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  • 1
    In: Biology of Blood and Marrow Transplantation, Elsevier BV, Vol. 25, No. 11 ( 2019-11), p. 2134-2142
    Type of Medium: Online Resource
    ISSN: 1083-8791
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 3056525-X
    detail.hit.zdb_id: 2057605-5
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  • 2
    In: Blood, American Society of Hematology, Vol. 106, No. 11 ( 2005-11-16), p. 3666-3666
    Abstract: RIC regimens are mainly used for patients who cannot benefit from the myelo-ablative (MA) approach, due to age, previous SCT, or comorbidities, based on an expected early toxicity of MA regimen. Some centers may also choose the RIC strategy in young patients because they have no facilities for the management of prolonged neutropenia. The development of RIC has been so encouraging that programs now compare MA and RIC in patients who could tolerate both approaches. However, RIC may fail, and MA SCT be secondary considered. Objective: The goal of this retrospective survey was to assess the toxicity and outcome of MA after RIC SCT. Patients: 17 patients (14–63 y; 6 CML, 4 AML, 2 CLL, 2 myeloma, 1 NHL, 1 CMML, 1 myelodysplastic syndrome) received a MA SCT after RIC, for relapse (n=12), graft rejection (n=4), or in a planned program (n=1), from an HLA-id sibling (n=12), a familial mismatched donor (n=1), an unrelated donor (n=3) or a cord blood (n=1). The reason for initial RIC approach was age in 4, a research program in 6, comorbidities in 3, and previous autologous SCT in 4 patients. RIC included Fludarabin (Flu)-Busulfan (BU) in 8, Flu-2Gy irradiation in 4, Cyclophosphamide (CPM)-antithymocyte globulin (ATG) in 1, and various Flu- regimens in 4. One patient had 2 consecutive RIC SCTs before MA SCT. The median delay between RIC and MA SCT was 9 months (range: 2.5–36 months). The same donor was used for the 1st and 2nd SCT in 12/17 cases. The MA transplant was conditioned with BU-CY (±VP16) in 9, Cyclo-TBI in 4, and other regimens in 4 patients. The median follow-up after MA SCT was 9 months Results: After the MA transplant, 1 patient developed veno-occlusive disease, 2 developed interstitial pneumonia. Five patients died from relapse between 8 and 21 mo after the MA SCT. Seven (41%) died from transplant-related causes at a median of 8 months (GVHD:3; infection:1; multi-organ failure:1; thrombotic microangiopathy:1; EBV proliferative disease:1). 5/17 (29.5%) patients are alive and well 4.5 to 26 months after MA transplant. Three of them have extensive chronic GVHD while they did not develop any GVHD after RIC. The delay between the 2 transplants did not influence the outcome. Conclusion: This survey shows that MA after RIC SCT is feasible, and considering that most of these patients have been initially eligible for RIC because of their age or comorbidities, MA SCT had an acceptable toxicity. It may be considered for patients who relapsed or rejected after RIC transplant.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2005
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 3
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 4335-4335
    Abstract: Abstract 4335 Background Primary induction failure or relapse in AML patients maintains a very poor prognosis despite the cytogenetic stratification and the introduction of new molecules. Nevertheless, allo-HSCT can improve the overall survival of some of these patients, although new strategies are needed especially in conditioning to allow a better outcome in this high risk population of patients. Aims The aim of this analysis was to investigate the safety and efficacy of FLAMSA sequential regimen in patients with high-risk acute leukaemia and MDS, in a multicenter retrospective French study. Methods We analyzed 79 patients, 44 males & 35 females with a median age of 55 years (19-69), there were 50 de novo acute leukaemias, 3 secondary leukaemias and 26 MDS, who underwent allo-HSCT after FLAMSA conditioning [fludarabine (30 mg/m2), high-dose AraC(2 g/m2), and amsacrine (100 mg/m2) from day -12 to -9 + cyclophosphamide (40 mg/kg with related donors, 60 mg/kg with unrelated or mismatched donors) on days -4 and -3, ATG 2.5mg/kg on days -4, -3, and -2 + TBI 4 Gy on day -5 (n=42) or Busilvex 3.2 mg/kg on days -4 & -5(n=37)] who were reported to the Societe Francaise Greffe de Moelle et de Therapie Cellulaire (SFGM-TC) registry. Thirteen patients had undergone previous HSCT (10 allogeneic and 3 autologous). The disease status at transplantation were: 19 (24%) of the patients in primary induction failure (PIF) or refractory disease, 14 (17,7%) in second relapse, 25 (32%) in early relapse, 8 (10%) in untreated disease and 13 (16.3%) in progressive disease. Thirty-four patients were transplanted from HLA identical siblings and 45 from unrelated donors. Sixty four grafts were PBSC, 5 bone marrow and 8 cord blood cells. Results After HSCT, 73 patients engrafted (6 non valuable early deaths) with a median time to neutrophil recovery of 16 days (8-41). There were 31 aGVHD (grade I: n=10, grade II: n=12, grade III: n=4 and grade IV: n=5) and 18 chronic GvHD (10 limited, 5 extensive and 3 unclassified). At the last follow-up, 32 patients are alive, after a median follow-up of 4.2 months, the probability of OS for the whole population at 2 years was 22.8% with 43.8% for untreated patients, 13.8% for patient in relapse, it was 47% for progressive and 23% for PIF patients. The univariate analysis showed a better significant OS according to 4 factors: disease status (untreated patients) (p= 0.04), kind of disease (p 〈 0.001); HLA matching (p=0.03) and HSC source (PBSC) (p=0.004) without any significant impact of age, sex-matching, CMV matching, ABO matching, conditioning regimen (TBI or Busilvex) and interval between diagnosis and transplantation. The multivariate analysis using Cox regression model showed the significant impact of 2 factors on OS: kind of disease; HR=0.284 [0.09-093] (p=0.03) and minor ABO incompatibility HR=2.55 [0.99-6.61] (p=0.05). The cumulative incidence of relapse and TRM at 6 months, 1 & 2 years were: 33%, 39.2% & 40.5% and 20.2%, 21% & 21.5% respectively without any TRM in the untreated group. The multivariate analysis showed also the significant impact of disease status on TRM (p 〈 0.001), and minor ABO incompatibility on relapse HR=5.35 [1.81-15-81] (p=0.002). The estimated cumulative incidence of death from leukaemia at 1 and 2 years from transplant was 62,7% (95% CI, 48,4%-73,1%) and 72,2% (95% CI, 57,3%-87,8%). Conclusion Our study showed a total OS of 23% at 2 years with a better survival in the untreated patients (44%) and progressive patients (47%); a worse survival for the PIF and relapsed patients group (23% & 12% respectively). When comparing to the German study, we observed similar results regarding TRM and relapse incidence, the only difference was the leukemia mortality with a higher rate in our patients which could be explained with the different relapse treatment. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
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  • 4
    In: Blood, American Society of Hematology, Vol. 124, No. 9 ( 2014-08-28), p. 1426-1433
    Abstract: Volasertib plus low-dose cytarabine increased the response rate and improved survival in AML patients ineligible for intensive treatment. Volasertib plus low-dose cytarabine resulted in responses across all AML genetic subgroups and had a clinically manageable safety profile.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2014
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 5
    In: Blood, American Society of Hematology, Vol. 103, No. 9 ( 2004-05-01), p. 3313-3319
    Abstract: The Stro-1 antigen potentially defines a mesenchymal stem cell (MSC) progenitor subset. We here report on the role of human ex vivo-expanded selected Stro-1+ or Stro-1- MSC subsets on the engraftment of human CD34+ cord blood cells in the nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mouse model. The data show that cotransplantation of expanded Stro-1- cells with CD34+ cells resulted in a significant increase of human CD45, CD34, CD19, and CD11b cells detected in blood or in bone marrow (BM) and spleen as compared with the infusion of CD34+ cells alone. Infusion into mice of expanded Stro-1+ and Stro-1- cells (without CD34+ cells) showed that the numbers of Stro-1+-derived (as assessed by DNA analysis of human β-globin with quantitative polymerase chain reaction [PCR]) were higher than Stro-1--derived cells in spleen, muscles, BM, and kidneys, while more Stro-1--derived than Stro-1+-derived cells were found in lungs. The transduction of expanded Stro-1+ cells with an enhanced green fluorescent protein (eGFP) gene did not modify their cytokine release and their homing in NOD/SCID mouse tissues. The difference between the hematopoietic support and the homing capabilities of expanded Stro-1+ and Stro-1- cells may be of importance for clinical therapeutic applications: Stro-1+ cells may rather be used for gene delivery in tissues while Stro-1- cells may rather be used to support hematopoietic engraftment. (Blood. 2004;103:3313-3319)
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2004
    detail.hit.zdb_id: 1468538-3
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  • 6
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 1972-1972
    Abstract: This analysis concerned 164 allogeneic HSCT after standard (Std) or reduced intensity conditioning (RIC) using double cord blood cells (CBC), reported to the SFGM-TC registry. There were 57 females (F) and 107 males (M) with a median age of 39.5 years (18–66). The diagnosis pretransplant were acute leukaemia: 93 (56 AML and 37 ALL), MDS: 9, MPS: 9 (CML: 4), CLL: 5, NHL: 18, HD: 7, MM: 13, AA: 7, other diseases: 3 (2 inborn errors and 1 solid tumour). The median interval between diagnosis and HSCT was 20.6 months (2.6–385.5). Among 154 evaluated patients (pts), disease status prior conditioning were 92 CR (CR1: 45, CR 2: 34, & gt;CR2: 12 and 1 non classified), 21 PR, 21 stable diseases (SD) (SD: 6, AA: 6, inborn errors: 2, CML in CP: 3, myelofibrosis: 2 and MDS: 2), 22 progressive diseases (PD) (PD: 4, relapses: 10 and refractory diseases: 8), 8 pts were not documented. Among 158 pts documented, 49 (31%) were completely sex matched and 109 (69%) sex mismatched [72 CBC1+2 (F+F or F+M) for a M recipient and 37 CBC1+2 (M+M or M+F) for a F recipient]. Among 158 documented, 42% of recipients, 37% of CBC1 and 38% of CBC2 were CMV+; there was a complete ABO compatibility between the 2 CBC and the recipient in 38 cases, 1 or 2 minor incompatibilities in 40 cases and almost 1 major incompatibility in 80 cases. For HLA matching, we distinguished 3 groups: group1 [n=78 (HLA compatibility at least 4/6 between recipient and CBC1+2) and between CB1 and CB2 including total HLA DRB1 matching)] , group 2 [n=55 (HLA compatibility at least 4/6 between recipient and CBC1+2) considering neither HLA compatibility between CBC1-CBC2 nor HLA DRB1 matching)] and group3 [n=25 (all others)] . At harvesting, the median number of total nucleated cells (TNC) (x107/kg) was 4.67(1.6–12.2), the CD34+ (x105/kg) 1.8 (0.3–10.8), the CFU-GM (x104/kg) 3.67 (0.94–25), and after thawing 3.24(0.58–12), 1.4(0.2–9.2) and 2(0.27–16.4) respectively. The TNC threshold number was set to 5x107/kg because more than 96% of pts received more than 3x107/kg. Among 135 documented, 26 (19%) received Std conditioning and 109 (81%) RIC. After transplantation, 129 pts (96%) engrafted with 86% (80–92) of neutrophil recovery at day 60 with no significant difference according to TNC ( & lt;5x107/kg: 88%, ≥ 5 x107/kg: 90%; p=0.28) and HLA matching (group1: 86.6%, group2: 89.6% and group3: 83.3%; p=0.81). Eighty-four pts developed an AGVHD: gr I: 20 and ≥ gr II: 60 (35 gr II, 16 gr III and 4 grade IV), 4 patients were not classified. At day 90, the cumulative incidence of AGVHD grI was 10.4%(5–16), gr ≥ II: 42%(33–51)[grII: 24%(16.5–32), grIII-IV: 18%(11–25)]. Moreover, we observed for AGVHD gr ≥ II according to HLA typing and TNC: group1: 41%(28–54), group2: 46%(31–60) and group3: 33%(8–58); TNC & lt;5x107/kg: 38%(25–51) and TNC & gt;5.107/kg: 46%(32–60). Twenty-one pts presented a chronic GVHD (9 limited and 12 extensive) and the cumulative incidence at 1 year was 13.7%(4–24) for limited and 20%(9–21) for extensive. With a median follow-up of 7.3 months, the probability of 1-year and 2-year overall survival and disease-free survival were 49.6% (40–61.5) and 38% (27–54), 43% (33.5–54.5) and 36% (25–51) respectively. The probabilities of OS, NRM and RM according to TNC, disease status pre-transplant, HLA matching and sex matching are shown in Figure 1 and Table1.The multivariate analysis showed a significant impact of 2 factors on OS: disease status PD vs CR: HR=6.16 (1.87–20.25) (p=0.002); HLA matching group2 vs group1: HR=0.29 (0.11–0.82) (p=0.01), and 3 significant factors on DFS: sex-matched HR=0.29 (0.09–0.94) (p=0.03), sex-mismatched (F recipient) HR=0.15 (0.04–0.61) (p=0.008) and HLA matching (group 2 vs group1) HR=0.32(0.11–0.88) (p=0.02).A refined chimerism analysis is ongoing and will be presented. In conclusion, this large retrospective analysis showed that the quantitative objective of double cord blood use for allogeneic HSCT is achieved (only 4% had received & lt; 3x107/kg TNC) with no further significant impact of TNC number on OS, NRM and RM. As usual in other types of allogeneic HSCT, we demonstrated the significant impact of disease status before transplantation on transplant outcome. Finally, the most interesting point was the better results observed in group 2 but which needs more precise analysis in the future. Table 1. Probability of OS, NRM, RM according to different variables. Probability of OS Probability of NRM Probability of RM Whole population (cummulative 1 year) 49.6%(40–61.5) 49.7%(39–60) 7.5%(2–17) TNC TNC & lt; 5 × 107/kg 50%(36.6–68.5)) 47%(32–62) 8%(0–16) TNC ≥ 5 × 107/kg 44.5%(29.6–67) 56.5%(38.5–74.5) 9.5%(0–20) Disease status pre-transplant CR 51%(38–68) PR 54%(31–92.5) SD 75%(43–100) PD relapse 35.5%(18–70) HLA compatibility Group 1: 4/6 or more for all(2/2 for DRBI) 34%(21–54) 62%(46–78) 10%(3–20) Group 2: 4/6 or more for R-CB1 and R-CB2 61%(45–81) 39%(21–57) 2%(0–6) Group 3: Others 61.6%(42–90) 42.5%(19–66) 10%(0–24.5) Sex matching M recipient with sexmismatch 35%(22–57) 63%(46–79) 8%(2–14) Sexmatch 61%(45–82) 43%(23.5–63) 4.5%(0–13.5) F recipient with sexmismatch 54%(36.5–80)) 42%(24–62) 9%(0–22) Figure 1: Probability of OS according to different HLA groups Figure 1:. Probability of OS according to different HLA groups
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
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  • 7
    In: Blood, American Society of Hematology, Vol. 104, No. 11 ( 2004-11-16), p. 4251-4251
    Abstract: Mesenchymal stem cells (MSCs) can inhibit T lymphocyte (TL) proliferation in mixed lymphocyte reaction (MLR) and are candidate to induce tolerance of allogeneic haematopoietic stem cell graft. Results of previous studies evaluating the role of cell contact between MSCs and TL are contradictory. Some soluble factors produced by MSCs have been shown to be involved in TL inhibition such as Transforming Growth Factor-b (TGF-b), Hepatocyte Growth Factor (HGF), and Indoleamine 2,3 dioxygenase (IDO). In this study inhibition of TL proliferation in MLR was evaluated in cultures with MSCs-TL contact and in cultures without MSCs-TL contact (transwell), at different concentration of MSCs (ratio MSCs/TL: 0.3, 0.1, 0.03, 0.01). Expression of mRNA encoding cytokines and adhesion molecules produced by MSCs were analysed by semi-quantitative RT-PCR. Inhibitory cytokines studied were IDO, HLA-G, LIF, IL-10, TGF-b and HGF; adhesion molecules studied were VCAM and LFA3. Results of MSCs dose effect. In MLR with MSCs-TL contact, inhibition of proliferative index was related to the dose of MSCs. The percentage of inhibition was 74%, 60%, 48%, and 28% at ratio 0.3, 0.1, 0.03 and 0.01 respectively (p & lt;0.05). In MLR without MSCs-TL contact, no dose effect was observed: the percentage of inhibition was 48%, 46% and 46% at ratio 0.3, 0.1 and 0.03 respectively; no inhibition was observed at ratio 0.01. Results of comparison between inhibition with cell contact and without cell contact. At ratio 0.3 the percentage of inhibition was 74% with cell contact and 48% without cell contact (p & lt;0.05), at ration 0.1 the percentage of inhibition was 60% and 46% respectively (p & lt;0.05). These results confirmed that TL inhibition is mediated by soluble factors but is increased when MSCs and TL are in contact. Results of mRNA RT-PCR in MSCs showed an overexpression of IDO, HLA-G and LIF in cultures with cell contact and without cell contact. In cultures with cell contact an overexpression of IL10 and TGF-b was observed, but not in cultures without cell contact. Adhesion molecules VCAM and LFA3 were overexpressed in both types of cultures with and without cell contact. In conclusion although cell contact is not mandatory to inhibit T cell proliferation, inhibition is higher when TL and MSCs are in contact, concomitantly an overexpression of additional inhibitory molecules is observed.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2004
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  • 8
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 4312-4312
    Abstract: Polyclonal or oligoclonal expansion of T cell large granular lymphocyte (T-LGL) after allogeneic haematopoietic stem cell transplantation (HSCT) has been described. A few cases of clonal T-LGL leukaemia of donor origin has been reported as a post transplantation lymphoproliferative disorder (PTLD) and described after allogeneic HSCT (Chang, Am J Clin Pathol, 2005). We report here a patient with a clonal T-LGL of recipient origin occurring after allogeneic HSCT for acute myeloid leukaemia (AML). A 56 year old male patient with an AML received an HLA mismatched (disparity on locus A) related HSCT from his sister in first complete remission. Conditioning regimen was myeloablative and combined Busilvex (12.8 mg/kg) and Cyclophosphomide (120 mg/kg) (BuCy2). Anti-Thymocyte Globulin (ATG Sangstat) was added because of the HLA disparity between donor and recipient at a dose of 15 mg/kg. Prophylaxis of Graft versus Host Disease (GVHD) combined cyclosporine and methotrexate. Complete engraftment was observed with full haematopoietic recovery and 100% donor type chimerism detected by real time quantitative PCR (RQ-PCR). A grade II acute GVHD resolved under steroid and CMV infection was treated with valganciclovir. Ten months post HSCT while all immunosuppressive treatment was discontinued, a severe neutropenia (poly morpho nuclear & lt;0.2 × 109/l) and an hyperlymphocytosis up to 10×109/l occurred with a thrombocytopenia of 100×109/l. Relapse of AML and viral infection (CMV, HHV6, EBV, HCV, HBV, HIV, HTLV1, parvovirus B19) were eliminated. Seach for autoantibodies was negative. No chronic GVHD was diagnosed. The predominant cells in blood films were typical LGLs. Flow cytometric analysis showed a population CD3+/CD8+/CD57+/CD56− consistent with T-LGL. Bone marrow biopsy confirmed agranulocytosis and T-LGL infiltration CD3+/CD8+/CD57+/CD56−. Secondarily agranulocytosis and thrombocytopenia spontaneously resolved within one month, but hyperlymphocytosis persisted with the same T-LGL profile. Chimerism by RQ-PCR on CD3+ and CD3− peripheral blood mononuclear cells (PBMNC) population at time of profound agranulocytosis revealed that donor cells were only 8.2 % and 1.2% on CD3+ and CD3− fractions respectively. Chimerism done when cytopenia resolved became mixed with 47% and 39% donor markers on CD3+ and CD3− fractions respectively. Chimerism was then performed on selected subpopulations; donor markers were 98% on CD14+/15+ myeloid cells, 100% on CD56+ natural killer (NK) cells and 78 % on CD19+ B cells. Cell sorting isolated two T-LGL subpopulations according to CD57 expression: CD57+bright and CD57+weak. Donor markers were 0.02% on CD3+/CD8+/CD57+bright T-LGL cells and 1.2% on CD3+/CD8+/CD57+weak T-LGL cells. These results were in favor of a recipient origin of the T-LGL population without loss of the graft. The diagnosis of clonal T-LGL population was confirmed by TCRg gene rearrangement performed on the selected CD3+/CD8+/CD57+bright and CD3+/CD8+/CD57+weak population. In addition a polyclonal background was observed only in the CD3+/CD8+/CD57+weak population. These data show that T-LGL leukaemia of recipient origin can occur after allogeneic HSCT for AML and can be included as a PTLD. The role of ATG as an intensive immunosuppressive treatment cannot be excluded in the occurrence of this PTLD. In this patient no treatment of T-LGL leukaemia and a wait and watch attitude were undertaken. Eighteen months post HSCT the patient is alive and well with the same stable PTLD profile and no relapse of AML The cytolytic activity of the recipient T-LGL clone could explained the absence of AML relapse and a transient toxicity against donor haematopoiesis. In vitro cytolytic assay will be done to confirm the cytotoxic activity of T-LGL against leukaemic cells and haematopoietic stem cells.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
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  • 9
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    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  The American Journal of Dermatopathology Vol. 43, No. 5 ( 2021-05), p. 394-395
    In: The American Journal of Dermatopathology, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. 5 ( 2021-05), p. 394-395
    Type of Medium: Online Resource
    ISSN: 0193-1091
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    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2041296-4
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  • 10
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    Wiley ; 2019
    In:  Clinical Case Reports Vol. 7, No. 3 ( 2019-03), p. 438-441
    In: Clinical Case Reports, Wiley, Vol. 7, No. 3 ( 2019-03), p. 438-441
    Abstract: Although uncommon, clinicians should be aware that polycythemia vera may be masked due to hemolysis. The report of such associations could help them in clinical practice to establish an early and accurate diagnosis that may be challenging in atypical presentations of myeloproliferative neoplasms.
    Type of Medium: Online Resource
    ISSN: 2050-0904 , 2050-0904
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2740234-4
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