Monocytosis

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Julia T Geyer - One of the best experts on this subject based on the ideXlab platform.

  • Oligomonocytic chronic myelomonocytic leukemia (chronic myelomonocytic leukemia without absolute Monocytosis) displays a similar clinicopathologic and mutational profile to classical chronic myelomonocytic leukemia
    Modern Pathology, 2017
    Co-Authors: Julia T Geyer, Wayne Tam, Yen-chun Liu, Zhengming Chen, Sa A Wang, Carlos Bueso-ramos, Jean Oak, Daniel A Arber, Eric Hsi, Heesun J Rogers
    Abstract:

    Chronic myelomonocytic leukemia is characterized by persistent absolute Monocytosis (≥1 × 10^9/l) in the peripheral blood and dysplasia in ≥1 lineages. In the absence of dysplasia, an acquired clonal genetic abnormality is required or causes for reactive Monocytosis have to be excluded. Oligomonocytic chronic myelomonocytic leukemia showing increased monocytes but no absolute Monocytosis in the peripheral blood occurs occasionally. These cases are likely classified as myelodysplastic syndrome or myelodysplastic/myeloproliferative neoplasm, unclassifiable. A subset eventually develop overt chronic myelomonocytic leukemia. Better characterization of oligomonocytic chronic myelomonocytic leukemia is essential since the distinction between chronic myelomonocytic leukemia and myelodysplastic syndrome is clinically relevant. We identified 44 cases of oligomonocytic chronic myelomonocytic leukemia (≥10% peripheral blood monocytes with absolute monocyte count of 0.5–1 × 10^9/l) and 28 consecutive chronic myelomonocytic leukemia controls. Clinicopathologic features were compared and mutation analysis was performed. Oligomonocytic chronic myelomonocytic leukemia patients were significantly younger (median age of 65 vs 72). They had lower WBC and absolute neutrophil count, while the monocyte percentage, hemoglobin and platelet counts were similar in the two groups. The myeloid to erythroid ratio was predominantly decreased or normal, compared with the characteristic increase in chronic myelomonocytic leukemia ( P =0.006). 38% of patients progressed to overt chronic myelomonocytic leukemia (median: 12 months). The overall percentage of mutations was significantly lower in oligomonocytic chronic myelomonocytic leukemia. However, the most frequent mutations in both groups were the ‘signature’ chronic myelomonocytic leukemia mutations in ASXL1 , TET2 and SRSF2 . Mutations in CBL were found exclusively in overt chronic myelomonocytic leukemia. In conclusion, we demonstrate clinical and genetic similarities between overt chronic myelomonocytic leukemia and oligomonocytic chronic myelomonocytic leukemia. The findings suggest that at least a subset of oligomonocytic chronic myelomonocytic leukemia represents early phase ‘dysplastic type’ chronic myelomonocytic leukemia.

  • Oligomonocytic chronic myelomonocytic leukemia (chronic myelomonocytic leukemia without absolute Monocytosis) displays a similar clinicopathologic and mutational profile to classical chronic myelomonocytic leukemia
    Modern pathology : an official journal of the United States and Canadian Academy of Pathology Inc, 2017
    Co-Authors: Julia T Geyer, Wayne Tam, Yen-chun Liu, Zhengming Chen, Carlos Bueso-ramos, Jean Oak, Daniel A Arber, Eric Hsi, A. Wang, Heesun J Rogers
    Abstract:

    Oligomonocytic chronic myelomonocytic leukemia (chronic myelomonocytic leukemia without absolute Monocytosis) displays a similar clinicopathologic and mutational profile to classical chronic myelomonocytic leukemia

  • development of Monocytosis in patients with primary myelofibrosis indicates an accelerated phase of the disease
    Modern Pathology, 2013
    Co-Authors: Leonardo Boiocchi, Julia T Geyer, Rosanny Espinalwitter, Julia Steinhilber, Irina Bonzheim, Daniel M Knowles, Falko Fend, Attilio Orazi
    Abstract:

    Primary myelofibrosis is a type of chronic myeloproliferative neoplasm characterized by progressive bone marrow failure with worsening cytopenia and in a subset of patients, progression to acute leukemia. Published data in patients with myelodysplastic syndromes have shown that the development of Monocytosis in the course of myelodysplastic syndromes is associated with a poor prognosis. A similar occurrence has been only sporadically reported in patients with primary myelofibrosis. Over a period of four years we identified 10 out of 237 cases of primary myelofibrosis who developed persistent absolute Monocytosis (>1 × 10(9)/l) during the course of disease (5 men and 5 women; median age/range: 68 years/52-82). Monocytosis developed at a median interval of 42 months from diagnosis (range: 1-180) and persisted for a median period of 23 months (range: 2-57). Five patients died after developing Monocytosis (range: 20-188 months) and two experienced worsening disease and became transfusion dependent. Monocytosis was associated with increased white blood cells, decreased hemoglobin, decreased platelet count, and the presence of circulating blasts. In three cases, bone marrow biopsies after the onset of Monocytosis showed marked myelomonocytic proliferation with morphological shifting from a typical primary myelofibrosis marrow appearance to aspects compatible with an overt 'secondary' chronic myelomonocytic leukemia. Before the development of Monocytosis, 5 of 10 patients carried the JAK2V617F mutation; five patients showed karyotypic alterations. No change in JAK2 mutational status or cytogenetic evolution were associated with the development of Monocytosis. Four of nine patients analyzed showed KRAS mutation in codon 12 or 13 with low allele burden. This is the first study correlating Monocytosis developing in primary myelofibrosis patients with bone marrow morphology, laboratory data, molecular analysis and clinical follow-up. Development of Monocytosis in patients with established primary myelofibrosis is associated with rapid disease progression and these patients should be considered as a high-risk group associated with short survival.

Heesun J Rogers - One of the best experts on this subject based on the ideXlab platform.

Ayalew Tefferi - One of the best experts on this subject based on the ideXlab platform.

  • Monocytosis in polycythemia vera clinical and molecular correlates
    American Journal of Hematology, 2017
    Co-Authors: Daniela Barraco, Terra L. Lasho, Rhett P. Ketterling, Naseema Gangat, Mrinal M. Patnaik, Sonia Cerquozzi, Christy Finke, Curtis A Hanson, Animesh Pardanani, Ayalew Tefferi
    Abstract:

    Monocytosis (absolute monocyte count, AMC ≥ 1 × 109 /L) might accompany a spectrum of myeloid neoplasms, other than chronic myelomonocytic leukemia (CMML). In the current study, we examined the prevalence, laboratory and molecular correlates, and prognostic relevance of Monocytosis in polycythemia vera (PV). Among 267 consecutive patients with World Health Organization (WHO)-defined PV, 55 (21%) patients displayed an AMC of ≥1 × 109 /L and 18 (7%) an AMC of ≥1.5 × 109 /L. In general, PV patients with Monocytosis were significantly older and displayed higher frequencies of leukocytosis (81% vs. 50% at AMC ≥1 × 109 /L) and TET2/SRSF2 mutations (57%/29% vs. 19%/1% at AMC ≥ 1.5 × 109 /L). In univariate analysis, AMC ≥1.5 × 109 /L adversely affected overall (OS; P = .004; HR 2.6, 95% CI 1.4-4.8) and myelofibrosis-free (MFFS; P = .02; HR 4.4, 95% CI 1.3-15.1) survival; during multivariable analysis, significance was borderline sustained for OS (P = .05) and MFFS (P = .06). Other independent risk factors for OS included unfavorable karyotype (P = .02, HR 3.39, 95% CI 1.17-9.79), older age (P < .0001, HR 3.34 95% CI 1.97-5.65), and leukocytosis ≥15 × 109 /L (P = .004, HR 2.04, 95% CI 1.26-3.29). In conclusion, in the current study, we encountered a higher than expected prevalence of Monocytosis in patients with PV and the mutation profile and age distribution of PV patients with Monocytosis is akin to those of patients with CMML and might partly contribute to their worse prognosis.

  • Monocytosis in polycythemia vera clinical and molecular correlates
    Blood, 2016
    Co-Authors: Daniela Barraco, Terra L. Lasho, Rhett P. Ketterling, Naseema Gangat, Mrinal M. Patnaik, Sonia Cerquozzi, Christy Finke, Curtis A Hanson, Animesh Pardanani, Ayalew Tefferi
    Abstract:

    Background Polycythemia Vera (PV) constitutes one of the three BCR-ABL1-negative myeloproliferative neoplasms and is characterized by clonal erythrocytosis and the almost invariable presence of JAK2 mutation. An absolute monocyte count (AMC) of ≥1 x 10(9)/L defines chronic myelomonocytic leukemia (CMML) but can also be seen in other myeloid disorders including myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPN). The presence or development of Monocytosis has previously been shown to confer poor prognosis in both primary myelofibrosis (PMF), which is one of the three BCR-ABL1-negative MPN (Leukemia Research 2007;31:1503, Mod Pathol. 2013 Feb;26(2):204) and MDS (Haematologica. 1997;82:25). In the current study, we examined the clinical, prognostic and molecular correlates of Monocytosis in PV. Methods Study patients were selected from our institutional database of MPN and fulfilled the 2008 World Health Organization (WHO) criteria for the diagnosis of PV (Blood. 2009;114:937). Cytogenetic and mutational analyses were performed according to conventional methods (Leukemia. 2014;28:2206) any assignment as unfavorable karyotype was per PMF criteria (Leukemia. 2011;25:82). Mutation screening included TET2, ASXL1 and SRSF2 because of their known association with CMML (Leukemia. 2014;28:2206) Statistical analyses considered clinical and laboratory parameters obtained at time of diagnosis. Results Patient characteristics: Analysis was conducted on 587 patients (median age 60 years; 48% males) who met WHO criteria for diagnosis of PV. Amongst them, accurate documentation of AMC was available in 237 patients, cytogenetic information in 239, and ASXL1, TET2 and SRSF2 mutational status in 133 patients. Median (range) values were for AMC 0.6 x 10(9)/L (0-4.7) and leukocytes 11.6 x 10(9)/L (3.8-171.6). 31% of 506 informative patients had palpable splenomegaly, 34% of 551 had microcirculatory symptoms, 30% of 566 had pruritus, 8% of 504 had erythromelalgia, 42% of 581 had hypertension, 9% of 584 had diabetes and 11% of 575 were active tobacco users. 25% of the patients presented with history of thrombosis and 22% developed thrombosis after diagnosis. Cytogenetic findings were abnormal in 19%, of whom 20% were unfavorable. TET2, ASXL1 and SRSF2 mutations were documented in 18%, 11% and 3%, respectively. During follow-up, 224 (38%) patients died and median follow-up for living patients was 109 months. Median survival was 16 years and leukemic or fibrotic transformations were documented in 4% and 14%, respectively. Comparison of patients with and without Monocytosis: Among 237 informative patients, 32 (14%) displayed Monocytosis (AMC ≥1 x 10(9)/L) at time of diagnosis. PV patients with Monocytosis were older (p=0.006) and displayed higher leukocyte count (p Among the 237 PV patients in whom information regarding AMC was available, 70 (30%) died during follow-up and 49 (21%), 23 (10%), 9 (4%) developed thrombosis, leukemic transformation or fibrotic progression, respectively. In univariate analysis, overall (p=0.009; HR 2.0, 95% CI 1.2-3.4) but not leukemia-free (p=0.79), myelofibrosis-free (p=0.13) or thrombosis-free (p=0.48) survivals were different between patients with or without Monocytosis. Furthermore, the significant difference in survival was no longer apparent when analysis was adjusted for age (p=0.13), unfavorable karyotype (0.17) or leukocytosis (p=0.06). Conclusions Monocytosis (AMC ≥1 x 10(9)/L) is not infrequent in PV (14%). However, the presence of Monocytosis does not appear to represent a significantly different phenotype in terms of molecular characteristics although it is associated with older age, leukocytosis and unfavorable karyotype. The latter associations account for the inferior survival seen in patients with Monocytosis. Disclosures No relevant conflicts of interest to declare.

  • Monocytosis is a powerful and independent predictor of shortened overall and leukemia free survival in primary myelofibrosis
    Blood, 2016
    Co-Authors: Sahrish Shah, Terra L. Lasho, Rhett P. Ketterling, Naseema Gangat, Daniela Barraco, Curtis A Hanson, Animesh Pardanani, Michelle A Elliott, Mythri Mudireddy, Ayalew Tefferi
    Abstract:

    Background The Dynamic International Prognostic Scoring System (DIPSS)-plus currently provides the most comprehensive prognostic model for primary myelofibrosis (PMF) (JCO 2011;29:392). DIPSS-pluse uses eight independent predictors of inferior survival: age >65 years, hemoglobin 25 x 109/L, circulating blasts ³1%, constitutional symptoms, unfavorable karyotype, red cell transfusion need and platelet count Methods Study patients fulfilled the 2016 WHO criteria for the diagnosis of PMF, including both pre-PMF and overt PMF (Blood. 2016;127:2391). Additional selection criteria included the availability of absolute monocyte count (AMC) and percentage at time of referral. Targeted next generation sequencing was used to screen for prognostically-relevant mutations (Blood 2015 126:354). Statistical analyses considered clinical and laboratory parameters obtained at time of initial referral to the Mayo Clinic. Results Patient characteristics: The study population included 454 patients (median age 64 years; 62% males); 293 (64%) patients harbored JAK2 mutations, 74 (16%) type 1/like CALR, 16 (3%) type 2/like CALR, 24 (5%) MPL and 47 (10%) were "triple-negative". DIPSS-plus risk distribution was 29% high, 38% intermediate-2, 17% intermediate-1 and 15% low; 27% displayed red cell transfusion-dependency, 29% constitutional symptoms, 70% palpable splenomegaly and 36% abnormal karyotype, including 13% with unfavorable karyotype. 301 patients were screened for ASXL1 mutations with 39% mutated, 297 for SRSF2 mutations with 15% mutated, 286 for U2AF1 with 18% mutated, 253 for SF3B1 with 6% mutated, 229 for EZH2 with 5% mutated and 110 for IDH1/2 with 7% mutated. Clinical, cytogenetic and molecular comparisons between PMF patients with and without Monocytosis: Among all study patients, 376 (83%) displayed AMC 3 x 10(9)/L; n=13) Monocytosis. Comparison of these three groups revealed that Monocytosis was significantly associated with older age (p=0.0001), higher leukocyte count (p Survival analysis: After a median follow up of 3.2 years, 265 (58%) deaths and 38 (8%) leukemic transformations were documented. In univariate analysis, all 8 variables included in DIPSS-plus were significantly associated with shortened survival (p 3 x 10(9)/L (p 3 x 10(9)L) was independent of each one of the eight DIPSS-plus variables, DIPSS-plus, driver mutational status, ASXL1 and SRSF2 mutations (p Conclusion The current study identifies Monocytosis as a powerful risk factor for both overall and leukemia-free survival in PMF and the effect was independent of currently established prognostic models and genetic risk factors. It was particularly noteworthy to document similar distribution of driver mutations among the three monocyte categories. Disclosures No relevant conflicts of interest to declare.

  • chronic myelomonocytic leukemia 2013 update on diagnosis risk stratification and management
    American Journal of Hematology, 2013
    Co-Authors: Sameer A Parikh, Ayalew Tefferi
    Abstract:

    Disease overview Chronic myelomonocytic leukemia (CMML) is a clonal hematopoietic stem cell disorder that is classified as a myelodysplastic/myeloproliferative neoplasm by the 2008 World Health Organization classification of hematopoietic tumors. It is characterized by absolute Monocytosis (>1 × 109/L) in the peripheral blood that persists for at least 3 months. Diagnosis The diagnosis of CMML rests on a combination of morphologic, histopathologic and chromosomal abnormalities in the bone marrow. It is important to exclude other myeloproliferative neoplasms and infectious/autoimmune conditions that can cause Monocytosis. Risk stratification Several CMML-specific prognostic models incorporating novel mutations have been recently reported. The Mayo prognostic model classified CMML patients into three risk groups based on: increased absolute monocyte count, presence of circulating blasts, hemoglobin 65 years, WBC >15 × 109/L, anemia, platelets <100 × 109/L, and ASXL1 mutation status. After a median follow-up of 2.5 years, survival ranged from not reached in the low-risk group to 14.4 months in the high-risk group. Risk-adapted therapy The Food and Drug Administration has approved azacitidine and decitabine for the treatment of patients with CMML. An allogeneic stem cell transplant can potentially offer a curative option to a subset of CMML patients. It is hoped that with the discovery of several novel mutations, targeted therapies will become available in the near future. Am. J. Heamtol. 88:968–974, 2013. © 2013 Wiley Periodicals, Inc.

  • Monocytosis is an independent risk factor for survival in agnogenic myeloid metaplasia
    Blood, 2006
    Co-Authors: Michelle A Elliott, David Dingli, Susan M Schwager, Ayalew Tefferi
    Abstract:

    Background: Young (age 30 × 109/L, and platelet count < 100 × 109/L (Dingli et al. Cancer 2006;106:623). In the current study, we identify absolute Monocytosis of ≥ 1 × 109/L as an additional independent risk factor for survival in AMM. Methods: A consecutive cohort of WHO-defined AMM patients diagnosed before the age of 60 years was identified. The impact of various clinical and laboratory parameters on overall survival was evaluated with univariate and multivariable analysis. Results: The study included 129 patients (median age 52 years, range 18–60; 69 males) with AMM. An overall median survival of 75 months was univariately affected by platelet count 30 × 109/L, Monocytosis of ≥ 1 × 109/L, and, where cytogenetic studies were available (n=41), presence of unfavorable cytogenetic abnormalities (p < 0.01 in each instance). On multivariable analysis, all but leukocyte count maintained their significance. The independent prognostic value of monocyte count was also validated against the modified Dupriez score (see above) and thus allowed further refinement of the particular CBC-based PSS that included Monocytosis of ≥ 1 × 109/L as a fourth risk factor; low-risk identified patients with none of the 4 risk factors, intermediate-risk with one risk factor, and high-risk with 2 or more risk factors (Figure 1). For comparison, Figure 2 illustrates survival curves according to the original Dupriez PSS. Conclusion: Monocytosis of ≥ 1 × 109/L is an independent risk factor for inferior survival in AMM. ![Figure 1. ][1] Figure 1. Mayo score ![Figure 2. ][1] Figure 2. Dupriez score [1]: pending:yes

Shunichi Hirose - One of the best experts on this subject based on the ideXlab platform.

  • thu0379 dichotomy in fc gamma receptor iib deficiency and autoimmune prone slam haplotype reveals the role of slam haplotype in Monocytosis and the significant effect of fc gamma receptor iib deficiency in yaa related lupus nephritis
    Annals of the Rheumatic Diseases, 2015
    Co-Authors: Keiko Nishikawa, Hirofumi Amano, Qingshun Lin, Hiromichi Tsurui, Shinya Kawano, K Kojo, Toshikazu Shirai, Shunichi Hirose
    Abstract:

    Background The inhibitory FcγRIIb-deficient mice develop autoimmune diseases, such as lupus nephritis, rheumatoid arthritis, and vasculitis with inflammatory cell infiltration [1,2]; however, the incorporation of FcγRIIb-linked autoimmune-prone SLAM haplotype in these gene targeting mice makes it difficult to isolate the role of FcγRIIb deficiency from SLAM haplotype in these diseases. Objectives In the present study, we genetically dissected the role of FcγRIIb deficiency and SLAM haplotype for these autoimmune diseases. Methods By extensively backcrossing 129-based FcγRIIb-deficient mice to B6 mice, three congenic mouse strains were established, the first with FcγRIIb deficiency and 129-derive autoimmune-prone SLAM haplotype (KO1), the second with FcγRIIb deficiency and B6 SLAM haplotype (KO2), and the third with wild-type FcγRIIb and 129 SLAM haplotype (SLAM 129 ). Results Lupus nephritis did not develop in KO1, KO2, and SLAM 129 ; however, KO1 and SLAM 129 showed age-associated Monocytosis and perivascular inflammatory cell infiltration. When introducing Yaa mutation, KO1. Yaa and KO2. Yaa mice developed severe nephritis. In contrast, SLAM 129 . Yaa mice developed mild form of lupus nephritis with the increased serum level of IgM, but not IgG, class autoantibodies. Conclusions Monocytosis was shown to be one of the characteristic features in murine models of lupus nephritis [3]. Our study suggests that autoimmune-prone SLAM haplotype plays a pivotal role for Monocytosis and resulting perivascular inflammatory cell infiltration; however, SLAM 129 alone is not enough for the development of lupus nephritis. FcγRIIb deficiency alone was not enough for both Monocytosis and lupus nephritis. In the presence of Yaa , FcγRIIb deficiency plays a significant role for the development of lupus nephritis with isotype switch of autoantibodies from IgM to pathogenic IgG class. Mild form of lupus nephritis in SLAM 129 . Yaa mice may be due to the deposition of IgM autoantibodies in glomeruli, which results in the up-regulation of chemokine production by activated mesangial cells and resultant inflammatory cell infiltration to glomeruli because of the high frequencies of monocytes in periphery. References Bollans S. and Ravetch JV. Immunity 13:277-285, 2000. Sato-Hayashizaki A, et al. Arthritis Rheum. 63:2930-2938, 2011. Wofsy D, et al. J. Exp. Med. 159:629-634, 1984. Disclosure of Interest None declared

Wayne Tam - One of the best experts on this subject based on the ideXlab platform.

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