{"title":"Incidental discovery of acquired factor X deficiency in a patient with multiple myeloma","authors":"Yousra Sbibih , Mohammed Bensalah , Abderrazak Saddari , Mounia Slaoui , Nabiha Trougouty , Abdelilah Berhili , Rachid Seddik","doi":"10.1016/j.lrr.2026.100592","DOIUrl":"10.1016/j.lrr.2026.100592","url":null,"abstract":"<div><div>Factor X deficiency is a very rare coagulopathy caused by a constitutional or acquired deficiency of factor X, or by the presence of a circulating anticoagulant in the blood. Factor X deficiency has already been described in patients with AL amyloidosis, the pathophysiological mechanism being related to factor X trapping in amyloid deposits. We report the case of a patient with multiple myeloma and acquired factor X deficiency, in whom the diagnosis of amyloidosis was excluded by all investigations. Factor X deficiency is exceptionally reported in the context of multiple myeloma, where the deficiency is related to plasma cell dyscrasia responsible for the production of monocolonal immunoglobulins of the light chain type. This case report reviews the procedures to be followed by clinicians and biologists in multiple myeloma hemopathy, and systematically includes a hemostasis work-up in the initial management of the disease. Acquired factor X deficiency can cause life-threatening bleeding if not properly managed.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"25 ","pages":"Article 100592"},"PeriodicalIF":0.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147858190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Christina Darwish, Don A. Baldwin, Peter Abdelmessieh
{"title":"Synchronous presentation of pH+ B cell acute lymphoblastic leukemia and chronic lymphocytic leukemia treated with blinatumomab","authors":"Christina Darwish, Don A. Baldwin, Peter Abdelmessieh","doi":"10.1016/j.lrr.2026.100598","DOIUrl":"10.1016/j.lrr.2026.100598","url":null,"abstract":"<div><div>CD19 directed immunotherapy with monoclonal antibodies and chimeric antigen receptor T (CAR-T) cell therapy has shown treatment efficacy in the relapsed/refractory setting for non-Hodgkin’s lymphoma (NHL) and chronic lymphocytic leukemia (CLL). However, the CD19 directed bispecific T-cell engager, blinatumomab, is currently only approved in B-cell acute lymphoblastic leukemia (ALL) and has largely not been investigated in other clinical contexts for CLL. We report a case of a patient who presented with both Philadelphia chromosome positive (pH+) ALL and CLL who achieved measurable residual disease (MRD) negative remission for both diseases with blinatumomab.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"26 ","pages":"Article 100598"},"PeriodicalIF":0.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13312526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148353981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A fatal posterior-fossa chloroma masquerading as tuberculous meningitis after peripartum BCR-ABL1 inhibitor cessation - a case report","authors":"Bhvika Zutshi, Sandeep Garg, Praveen Bharti, Amit Kumar, Annesha Chakraborty, Saarthak Miglani, Ajay Kumar Meena, Arpit Singh Chahal, Sankha Sekhar Ghosh","doi":"10.1016/j.lrr.2026.100607","DOIUrl":"10.1016/j.lrr.2026.100607","url":null,"abstract":"<div><div>Intracranial myeloid sarcoma complicating chronic myeloid leukemia (CML) is exceptional; when its cerebrospinal-fluid profile simultaneously mimics tuberculous meningitis (TBM), the diagnostic trap becomes fatal. A 27-year-old postpartum woman with Ph⁺ CML, initially presenting in B-cell acute lymphoblastic leukemia lymphoid blast crisis, developed rapidly progressive posterior-fossa syndrome following peripartum tyrosine kinase inhibitor (TKI) discontinuation. CSF revealed lymphocyte-predominant pleocytosis, hypoglycorrhachia, hyperproteinorachia, and adenosine deaminase 33 U/L, with negative CBNAAT, malignant cytology, and flow cytometry; BCR-ABL1 P210 registered an International Scale of 49.196%. Contrast-enhanced MRI demonstrated a dural-based, homogeneously enhancing, diffusion-restricting cerebellopontine mass with pachymeningeal involvement, consistent with granulocytic sarcoma. Death from tonsillar herniation occurred within one week, before tissue confirmation. Three imperatives emerge: CSF adenosine deaminase elevation lacks specificity for TBM in hematological malignancy; Ph⁺ CML can undergo myeloid CNS relapse following peripartum TKI cessation; and a posterior-fossa dural mass in leukemia demands urgent tissue diagnosis.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"26 ","pages":"Article 100607"},"PeriodicalIF":0.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Phuong Thao Pham, Hoang Viet Nguyen, Minh Phuong Vu
{"title":"The prognostic value of KRAS, NRAS, and BRAF genes mutations in patients with newly diagnosed multiple myeloma","authors":"Phuong Thao Pham, Hoang Viet Nguyen, Minh Phuong Vu","doi":"10.1016/j.lrr.2026.100615","DOIUrl":"10.1016/j.lrr.2026.100615","url":null,"abstract":"<div><h3>Background</h3><div><em>KRAS, NRAS,</em> and <em>BRAF (RAS/RAF)</em> genes mutations play a role in the pathogenesis of multiple myeloma (MM). We conducted this study to investigate whether <em>RAS/RAF</em> genes mutations have a prognostic value in patients with MM.</div></div><div><h3>Material and methods</h3><div>117 newly diagnosed MM patients underwent the FISH technique to detect high-risk cytogenetic abnormalities and next-generation sequencing (NGS) to detect <em>KRAS, NRAS, BRAF</em> and <em>TP53</em> mutations.</div></div><div><h3>Results</h3><div>In the study patient group, patients with the <em>KRAS</em> mutation had significantly longer OS and PFS compared to those with the <em>TP53</em> mutation; patients with the <em>BRAF</em> mutation had significantly longer OS compared to those with the <em>TP53</em> mutation. In the patient without high-risk cytogenetics based on FISH, patients with the <em>KRAS</em> mutation had significantly longer OS and PFS compared to those with the <em>TP53</em> mutation. Conversely, in the patients with high-risk cytogenetics based on FISH, no difference in survival time has been observed among patient groups harboring different gene mutations.</div></div><div><h3>Conclusions</h3><div><em>RAS/RAF</em> gene mutations may have important prognostic implications for MM but should be considered in conjunction with other abnormalities, such as chromosomal abnormalities and <em>TP53</em> mutations.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"26 ","pages":"Article 100615"},"PeriodicalIF":0.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149199164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Aplastic anaemia with small paroxysmal nocturnal haemoglobinuria clones developing during osimertinib therapy for non-small cell lung cancer","authors":"Hayata Morimoto , Seiichiro Katagiri , Tomokazu Omori , Shunsuke Otsuki , Seiichiro Yoshizawa , Nahoko Furuya , Hiroaki Fujimoto , Hironori Takeuchi , Akihiko Gotoh , Daigo Akahane","doi":"10.1016/j.lrr.2026.100572","DOIUrl":"10.1016/j.lrr.2026.100572","url":null,"abstract":"<div><div>We report two cases of aplastic anaemia (AA) with small populations of paroxysmal nocturnal haemoglobinuria (PNH)-phenotype cells that developed during osimertinib (OSIM) therapy for epidermal growth factor receptor mutation-positive lung adenocarcinoma (EGFR-LUAD). The first case was a 76-year-old woman with EGFR-LUAD accompanied by pleural dissemination. She developed pancytopenia 9 months after starting OSIM therapy. We diagnosed the patient with moderately severe AA and observed hematopoietic recovery following treatment with anabolic steroids and eltrombopag. The second case involved a 63-year-old woman diagnosed with EGFR-LUAD who received adjuvant chemotherapy with OSIM. She developed pancytopenia 6 months later and was diagnosed with non-severe AA. Cyclosporine and romiplostim treatment were effective, allowing for outpatient management. In the two cases described herein, a small number of PNH-phenotype cells were confirmed. The clinical importance of the small PNH-phenotype populations and the mechanism underlying AA during OSIM therapy remain unclear and warrant further investigation.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"25 ","pages":"Article 100572"},"PeriodicalIF":0.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147395028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vincent T. Taillefer , Marianne Emond , Marie-Hélène Leblanc , Stephane Doucet , Jean-Philippe Adam
{"title":"Gemcitabine, dexamethasone and cisplatin with or without rituximab is highly effective as a mobilization regimen in relapsed or refractory lymphoma","authors":"Vincent T. Taillefer , Marianne Emond , Marie-Hélène Leblanc , Stephane Doucet , Jean-Philippe Adam","doi":"10.1016/j.lrr.2026.100566","DOIUrl":"10.1016/j.lrr.2026.100566","url":null,"abstract":"<div><h3>Introduction</h3><div>A combination of Gemcitabine, Dexamethasone and Cisplatin (GDP) with or without rituximab (±R) is an outpatient treatment widely used for relapsed or refractory (R/R) lymphoma. Limited data are available on stem cell mobilization following GDP treatment.</div></div><div><h3>Method</h3><div>A retrospective multicenter study was conducted from January 1st, 2014, to December 31st, 2020. Patients received GDP±R before autologous stem cell transplantation (ASCT) and were mobilized with either GDP±R or intermediate-dose cyclophosphamide (ID-CY). The primary objective was to determine the percentage of patients achieving ≥2 × 10<sup>6</sup> CD34<sup>+</sup>/kg, median CD34<sup>+</sup> yield, and number of apheresis days. The secondary objective compared these results with ID-CY.</div></div><div><h3>Results</h3><div>Ninety-two patients (median age 54) were treated for diffuse large B-cell (40%), Hodgkin (36%), or follicular lymphoma (16%). Of these, 83 were mobilized with GDP±R and 9 with ID-CY. G-CSF was administered at 5 mcg/kg (61%) or 10 mcg/kg (37%) daily, typically starting on day 9, after two GDP cycles. A successful stem cell collection at the first attempt occurred in 96% of GDP±R patients, and 94% of patients proceeded to ASCT. No significant difference was found between GDP±R and ID-CY in terms of successful collection (96% vs. 100%, <em>p</em>=NS), but fewer hospitalizations occurred within 21 days of mobilization (1% vs. 22%, <em>p</em> = 0.02).</div></div><div><h3>Conclusion</h3><div>This study demonstrated the feasibility of performing a peripheral blood stem cell mobilization at day 15 following GDP±R. It is highly effective and represents a better option due to its simplicity of administration, low rate of hospitalization and low cost.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"25 ","pages":"Article 100566"},"PeriodicalIF":0.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A rare case of variant acute promyelocytic leukemia with FIP1L1-RARA fusion gene: case report and literature review","authors":"Yanyan Qiu, Huarong Zhou, Shaoyuan Wang","doi":"10.1016/j.lrr.2025.100553","DOIUrl":"10.1016/j.lrr.2025.100553","url":null,"abstract":"<div><div>Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia characterized by the promyelocytic leukemia-retinoic acid receptor alpha (<em>PML-RARA</em>) fusion gene and exceptional responsiveness to differentiation therapy with all-trans retinoic acid (ATRA) and arsenic trioxide (Arsenic Trioxide). However, rare variant forms of APL involving alternative <em>RARA</em> fusion partners, such as <em>FIP1L1-RARA</em>, are typically resistant to ATRA/ATO-based regimens and are associated with poor clinical outcomes. We report a rare case of <em>FIP1L1-RARA</em>-positive APL in a patient who initially presented with clinical, morphological, and immunophenotypic features consistent with classical APL. Standard diagnostic evaluations, including morphology, flow cytometry, and fluorescence in situ hybridization (FISH), failed to detect the fusion abnormality. The diagnosis was ultimately confirmed by RNA sequencing (RNA-Seq). Empirical induction with ATRA and ATO was initiated but resulted in persistent and progressive promyelocytosis. Anthracycline-based chemotherapy was subsequently administered, followed by azacitidine combined with venetoclax in the subsequent course of treatment. Although partial hematologic improvement was observed, the overall response remained suboptimal. This case underscores the diagnostic challenges of atypical APL and highlights the pivotal role of RNA-Seq in identifying cryptic <em>RARA</em> rearrangements. A literature review suggests that <em>FIP1L1-RARA</em>-positive APL represents a biologically and clinically distinct entity with highly variable treatment responses and poor prognosis. Early molecular diagnosis and prompt implementation of conventional chemotherapy or targeted therapies such as venetoclax may be essential to improving outcomes in this rare APL subtype.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"25 ","pages":"Article 100553"},"PeriodicalIF":0.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145625109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"FLT3 inhibitor and venetoclax therapy in elderly patients with relapsed/refractory FLT3-ITD+ AML: A report of three cases","authors":"Daisuke Ikeda , Satoshi Uchiyama , Yong-Mei Guo , Nobue Sato , Hirotaka Nakamura , Akihito Nagata , Chi Song-Gi , Yosuke Minami , Junichiro Yuda","doi":"10.1016/j.lrr.2026.100591","DOIUrl":"10.1016/j.lrr.2026.100591","url":null,"abstract":"<div><div>This case report examines three patients with relapsed/refractory <em>FLT3-ITD</em>+ acute myeloid leukemia (AML) treated with FLT3 inhibitors (FLT3i) and venetoclax (VEN). While the combination therapy showed promising antileukemic activity, all patients experienced severe myelosuppression, leading to treatment interruptions. Two patients died following disease progression after therapy discontinuation, while one maintained remission with an alternating treatment schedule. These cases highlight the importance of minimizing treatment interruptions while balancing infection risks and suggest that combination or sequential therapy with VEN and FLT3i may be effective for relapsed/refractory (R/R) <em>FLT3-ITD</em>+ AML when treatment duration and dosing are properly managed.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"25 ","pages":"Article 100591"},"PeriodicalIF":0.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147784159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sondus Alsharidah, Eman Almatter, Hana' Nofal, Maha Bourusly, Mohammad Obaid
{"title":"Multidisciplinary approaches to coexisting Glanzmann thrombasthenia and juvenile polyposis syndrome","authors":"Sondus Alsharidah, Eman Almatter, Hana' Nofal, Maha Bourusly, Mohammad Obaid","doi":"10.1016/j.lrr.2026.100583","DOIUrl":"10.1016/j.lrr.2026.100583","url":null,"abstract":"<div><div>Glanzmann thrombasthenia (GT) is a rare autosomal recessive bleeding disorder from defects in the αIIbβ3 integrin receptor, impairing platelet aggregation and often overlooked due to normal platelet counts. Juvenile polyposis syndrome (JPS) is an autosomal dominant disorder with multiple gastrointestinal polyps and increased colorectal cancer risk. Their co-occurrence is exceedingly rare and challenging. We report a 19-year-old male who was diagnosed with GT at age 5 after rectal bleeding from a gastrointestinal polyp requiring polypectomy and transfusions; platelet aggregation studies confirmed GT. At age 9, genetic testing established JPS. In 2014 he developed recurrent severe bleeding—hematochezia, melena, and hemarthrosis—managed with recombinant activated factor VII (rFVIIa), blood transfusions, and supportive care including vitamin D. Additional findings included duodenal lymphangioma requiring resection, vitamin D deficiency with bone pain and complex regional pain syndrome, and chronic idiopathic hypertension treated with antihypertensives. This case highlights rFVIIa effectiveness and the need for multidisciplinary, long-term follow-up and care.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"25 ","pages":"Article 100583"},"PeriodicalIF":0.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147746584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anna Mira Lubis , Muhammad Orri Baskoro , Gabriella Anindyah , Agnes Stephanie Harahap
{"title":"JAK2 V617F mutations and thrombosis in BCR-ABL1 negative myeloproliferative neoplasms: clinical profile and hematologic insights","authors":"Anna Mira Lubis , Muhammad Orri Baskoro , Gabriella Anindyah , Agnes Stephanie Harahap","doi":"10.1016/j.lrr.2026.100588","DOIUrl":"10.1016/j.lrr.2026.100588","url":null,"abstract":"<div><h3>Background</h3><div>The interplay between JAK2 mutation, thrombosis, and the baseline clinical and hematologic profile of MPN remains poorly understood. This study aims to provide insight on the relationship between the clinical profile and hematologic findings, JAK2 V617F mutation, and the occurrence of thrombotic events in BCR-ABL1 negative MPNs.</div></div><div><h3>Materials and methods</h3><div>We retrospectively analyzed 198 patients with BCR-ABL1-negative MPNs to assess associations between JAK2 V617F mutation status, hematologic parameters, clinical features, and thrombotic events.</div></div><div><h3>Results</h3><div>Patients under 40 years old were associated with JAK2 V617F-negative MPN (p<0.05). In PV patients, cardiovascular comorbidities were associated with a 4.5-fold increased risk of thrombosis (OR 4.59; CI 1.57-13.43; p=0.005). Mutated-JAK2 V617F MPN was associated with lower platelets and higher WBC count, while thrombosis was associated with higher hemoglobin and hematocrit (p<0.01). However, we found no associations between JAK2 V617F mutation and thrombotic events across all MPN subtypes.</div></div><div><h3>Conclusion</h3><div>Cardiovascular comorbidity are an independent risk factor for thrombosis in PV. While JAK2 V617F mutation was associated with distinct hematologic profiles, it was not independently linked to thrombotic risk. These findings highlight the significance of clinical comorbidities and hematologic parameters in thrombotic event occurrences in MPN patients.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"25 ","pages":"Article 100588"},"PeriodicalIF":0.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147746585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}