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1.
Am J Transplant ; 21(12): 3894-3906, 2021 12.
Artigo em Inglês | MEDLINE | ID: mdl-33961341

RESUMO

Graft-versus-host disease after liver transplantation (LT-GVHD) is rare, frequently fatal, and associated with bone marrow failure (BMF), cytopenias, and hyperferritinemia. Given hyperferritinemia and cytopenias are present in hemophagocytic lymphohistiocytosis (HLH), and somatic mutations in hematopoietic cells are associated with hyperinflammatory responses (clonal hematopoiesis of indeterminate potential, CHIP), we identified the frequency of hemophagocytosis and CHIP mutations in LT-GVHD. We reviewed bone marrow aspirates and biopsies, quantified blood/marrow chimerism, and performed next-generation sequencing (NGS) with a targeted panel of genes relevant to myeloid malignancies, CHIP, and BMF. In all, 12 marrows were reviewed from 9 LT-GVHD patients. In all, 10 aspirates were evaluable for hemophagocytosis; 7 had adequate DNA for NGS. NGS was also performed on marrow from an LT cohort (n = 6) without GVHD. Nine of 10 aspirates in LT-GVHD patients showed increased hemophagocytosis. Five (71%) of 7 with LT-GVHD had DNMT3A mutations; only 1 of 6 in the non-GVHD LT cohort demonstrated DNMT3A mutation (p = .04). Only 1 LT-GVHD patient survived. BMF with HLH features was associated with poor hematopoietic recovery, and DNMT3A mutations were over-represented, in LT-GVHD patients. Identification of HLH features may guide prognosis and therapeutics. Further studies are needed to clarify the origin and impact of CHIP mutations on the hyperinflammatory state.


Assuntos
Doença Enxerto-Hospedeiro , Transplante de Fígado , Linfo-Histiocitose Hemofagocítica , Transtornos da Insuficiência da Medula Óssea , Transplante de Medula Óssea/efeitos adversos , Doença Enxerto-Hospedeiro/genética , Humanos , Transplante de Fígado/efeitos adversos , Linfo-Histiocitose Hemofagocítica/genética , Mutação/genética
3.
Leuk Lymphoma ; 59(6): 1391-1398, 2018 06.
Artigo em Inglês | MEDLINE | ID: mdl-28868942

RESUMO

Accurate subclassification of aggressive B cell lymphomas (ABCLs) requires integration of morphologic, immunohistochemical (IHC), and cytogenetic information. Optimal strategies have not been well defined for diagnosis of high grade B cell lymphoma with MYC and BCL2 and/or BCL6 rearrangements (HGBLwR) and double expressor lymphomas with MYC and BCL2 protein overexpression. One hundred and eighty seven ABCLs were investigated with complete IHC and FISH analysis. Morphologic and IHC analysis was insufficient to identify clinically relevant HGBLwR. Approximately, 75% of cases classified as HGBLwR showed conventional DLBCL morphologic features. Fourteen percent of MYC-rearranged cases were negative by IHC. Conversely, 60% of cases positive for MYC by IHC did not demonstrate a MYC rearrangement. Analysis by FISH without MYC and BCL2 IHC would miss 41 cases of double expressor lymphoma. Complete IHC and FISH analysis is recommended in the evaluation of all ABCLs.


Assuntos
Biomarcadores Tumorais , Linfoma de Células B/genética , Linfoma de Células B/metabolismo , Proteínas Proto-Oncogênicas c-myc/genética , Proteínas Proto-Oncogênicas c-myc/metabolismo , Análise Citogenética , Expressão Gênica , Variação Genética , Humanos , Imuno-Histoquímica , Hibridização in Situ Fluorescente , Antígeno Ki-67/genética , Antígeno Ki-67/metabolismo , Linfoma de Células B/diagnóstico , Gradação de Tumores , Estadiamento de Neoplasias , Reprodutibilidade dos Testes
4.
Cytometry B Clin Cytom ; 72(3): 189-95, 2007 May.
Artigo em Inglês | MEDLINE | ID: mdl-17226861

RESUMO

BACKGROUND: Patients with B-cell chronic lymphocytic leukemia (B-CLL) often demonstrate variable responses to similar treatments. It would be highly desirable to develop a personalized therapeutic strategy for selection of appropriate drugs or regimens based on the drug sensitivity profiles of leukemic cells from individuals. METHODS: We applied a multiparameter flow cytometric drug cytotoxicity assay to evaluate drug effects specifically on B-CLL cells from 43 individuals after leukemic cells were incubated in vitro with fludarabine, chlorambucil, cladribine, or prednisolone. RESULTS: We demonstrated that different B-CLL cell populations from 43 individuals showed a marked variability in drug sensitivity. In vitro resistance to fludarabine was greatest in B-CLL cells with deletions of p53, a cytogenetic abnormality that is almost invariably associated with a poor therapeutic response clinically. CONCLUSIONS: In vitro drug sensitivity profiles analyzed by a multiparameter flow cytometric cytotoxicity assay may serve as a tool to facilitate individualized selection of appropriate drugs for treatment in B-CLL. Prospective trials will be needed to validate the clinical utility of this flow cytometric cytotoxicity assay.


Assuntos
Antineoplásicos/efeitos adversos , Resistencia a Medicamentos Antineoplásicos , Citometria de Fluxo/métodos , Leucemia Linfocítica Crônica de Células B/tratamento farmacológico , Testes de Toxicidade/métodos , Adulto , Idoso , Idoso de 80 Anos ou mais , Resistencia a Medicamentos Antineoplásicos/genética , Feminino , Deleção de Genes , Genes p53 , Humanos , Leucemia Linfocítica Crônica de Células B/genética , Masculino , Pessoa de Meia-Idade , Prognóstico , Resultado do Tratamento , Vidarabina/análogos & derivados , Vidarabina/uso terapêutico
6.
J Gastrointest Surg ; 21(4): 607-613, 2017 04.
Artigo em Inglês | MEDLINE | ID: mdl-28083838

RESUMO

INTRODUCTION: We hypothesized that serum neutrophil-to-lymphocyte and platelet-to-lymphocyte ratios may predict pathologic complete response to neoadjuvant chemoradiotherapy in esophageal cancer patients. The ability to predict favorable treatment response to therapy may aid in determining optimal treatment regimens. MATERIALS AND METHODS: A retrospective review of a prospective esophageal disease registry was conducted. Neutrophil-to-lymphocyte ratio was defined as the pre-chemoradiotherapy serum neutrophil count divided by lymphocyte count. Platelet-to-lymphocyte ratio was similarly defined. Logistic regression was applied to analyze these ratios and their effect on pathologic complete response. A Cox proportional-hazards model was used to analyze survival. RESULTS: Sixty patients were included. Elevated neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio were both negative predictors of pathologic complete response (odds ratio: 0.62; 95% confidence interval: 0.37-0.89, P = 0.037 and odds ratio: 0.91; 95% confidence interval: 0.82-0.98, P = 0.028, respectively). Only platelet-to-lymphocyte ratio was predictive of decreased overall survival (hazard ratio: 1.05, 95% confidence interval: 0.94-1.16, P = 0.40). CONCLUSION: Elevated neutrophil and platelet-to-lymphocyte ratios were significant predictors of a poor treatment response to neoadjuvant therapy. Only elevated platelet-to-lymphocyte ratio was predictive of worse overall survival. Neutrophil-to-lymphocyte and platelet-to-lymphocyte ratios may offer a simple serum test to assess the likelihood of a pathologic complete response after neoadjuvant therapy in esophageal cancer.


Assuntos
Plaquetas , Neoplasias Esofágicas/sangue , Neoplasias Esofágicas/terapia , Linfócitos , Neutrófilos , Idoso , Quimiorradioterapia Adjuvante , Neoplasias Esofágicas/patologia , Feminino , Humanos , Contagem de Linfócitos , Masculino , Pessoa de Meia-Idade , Terapia Neoadjuvante , Estadiamento de Neoplasias , Valor Preditivo dos Testes , Prognóstico , Modelos de Riscos Proporcionais , Estudos Retrospectivos , Taxa de Sobrevida
8.
J Mol Diagn ; 8(5): 604-12, 2006 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-17065430

RESUMO

Oncogenic mutations of the receptor tyrosine kinase KIT contribute to the pathogenesis of gastrointestinal stromal tumors, systemic mastocytosis (SM), and some cases of acute myelogenous leukemia (AML). The D816V substitution in the activation loop of KIT results in relative resistance to the kinase inhibitor imatinib (Gleevec). Because this mutation occurs in 80 to 95% of adult SM, its detection has diagnostic and predictive significance. Unfortunately, the fraction of mutation-positive cells in clinical SM samples is often below the 20 to 30% threshold needed for detection by direct DNA sequencing. We have developed an allele-specific polymerase chain reaction assay using a mutation-specific primer combined with a wild-type blocking oligonucleotide that amplifies D816V at the level of 1% mutant allele in DNA extracted from formalin-fixed, paraffin-embedded tissue. There were no amplifications among 64 KIT wild-type tumors and cell lines, whereas all D816V-mutant samples (eight AML and 11 mast cell disease) were positive. Other D816 substitutions associated with resistance to imatinib in vitro are rare in SM. Among these D816F was detectable with the assay whereas D816H, D816Y, and D816G did not amplify. Nine biopsies (bone marrow, skin, or colon) with suspected SM were negative by denaturing high performance liquid chromatography and/or DNA sequencing but positive by allele-specific polymerase chain reaction. Thus, the assay may be useful in confirming the diagnosis of SM.


Assuntos
Alelos , Leucemia Mieloide Aguda/diagnóstico , Mastocitose/diagnóstico , Mutação , Piperazinas/uso terapêutico , Reação em Cadeia da Polimerase/métodos , Pirimidinas/uso terapêutico , Receptores Proteína Tirosina Quinases/genética , Adulto , Idoso , Animais , Benzamidas , Linhagem Celular , Feminino , Genes ras , Humanos , Mesilato de Imatinib , Leucemia Mieloide Aguda/genética , Masculino , Mastocitose/genética , Camundongos , Pessoa de Meia-Idade , Inibidores de Proteínas Quinases/uso terapêutico , Sensibilidade e Especificidade
9.
JAMA Surg ; 151(11): e162743, 2016 11 16.
Artigo em Inglês | MEDLINE | ID: mdl-27627765

RESUMO

Importance: Pathologic complete response (pCR) after neoadjuvant chemoradiotherapy (CRT) may be a clinical prognostic marker of superior outcomes. In patients with esophageal cancer, pCR is associated with increased survival. While mechanisms for increasing the likelihood of pCR remain unknown, in other solid tumors, higher rates of pCR have been associated with longer time intervals between CRT completion and surgical procedures. Objective: To determine the association between time intervals from the completion of CRT to surgical procedure with rates of pCR in patients with esophageal cancer. Design, Setting, and Participants: A prospectively maintained multidisciplinary foregut database was reviewed for consecutively enrolled patients with esophageal cancer from January 2000 to July 2015 presenting for surgical evaluation at a single National Cancer Institute-designated cancer center within a quaternary academic medical center. Interventions: Included patients successfully completed neoadjuvant CRT followed by esophagectomy. Main Outcomes and Measures: Rate of pCR by logistic regression based on a categorized time interval (ie, 0 to 42, 43 to 56, 57 to 70, 71 to 84, 85 to 98, and 99 or more days) from the completion of CRT to surgical resection, adjusted for clinical stage, demographic information, and CRT regimen. Results: Of the 234 patients who met inclusion criteria, 191 (81.6%) were male, and the median (range) age was 64 (58-70) years; 206 (88.0%) were diagnosed as having adenocarcinoma, and 65 (27.9%) had a pCR. Patients in the 85 to 98-day group had significantly increased odds of a pCR compared with other groups (odds ratio, 5.46; 95% CI, 1.16-25.68; P = .03). No significant differences in survival were seen between time groups overall or among patients with residual tumor. Conclusions and Relevance: This study suggests that a time interval of 85 to 98 days between CRT completion and surgical resection is associated with significantly increased odds of a pCR in patients with esophageal cancer. No adverse association with survival was detected as a result of delaying resection, even in patients with residual tumor.


Assuntos
Adenocarcinoma/terapia , Carcinoma de Células Escamosas/terapia , Neoplasias Esofágicas/terapia , Idoso , Quimiorradioterapia Adjuvante , Esofagectomia , Feminino , Humanos , Estimativa de Kaplan-Meier , Masculino , Pessoa de Meia-Idade , Terapia Neoadjuvante , Neoplasia Residual , Taxa de Sobrevida , Fatores de Tempo
10.
Am J Clin Pathol ; 123(6): 826-32, 2005 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-15899772

RESUMO

The diagnosis of B-cell chronic lymphoproliferative disorders is a great challenge when made in a background of polyclonal B cells. We studied the diagnostic usefulness of aberrant CD22 expression for differentiating neoplastic from benign B cells by 4-color flow cytometry. Of 56 cases of B-cell chronic lymphoproliferative disorders, we found that neoplastic cells showed aberrant CD22 expression in 39 (70%) of 56 cases, including chronic lymphocytic leukemia, mantle cell lymphoma, marginal zone lymphoma, hairy cell leukemia, and follicular lymphoma. In 4 cases, monoclonality was detected definitively only by evaluating the immunoglobulin light chain restriction in B cells with aberrant CD22 expression because numerous polyclonal B cells were present. Aberrant CD22 expression is a useful marker for detection of monoclonal B cells admixed with numerous benign polyclonal B cells.


Assuntos
Antígenos CD/biossíntese , Antígenos de Diferenciação de Linfócitos B/biossíntese , Linfócitos B/citologia , Biomarcadores Tumorais/análise , Moléculas de Adesão Celular/biossíntese , Lectinas/biossíntese , Leucemia Linfocítica Crônica de Células B/diagnóstico , Linfoma de Células B/diagnóstico , Linfócitos B/metabolismo , Diferenciação Celular , Citometria de Fluxo , Humanos , Cadeias Leves de Imunoglobulina/imunologia , Imunofenotipagem , Leucemia Linfocítica Crônica de Células B/imunologia , Linfoma de Células B/imunologia , Estudos Retrospectivos , Lectina 2 Semelhante a Ig de Ligação ao Ácido Siálico
11.
Cancer Genet Cytogenet ; 159(2): 151-4, 2005 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-15899388

RESUMO

Mesenchymal chondrosarcoma is a rare malignant tumor that comprises about 3-10% of all sarcomas. Reports of cytogenetic studies of mesenchymal chondrosarcoma are limited and no consistent cytogenetic abnormality has surfaced. Some mesenchymal chondrosarcomas have a t(11;22) translocation suggesting a relationship with the PNET/Ewing tumor family. We report what to our knowledge is the first case of trisomy 8 as the sole cytogenetic abnormality in a mesenchymal chondrosarcoma.


Assuntos
Condrossarcoma Mesenquimal/genética , Cromossomos Humanos Par 8 , Neoplasias de Tecidos Moles/genética , Trissomia , Criança , Feminino , Humanos , Hibridização in Situ Fluorescente , Cariotipagem , Neoplasias de Tecidos Moles/patologia , Coxa da Perna
13.
Am J Clin Pathol ; 144(2): 253-62, 2015 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-26185310

RESUMO

OBJECTIVES: Human epidermal growth factor receptor 2 (HER2, ERBB2) testing is an important prognostic/predictive marker in breast cancer management, especially in selecting HER2-targeted treatment. American Society of Clinical Oncology (ASCO)/College of American Pathologists (CAP) guidelines address HER2 status and were recently revised in 2013, replacing the 2007 version. For in situ hybridization interpretation, 2013 guidelines return to the prior threshold of a HER2/CEP17 ratio of 2.0 or greater for positive and eliminate 1.8 to 2.2 as the equivocal range. Also, the HER2 signal/nucleus ratio is accounted for, with 6.0 or greater for positive and 4.0 to less than 6.0 for equivocal, even in cases with a HER2/CEP17 ratio less than 2.0. METHODS: With institutional review board approval, we reviewed our 2006 to 2012 HER2 fluorescence in situ hybridization (FISH) results and classified them according to both the 2007 and 2013 guidelines as negative, positive, or equivocal. RESULTS: Of 717 HER2 FISH results, 55 (7.7%) changed category when reassessed by 2013 guidelines. Nineteen of 25 results in the 2007 equivocal category were reassigned as positive (n = 13) or negative (n = 6). Thirty-five previously negative cases became equivocal in the 2013 scheme, 12 of these with 1+ immunohistochemistry. The positive category increased from 71 to 85. CONCLUSIONS: The 2013 ASCO/CAP guidelines increased the number of HER2 FISH positive and equivocal results. The equivocal group is substantially different, posing a dilemma for clinical management.


Assuntos
Biomarcadores Tumorais/análise , Hibridização in Situ Fluorescente/normas , Patologia Molecular/normas , Guias de Prática Clínica como Assunto/normas , Receptor ErbB-2/análise , Neoplasias da Mama , Feminino , Humanos
14.
J Gastrointest Surg ; 19(7): 1201-7, 2015 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-25910454

RESUMO

INTRODUCTION: The purpose of this study was to evaluate the effects of neoadjuvant therapy on lymph node harvest (LNH), lymph node ratio (LNR), and overall survival rates after esophagectomy. METHODS: A retrospective analysis of 111 patients who underwent esophagectomy for esophageal adenocarcinoma from 2001 to 2010 was performed. Patients were divided into two groups: neoadjuvant chemoradiotherapy prior to surgery (NEOSURG) versus surgery alone (SURG). RESULTS: There were 83 patients (75%) in the NEOSURG group and 28 (25%) in the SURG group with a mean age of 66 and 67 years, respectively. The median LNH in the NEOSURG group and SURG group was 16.0 and 15.5, respectively (p = 0.57). Within the NEOSURG group, the median LNH was 16 for complete responders, 14 for partial responders, 16 for nonresponders, and 18 in those who were pathologically upstaged (p = 0.434). The median LNR was 0, 0, 0.1, and 0.2, respectively (p < 0.001). Complete response after neoadjuvant therapy demonstrated a trend toward improved survival (p = 0.056). CONCLUSION: The LNH was not significantly influenced by neoadjuvant treatment or pathologic response. The LNR was inversely related to pathologic response after neoadjuvant therapy. Complete pathologic response to neoadjuvant therapy trends to improve survival rates.


Assuntos
Quimiorradioterapia Adjuvante , Neoplasias Esofágicas/patologia , Neoplasias Esofágicas/terapia , Excisão de Linfonodo , Linfonodos/cirurgia , Adenocarcinoma , Idoso , Esofagectomia , Feminino , Humanos , Linfonodos/patologia , Masculino , Pessoa de Meia-Idade , Terapia Neoadjuvante , Estadiamento de Neoplasias , Estudos Retrospectivos , Taxa de Sobrevida , Resultado do Tratamento
15.
Diagn Cytopathol ; 26(2): 113-6, 2002 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-11813330

RESUMO

Anaplastic large cell lymphoma (ALCL), according to the new WHO classification, is a diagnosis limited to T/NK cell lymphomas. We present a case that demonstrates a new morphologic variant of ALCL with significant possible pitfalls for the cytopathologist. A fine-needle aspiration biopsy of a cervical lymph node showed a cellular aspiration comprised of medium-sized plasmacytoid cells in a discohesive and focally loosely cohesive pattern. The cytologic diagnosis confirmed the presence of malignancy and noted the prominent plasmacytoid features. An accompanying comment favored melanoma and included a broad differential. No cell block was available for immunohistochemical stains. Immunophenotyping of the subsequent excisional node biopsy showed an anaplastic lymphoma kinase (ALK)-positive ALCL. This case illustrates a new variant of ALCL. Although ALCL variants, such as small cell and lymphohistiocytic, are well recognized, the plasmacytoid features are an additional potential source for misdiagnosis. This case report shows that a cytopathologist should include ALK-positive ALCL in the differential diagnosis of plasmacytoid proliferations cell because of the clinical importance of the ALK-positive ALCL.


Assuntos
Leucemia Linfocítica Crônica de Células B/patologia , Linfoma Anaplásico de Células Grandes/patologia , Plasmócitos/patologia , Biomarcadores Tumorais/análise , Biópsia por Agulha , Diagnóstico Diferencial , Humanos , Imuno-Histoquímica , Imunofenotipagem , Leucemia Linfocítica Crônica de Células B/classificação , Leucemia Linfocítica Crônica de Células B/imunologia , Linfonodos/patologia , Linfoma Anaplásico de Células Grandes/classificação , Linfoma Anaplásico de Células Grandes/imunologia , Masculino , Melanoma/patologia , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Plasmócitos/imunologia
18.
Hum Pathol ; 43(12): 2167-76, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-22658276

RESUMO

Classification of acute myeloid leukemia increasingly depends on genetic analysis. However, the number of known mutations in acute myeloid leukemia is expanding rapidly. Therefore, we tested a high-throughput screening method for acute myeloid leukemia mutation analysis using a multiplex mass spectrometry-based approach. To our knowledge, this is the first reported application of this approach to genotype leukemias in a clinical setting. One hundred seven acute myeloid leukemia cases were screened for mutations using a panel that covers 344 point mutations across 31 genes known to be associated with leukemia. The analysis was performed by multiplex polymerase chain reaction for mutations in genes of interest followed by primer extension reactions. Products were analyzed on a Sequenom MassARRAY system (San Diego, CA). The multiplex panel yielded mutations in 58% of acute myeloid leukemia cases with normal cytogenetics and 21% of cases with abnormal cytogenetics. Cytogenetics and routine polymerase chain reaction-based screening of NPM1, CEBPA, FLT3-ITD, and KIT was also performed on a subset of cases. When combined with the results of these standard polymerase chain reaction-based tests, the mutation frequency reached 78% in cases with normal cytogenetics. Of these, 42% harbored multiple mutations primarily involving NPM1 with NRAS, KRAS, CEBPA, PTPN11, IDH1, or FLT3. In contrast, cases with abnormal cytogenetics rarely harbored more than 1 mutation (1.5%), suggesting different underlying biology. This study demonstrates the feasibility and utility of broad-based mutation profiling of acute myeloid leukemia in a clinical setting. This approach will be helpful in defining prognostic subgroups of acute myeloid leukemia and contribute to the selection of patients for enrollment into trials with novel inhibitors.


Assuntos
Biomarcadores Tumorais/genética , Análise Mutacional de DNA/métodos , Ensaios de Triagem em Larga Escala , Leucemia Mieloide Aguda/genética , Reação em Cadeia da Polimerase Multiplex/métodos , Proteínas Estimuladoras de Ligação a CCAAT/genética , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Proteínas Nucleares/genética , Nucleofosmina , Prognóstico , Proteínas Proto-Oncogênicas c-kit/genética , Tirosina Quinase 3 Semelhante a fms/genética
19.
Am J Clin Pathol ; 135(5): 709-19, 2011 May.
Artigo em Inglês | MEDLINE | ID: mdl-21502425

RESUMO

Myeloproliferative neoplasms and myelodysplastic/myeloproliferative neoplasms are heterogeneous disorders. JAK2 mutation testing and karyotyping are routinely used for diagnosis but have not been incorporated into risk stratification in Philadelphia chromosome-negative myeloproliferative neoplasms. This study correlated cytogenetic abnormalities with disease stage and JAK2 status. A total of 179 cases were analyzed for the JAK2 mutation. Among them, cytogenetic data were available for 97 cases-45 of 106 JAK2+ and 52 of 73 JAK2-. The JAK2+ group showed a higher frequency of cytogenetic anomalies than the JAK2- group (23/45 [51%] vs 14/52 [27%]). Chromosome 9, chromosome 7, and 20q- were recurrent abnormalities in the JAK2+ group, whereas 13q- and trisomy 21 were common in the JAK2- group. In the JAK2+ group, chromosome 7 and complex cytogenetic abnormalities were associated with excess blasts/blastic transformation (P < .05), whereas no cases with 20q- underwent blastic transformation. Our results suggest that incorporation of JAK2 mutation testing and karyotyping allows for monitoring of disease progression with prognostic and therapeutic implications.


Assuntos
Aberrações Cromossômicas , Janus Quinase 2/genética , Mutação , Doenças Mieloproliferativas-Mielodisplásicas/enzimologia , Doenças Mieloproliferativas-Mielodisplásicas/genética , Transtornos Mieloproliferativos/enzimologia , Transtornos Mieloproliferativos/genética , Transformação Celular Neoplásica , Cromossomos Humanos Par 13/genética , Cromossomos Humanos Par 20/genética , Cromossomos Humanos Par 21/genética , Cromossomos Humanos Par 7/genética , Cromossomos Humanos Par 9/genética , Progressão da Doença , Humanos , Cariotipagem , Doenças Mieloproliferativas-Mielodisplásicas/patologia , Transtornos Mieloproliferativos/patologia
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