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Abstract: Abstract Acute myeloid leukemia (AML) is a genetic disorder of hematopoietic stem cells (HSCs) followed by clonal selection and uncontrolled proliferation leading to malignant neoplasm. Inappropriate regulation of apoptosis contributes to many human disorders including cancer. Caspase 9 (CASP9) is associated with the intrinsic pathway of apoptosis. Functional single-nucleotide polymorphisms (SNPs) in CASP9 might influence gene expression leading to altered apoptosis and increased AML risk. Previously, two CASP9 promoter polymorphisms (CASP9 1263 rs4645978A > G and CASP9 712 rs4645981C > T) were shown to be associated with increased risk of developing AML and inferior AML survival in South Indian subjects. This study was to evaluate these polymorphisms in an independent cohort of AML patients and controls in Egypt. PCR–RFLP for CASP9 1263 rs4645978 A > G and CASP9 712 rs4645981 C > T genotypes were done in 60 de novo AML cases and 40 healthy control subjects. Our study showed that CASP9 712 rs4645981 C > T gene polymorphism is associated with increased risk of developing AML and poor disease outcome (p value = 0.006, < 0.001; OR = 3.644, 26; and 95% CI = 1.39–9.528, 6.5–103.5, respectively). In contrast, CASP9 1263 rs4645978 A > G showed no significant difference between AML patients and the controls regarding the risk of developing AML or disease outcome (p value = 0.301, 0.573, respectively). CASP9 712 rs4645981 C > T could be involved in the pathophysiology and development of AML in Egypt and may be useful as a predictive molecular markers for inferior prognosis in AML. Notably, risk was highest and outcomes worst in patients with both the 712C > T and 1263A > G alleles. PubDate: 2022-08-06
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Abstract: Abstract De novo AMLs with typical nonrandom chromosomal abnormalities are often associated with specific morphology subtypes. The t(8;21) is one of the most prominent recurrent cytogenetic aberrations (RCA) in AML, frequently associated with AML with maturation, and is characterized as a good prognostic marker. On the contrary, BCR::ABL1 rearrangement is rarely observed in AMLs, without specific morphology, carrying poor prognosis. Its distinction from blastic transformation of chronic myeloid leukemia has been a matter of long debate. The revised WHO classification (2016) recognized AML with BCR::ABL1+ as a provisional entity. The occurrence of additional cytogenetic aberrations in AML RCA within the same leukemic clone has been detected, albeit rare cases of BCR::ABL1+ were reported, mainly as subclones. Those additional cytogenetic and molecular findings seem to significantly affect patient prognosis. Conventional cytogenetic analysis, fluorescent in situ hybridization (FISH), and polymerase chain reaction (PCR) were applied at presentation and during the follow-up of the patient. We present a 34-year-old male patient with de novo AML harboring concomitant t(8;21) and t(9;22) in a single clone. The presence of both t(8;21) and Philadelphia chromosome (Ph+) in the same metaphases but in less than 100% of the analyzed cells, the p190 BCR::ABL transcript type, and absence of splenomegaly support that additional BCR::ABL1+ is a part of the main leukemic clone. These findings, accompanied with an encouraging outcome of continuous cytogenetic and molecular remission after induction therapy, support BCR::ABL1 being a secondary genetic event in AML with t(8;21). PubDate: 2022-07-31
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Abstract: Abstract Epstein-Barr virus (EBV) is one of the most common viruses associated with multiple malignancies including hematopoietic, epithelial, and mesenchymal neoplasms. EBV is linked to B- and T-cell lymphomas, ranging from indolent to highly aggressive neoplasms. EBV-positive follicular lymphoma (FL) is not well characterized due to its low prevalence. In this report, we describe a case of EBV-positive FL and concurrent EBV-negative diffuse large B-cell lymphoma (DLBCL), and discuss their clonal relationship, and EBV status in the process of disease progression. Histology, immunohistochemistry, in situ hybridization, and next-generation sequencing studies were performed as previously described. The 58-year-old male presented with extensive axillary and subpectoral lymphadenopathy. The patient had a history of mixed connective tissue disease treated in the past with steroids and methotrexate, and at the time of current presentation with hydroxychloroquine. The excision of axillary lymph node showed coexistent EBV-positive FL (grade 3B) and EBV-negative DLBCL. There was no evidence of BCL2 gene rearrangement; however, both EBV-positive neoplastic follicles and diffuse component harbored MYC/IGH rearrangement. Next-generation sequencing suggested branching evolution with shared DDX3X mutation, a number of private mutations, and unique IGH usage in FL and DLBCL. The patient was treated with six cycles of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) with involved-field radiotherapy and remains in complete remission. To the best of our knowledge, this is the first report of BCL2 rearrangement negative, MYC/IGH-positive and EBV-positive FL, and concurrent EBV-negative DLBCL, which supports branched evolution model. PubDate: 2022-07-28
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Abstract: Abstract The patient is a woman in her 60s with a history of plasma cell myeloma, status post high-dose melphalan and autologous stem cell transplant, followed by maintenance lenalidomide. She was admitted for severe headaches with concern for meningitis. CSF culture yielded Cryptococcus neoformans. Cryptococcal antigen was present at high titer in the CSF (1:640) but was negative in serum. A diagnosis of cryptococcal meningitis was rendered. She was treated with over 2 weeks of intravenous amphotericin plus flucytosine. Upon discharge, her CSF cryptococcal antigen test remained positive (1:2560) but CSF culture was negative. She continued to experience mild headaches after discharge and was maintained on daily oral fluconazole. Several months later, a bone marrow biopsy was performed to evaluate for residual myeloma post-transplant. There was no morphologic, immunohistochemical, or flow cytometric evidence of residual plasma cell neoplasm. However, the core biopsy revealed suspicious clusters of histiocytes (A) with numerous cytoplasmic inclusions, some of which appeared to contain thick cell wall-like structures (B). Special stains, including periodic acid-Schiff (PAS, C) and Grocott’s methenamine silver (GMS, D), identified variably sized yeast forms, morphologically compatible with Cryptococcus. Infected histiocytes were not visualized on the aspirate smears. A repeat serum cryptococcal antigen test was positive (1:640). She was kept on daily oral fluconazole and is being closely followed by infectious disease. Immunocompromised patients are at increased risk for a variety of marrow infections, including Cryptococcus. Patients with plasma cell myeloma are at risk for invasive fungal infections after autologous stem cell transplant and while taking lenalidomide, which alters CD4 + and CD8 + T-cell function through multiple mechanisms. Due to a lack of standardized treatment protocols for therapy-refractory non-pulmonary non-meningeal cryptococcal disease, therapy regimens are often tailored on a case-by-case basis. PubDate: 2022-07-21
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Abstract: Abstract Extramedullary hematopoiesis (EMH), as a compensatory phenomenon, refers to the blood cell formation outside of the bone marrow that occurs once the cells in the circulatory system fail to meet individuals’ needs. EMH is rare in moderate to severe beta thalassemia because most symptomatic patients are effectively managed with transfusion. However, patients that fail to receive transfusions like β-thalassemia intermedia (β-TI) as indicated are at increased risk for developing EMH. This paper describes the case of a 15-year-old female adolescent with β-thalassemia major (β-TM), suffering from a rare form of EMH affecting the sinus cavities, characterized by headache, sinusitis, and nasal obstruction, as confirmed by physical-pathological examinations and computerized tomography (CT) scan findings. The EMH in this patient could be significantly attributed to the lack of regular blood transfusions in recent years. It was concluded that β-TM along with the occurrence of EMH in the sinus cavities had led to a complex case, carrying a heavy burden of the disease for the patient. PubDate: 2022-07-15
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Abstract: Abstract Familial hemophagocytic lymphohistiocytosis (FHLH) with Epstein–Barr virus (EBV) infection can mimic chronic active EBV infection of T- and NK-cell type (CAEBV-T/NK) in its clinical manifestation and pathomorphology. FHLH with genetic susceptibility to EBV has not been previously reported. The development of FHLH in conjunction with EBV infection is rare and needs further investigation to understand and characterize it. We report a rare case of FHLH with EBV infection that mimicked CAEBV-T/NK, but progressed to childhood aggressive natural killer cell leukemia (ANKL). The patient is in clinical remission following allogeneic hematopoietic stem cell transplantation (allo-HSCT). Our reported case suggests that patients with FHLH and EBV infection, especially those with symptoms similar to those of CAEBV-T/NK, may rapidly progress to ANKL or other neoplastic diseases. Therefore, we must be aware of these cases to ensure that patients are diagnosed correctly so they can be treated appropriately and in a timely manner. PubDate: 2022-07-14
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Abstract: Abstract Primary mediastinal B-cell lymphoma (PMBL) is a rare but aggressive form of non-Hodgkin lymphoma (NHL) that shares significant overlap with Diffuse large B-cell lymphoma (DLBCL). Double- (DH) and triple-hit (TH) lymphomas are aggressive B-cell lymphomas with translocations involving MYC + BCL2 or BCL6 and MYC + BCL2 + BCL6, respectively. There are only 2 previous reports of DH in PMBL and no reports of TH. Here, we present the case of a 23-year-old female with post-treatment relapse of PMBL into a PMBL-TH, after initially presenting with MYC but without either BCL2 or BCL6 rearrangement. Immunohistochemistry (IHC), fluorescence in situ hybridization (FISH), and the Lymph3Cx gene expression assay were used to confirm the diagnosis. This case initiates the literature for PMBL-TH and expands the overall knowledge base regarding DH/TH in B-cell lymphomas. It also further emphasizes the utility of genetic and molecular assays in clinical identification of unique B-cell lymphoma subtypes when considering potential treatment courses. PubDate: 2022-07-14
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Abstract: Abstract We chronicle a case of an atypical plasmablastic proliferation in a patient occurring in the context of vedolizumab, a novel therapy for the treatment of inflammatory bowel disease (IBD). No documented cases exist of this potential association, and we propose a pathogenic mechanism. A 22-year-old female with IBD had a flare of colitis and required a subtotal colectomy. She had been on vedolizumab for 2 years. Histology revealed indeterminate colitis but discovered a densely cellular polypoid lesion of plasmablasts and plasma cells of varying maturation, positive for MUM1, BLIMP1, c-myc, IgG, and CD138, with a lambda light chain restriction, but negative for CD20 and PAX5. The combined diagnosis was of an atypical plasmablastic proliferation that mimicked a plasmablastic lymphoma; however, this diagnosis was confounded by its atypical presentation: a young female on vedolizumab, and we queried what pathogenic role vedolizumab may have had. Vedolizumab selectively targets α4β7 integrin, a leucocyte adhesion molecule, to inhibit gut lymphocyte accretion and reduce inflammation. A similar phenomenon occurs with HIV-infection. HIV-gp120 binding with α4β7 leads to a loss of gut CD4 + lymphocytes and the potential to develop plasmablastic lymphoma, an AIDS-defining diagnosis. Concurrent use of vedolizumab at diagnosis suggests a synergistic causal effect given the molecular mimicry of its target α4β7 seen also with HIV-infection. This is the first documented case of a plasmablastic proliferation, or of any clonal cellular proliferation, to occur in the context of vedolizumab. α4β7 integrin antagonism may carry oncogenic sequelae, and we recommend further investigation to understand its pathogenesis. PubDate: 2022-07-13
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Please help us test our new pre-print finding feature by giving the pre-print link a rating. A 5 star rating indicates the linked pre-print has the exact same content as the published article.
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Abstract: Abstract Chronic myeloid leukemia (CML) is a common myeloproliferative neoplasm (MPN). However, CML presenting with isolated thrombocytosis and lacking all the typical features of CML is quite rare. The purpose of this report is to demonstrate the importance of BCR::ABL1 testing for correct diagnosis and treatment even when the presenting features are unusual for CML. We report a case of isolated thrombocytosis with subsequently discovered alternative splicing of JAK2 resulting in skipping of exon 15 in the peripheral blood as the initial presentation of CML in a 67-year-old male with metastatic hepatocellular carcinoma, with BCR::ABL1 detected in the bone marrow aspirate. Bone marrow aspirate was collected in EDTA for evaluation and testing. Bone marrow clot and core sections were obtained and the core was decalcified, then each was fixed in neutral-buffered formalin (10%). The clot and core were embedded in formalin and sectioned at 4 microns for evaluation. Bone marrow aspirate and biopsy demonstrated markedly increased megakaryocytes with clustering. The chromosome analysis demonstrated t(9;22) and molecular studies for BCR::ABL1 were positive. JAK2, MPL, and CALR mutations were negative. The patient did not show a response to hydroxyurea (HU) as the initial treatment. His platelet count normalized within 1 month after treatment with Tyrosine kinase inhibitor (TKI) Imatinib. This report highlights the importance of pursuing BCR::ABL1 testing in the workup of patients with isolated thrombocytosis, even in the presence of abnormal JAK2 transcripts and unusual bone marrow features. PubDate: 2022-05-10 DOI: 10.1007/s12308-022-00496-6
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Abstract: Abstract T-lymphoblastic leukemia/lymphoma (T-ALL/LBL) is an aggressive lymphoid malignancy, frequently involving the central nervous system (CNS). However, exclusive CNS infiltration of T-ALL without leukemic presentation at initial diagnosis is extremely rare. Herein, we report the case of a 19-year-old male patient who presented with progressively worsening head and neck pain, dysphagia, and dizziness. No leukemic cells were detected in peripheral blood or bone marrow samples. Computed tomography revealed only a small anterior mediastinal mass and mildly high density in some areas of the bone marrow. Although brain magnetic resonance imaging (MRI) showed no abnormal findings, spine MRI revealed slight contrast enhancement of the cauda equina. A spinal tap revealed massive infiltration of abnormal lymphoid cells that were diagnosed as T-ALL/LBL based on morphological and immunophenotypic findings. Urgent intravenous and intrathecal chemotherapeutic intervention resulted in a rapid reduction in leukemic cells in the cerebrospinal fluid, with relief of symptoms. Since T-ALL/LBL usually exhibits leukocytosis associated with a high frequency of CNS involvement, this case is considered an exceptional presentation. Recognition of such a rare presentation of T-ALL/LBL, which mimics other neurological diseases such as meningoencephalitis and demyelinating diseases, is important to avoid delayed diagnosis and treatment that could result in early death or severe neurological sequelae. PubDate: 2022-04-26 DOI: 10.1007/s12308-022-00495-7
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Abstract: Abstract B-lymphoblastic leukemia/lymphoma (B-ALL/LBL), not otherwise specified, is a neoplasm of B-cell precursor lymphoid cells. Most of these tumors tend to manifest in children. B-LBL constitutes about 10% of the lymphoblastic lymphomas; however, in older adults, it is extremely rare. We present a case of a 46-year-old man with no pertinent medical or surgical history who presented with severe abdominal pain, nausea, and emesis. An abdominal CT scan was suggestive of strangulation of the distal small bowel and ischemia, showed extensive matted lymphadenopathy in the mesentery, and multiple left suprarenal periaortic nodes. A bowel resection was performed and there was an ileocolonic intussusception with the right colon filled with the intussuscepted terminal ileum. Opening the specimen revealed a submucosal ileal mass that measured 3 × 2.2 × 1.3 cm with a well-circumscribed, yellow-white cut surface. Histological examination showed a diffuse infiltrate composed of small- and medium-sized cells extending through the ileal wall from mucosa to subserosa, with irregular nuclear contours, open chromatin, inconspicuous nucleoli, occasional mitoses, and frequent apoptotic bodies. Flow cytometric analysis revealed 29% B-lymphoblasts corresponding to the diagnosis of B-LBL. BCR/ABL translocation by FISH was not detected. Cytogenetics analysis showed a normal male karyotype 46,XY. B-LBL is a rare neoplasm in older adults and can involve nodal and extranodal sites; however, the gastrointestinal tract is rarely compromised, with only a few cases reported in the literature. PubDate: 2022-04-23 DOI: 10.1007/s12308-022-00494-8
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Abstract: Abstract World Health Organization (WHO) guidelines, 2008 and 2016, have laid down strict criteria for assigning the lineage to blast cells in the diagnosis and classification of acute leukemia. While cytoplasmic (c) CD22 has been recommended by WHO as a strong B lymphoid lineage-associated marker along with surface (s) CD19, cCD79a, and sCD10, there is no reference to sCD22 as a diagnostic marker in these guidelines. In view of the above fact and the technological advantage surface immunophenotyping assays provide over the cytoplasmic assays, we examined the sensitivity and specificity of sCD22 for B lymphoid lineage. Blast cells in 232 cases of B-acute lymphoblastic leukemia (B-ALL) were examined by flow cytometric immunophenotyping for expression of sCD10, sCD19, sCD20, sCD22, and cCD79a in addition to a host of other lineage-associated CD markers as a part of an antibody reagent panel. In 124/126 (98%) cases of B-ALL, the blast cells expressed sCD22, thereby confirming its high sensitivity as a B lymphoid marker. In 52/54 (96%) of these cases wherein cCD79a (another B lineage marker recommended by the WHO) expression was examined in parallel, both markers were positive suggesting a very high degree of correlation between sCD22 and c79a expression. sCD22 also showed 100% specificity for the B lymphoid lineage. Our data show that sCD22 can be used as a reliable and preferred marker for the diagnosis of B-ALL in place of cCD22 and cCD79a in view of its associated technological advantages. These findings also provide the basis for an increasing use of anti-CD22 antibody and/or CD22 CAR T cell therapy in B-ALL. PubDate: 2022-04-23 DOI: 10.1007/s12308-022-00492-w
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Abstract: Abstract Aggressive subtypes of non-Hodgkin lymphoma may uncommonly be referred to clinical oncologists for treatment of acute leukemia, due to an elevated or rapidly rising white blood cell count (WBC), with circulating neoplastic cells that morphologically resemble leukemic blasts seen in acute myeloid or lymphoblastic leukemia. We describe six cases of non-Hodgkin lymphoma that mimicked acute leukemia and were identified in the pathology records of the Brigham and Women's Hospital. The patients were older adults (mean age 70 years), who presented with leukocytosis (mean 79.7 × 109/L) with circulating neoplastic cells (mean 57%), which mimicked leukemic blasts, thrombocytopenia, and anemia (4/6 patients). In each case, immunophenotypic analysis identified a population of mature B cells or mature T cells. We identified 15 additional cases of non-Hodgkin lymphoma in the literature that mimicked acute leukemia; considering all 21 cases, 11 had an appearance of acute lymphoblastic leukemia, 4 had an appearance of acute monocytic leukemia, and 6 had an appearance of acute leukemia unable to be further categorized. In general, patients exhibited poor overall survival. These cases illustrate the importance of comprehensive immunophenotypic analysis in the initial evaluation of hematolymphoid neoplasms, and that occasional cases of non-Hodgkin lymphomas can resemble acute leukemia at initial presentation. PubDate: 2022-04-23 DOI: 10.1007/s12308-022-00493-9
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Abstract: Abstract Primary central nervous system lymphoma (PCNSL) is a highly aggressive non-Hodgkin lymphoma confined to the central nervous system. Diffuse large B cell lymphoma (DLBCL) is the most common subtype, and it follows a much more aggressive course than its systemic counterpart. Differential diagnosis of PCNSL and systemic DLBCL depends on clinical staging, which is expensive and time consuming. Protein kinase C delta (PKCD) is a protein with proapopitotic properties and has a major role in negative selection of B cells in germinal centers, a regulatory function in B cell receptor (BCR) pathway and MHC II expression. Mutations identified in its gene are reported to be unique for PCNSL and not encountered in systemic DLBCL. Our aim is to evaluate immunohistochemical (IHC) expression and the mutation status of PKCD in PCNSLs and systemic DLBCLs in order to find out whether PKCD could be a novel marker that could be used in differential diagnosis of both entities. A total of 43 cases diagnosed with PCNSL, and 43 cases diagnosed with systemic DLBCL were included in the study. Immunohistochemistry for PKCD antibody and Sanger sequencing targeting exon 16 and exon 18 of PKCD gene were performed. Although immunoreactivity for PKCD was observed in all PCNSL and 95.3% of systemic DLBCL cases, strong and diffuse staining was found to be more frequent in PCNSL than systemic diffuse large B cell lymphomas (p < 0.001). However, mutations defined in literature were not encountered in our cohort. While clinical staging is still the primary way for differential diagnosis of PCNSL and systemic DLBCL, the diffuse and strong PKCD expression can be used as a supportive feature for PCNSL diagnosis. PubDate: 2022-04-04 DOI: 10.1007/s12308-022-00490-y
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Abstract: Abstract In some patients with chronic myeloproliferative neoplasms, myelofibrosis (MF) develops as natural evolution of the disease. The aim of this study was to analyze predictive factors that may cause MF in polycythemia vera (PV) and essential thrombocythemia (ET) patients. This retrospective study was conducted on PV and ET patients who attended our hospital between 2008 and 2019. The development of MF during follow-up was recorded, and comparisons were made of the patients who developed MF and those who did not develop MF. Evaluation was made of 126 ET and 105 PV patients. During follow-up period, MF had developed 5.7% of PV and 7.1% of ET patients. It was determined that JAK-2 mutant allele burden, lymphocyte count, vitaminB12 levels, and grade of bone marrow fibrosis at diagnosis had statistically significant impact on the development of MF in all patients. In the logistic-regression analysis, it was found that initial hemoglobin, hematocrit, neutrophil-to-lymphocyte ratio, and monocyte count for PV patients; vitaminB12, the presence of splenomegaly; and BM fibrosis at diagnosis for ET patients have statistically significant effect on MF development. The results of the current study demonstrated that some parameters especially vitamin B12 levels can be used as predictive markers for the development of MF. PubDate: 2022-03-28 DOI: 10.1007/s12308-022-00488-6
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Abstract: Abstract Chronic myeloid leukaemia most commonly presents in chronic phase (CML-CP) and it is characterised by granulocytic proliferation. Many patients have an excellent response to tyrosine kinase inhibitor therapy; however, a small proportion will develop lymphoid or myeloid blast crisis, with inferior clinical outcomes. Detection of lymphoblasts at diagnosis of CML-CP has been reported in small case series with conflicting results on the risk of subsequent blast crisis. The aim of this study was to identify the incidence and immunophenotype of abnormal lymphoblast populations in CML-CP. Retrospective review of bone marrow flow cytometry results of consecutive patients with newly diagnosed CML-CP between June 2012 and February 2021 was performed. Lymphoblasts, myeloblasts, haematogones, and mature lymphocytes were evaluated. Fifty-nine patients had bone marrow flow cytometry results available for review. Abnormal lymphoblast populations were detected in four patients (7%) comprising 0.05–0.19% of bone marrow events. The immunophenotype was similar but distinct from haematogones. The most common distinguishing features of the abnormal lymphoblast populations were abnormally bright expression of CD19 or CD10, weak CD38 or aberrant CD20 expression on CD34 + cells. The clinical case of one of the patients with abnormal lymphoblasts detected at diagnosis who went on to subsequent blast crisis is discussed. Abnormal lymphoblasts can be identified in CML-CP and may be under-recognised. Their detection requires careful analysis in order to distinguish them from normal precursors. The clinical significance of such populations requires further study. PubDate: 2022-03-10 DOI: 10.1007/s12308-022-00487-7
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