraham, Samir HenniAbstractTyrosine kinase inhibitors are considered as highly effective and relatively safe drugs for the treatment of chronic myeloid leukemia. (medworm.com)
  • We explored this hypothesis using the human monocytic leukemia cell line, THP-1, and recombinant BmpA (rBmpA). (medworm.com)