Myeloproliferative Neoplasm with BCR-FGFR1 Fusion Presenting as Eosinophilic Myeloproliferative Syndrome

Myeloproliferative Neoplasm with BCR-FGFR1 Fusion Presenting as Eosinophilic Myeloproliferative Syndrome | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Myeloproliferative Neoplasm with BCR-FGFR1 Fusion Presenting as Eosinophilic Myeloproliferative Syndrome Sanchit Chhabra, Sunil Kumar, Lalit Raut, Keshav Yadav, Nidhi Bardiya This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7790354/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Myeloproliferative neoplasms with FGFR1 rearrangements, historically described as the 8p11 myeloproliferative syndrome, represent a rare but highly aggressive group of hematologic disorders driven by constitutive activation of the FGFR1 tyrosine kinase. These neoplasms often manifest with striking eosinophilia and carry a significant risk of progression to acute leukemia. Among the different FGFR1 fusion partners, the BCR-FGFR1 rearrangement is particularly uncommon and portends a challenging clinical course.[ 1 ] We describe the case of a middle-aged woman who presented with fatigue, weight loss, and splenomegaly, accompanied by pronounced leukocytosis and eosinophilia. Cytogenetic analysis revealed a t(8;22)(p11;q11) translocation resulting in a BCR-FGFR1 fusion. Despite initial cytoreductive therapy, her disease evolved rapidly, underscoring the aggressive nature of this entity. She ultimately required intensive therapy and consideration for allogeneic stem cell transplantation. This case highlights the diagnostic and therapeutic challenges of BCR-FGFR1–positive neoplasms and emphasizes the importance of early recognition, molecular testing, and timely referral for potentially curative interventions. In the era of emerging FGFR inhibitors, documenting such cases adds valuable insight into the natural history and management strategies for this rare and devastating disorder. Myeloproliferative neoplasm FGFR1 rearrangement t(8 22)(p11 q11) Eosinophilia 8p11 myeloproliferative syndrome Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Introduction Myeloproliferative neoplasms with eosinophilia and FGFR1 rearrangements represent a rare but distinct group of hematologic disorders, formally recognized as separate entities in the World Health Organization (WHO) classification. These neoplasms are unified by constitutive activation of the FGFR1 tyrosine kinase, which drives uncontrolled cellular proliferation and confers an aggressive clinical course.[ 2 ] Among the various FGFR1 fusion partners described, the BCR-FGFR1 rearrangement , resulting from the translocation t(8;22)(p11;q11) , is particularly uncommon. Patients with this fusion often present with features resembling chronic myeloproliferative disorders, including leukocytosis, marked eosinophilia, and splenomegaly, but unlike more indolent conditions, these neoplasms frequently progress to acute leukemia—most commonly acute myeloid leukemia or T-lymphoblastic lymphoma/leukemia—within a short period of time.[ 3 ] Because of its rarity, BCR-FGFR1–positive disease is often under-recognized, leading to delays in diagnosis and missed opportunities for timely intervention. Early identification is critical, as the natural history is aggressive and conventional therapies, including standard tyrosine kinase inhibitors such as imatinib, are ineffective. At present, allogeneic hematopoietic stem cell transplantation remains the only curative strategy, although emerging FGFR inhibitors offer new hope for targeted treatment.[ 4 ] Here, we report the case of a middle-aged woman with BCR-FGFR1–positive myeloproliferative neoplasm presenting with eosinophilia, highlighting the diagnostic challenges, clinical course, and therapeutic considerations associated with this rare entity. Case Presentation A 37-year-old woman, previously healthy and working as a house wife, presented to the emergency department with a 7-day history of high-grade fever accompanied by chills and drenching night sweats. She had fatigue, generalized body aches, and a persistent dull pain in her lower back that worsened with movement. Over the past month, she had progressive loss of appetite, significant weight loss (around 5 kilograms), and increasing exhaustion that was beginning to interfere with her ability to work and perform daily activities. On arrival, she was febrile (temperature 39.1°C), had tachycardia (Pr-112 bpm), and was hypotensive (BP 92/60 mmHg). Her respiratory rate was increased, though she was not in distress. Physical examination revealed mild hepatosplenomegaly and localized tenderness in the lower lumbar region, but no focal signs of infection or neurological deficit. Initial laboratory investigations revealed that she had total leukocyte count of 62600/mm³. Platelet count was low at 55,000/mm³. CRP(102) was significantly elevated, and procalcitonin(10) was raised, suggesting a severe inflammatory response. Liver and kidney functions were within normal limits as shown in table 1. Blood and urine cultures were drawn, and she was empirically started on broad-spectrum intravenous antibiotics and fluids for presumed sepsis. Table 1 shows various initial laboratory investigations. Test Value Reference Range TLC (Total Leukocyte Count) 62,600 /µL 4,000 – 11,000 /µL Neutrophils 49% 40 – 75% Eosinophils 37% 1 – 6% Lymphocytes 4% 20 – 45% Platelet Count 55,000 /µL 150,000 – 450,000 /µL CRP (C-Reactive Protein) 102 mg/L <5 mg/L Procalcitonin 10 ng/mL <0.05 ng/mL Urea 20 mg/dL 10 – 50 mg/dL Creatinine 1.0 mg/dL 0.6 – 1.2 mg/dL Sodium (Na⁺) 132 mEq/L 135 – 145 mEq/L Potassium (K⁺) 4.0 mEq/L 3.5 – 5.0 mEq/L SGOT (AST) 32 U/L up to 40 U/L SGPT (ALT) 30 U/L up to 40 U/L Total Bilirubin 0.6 mg/dL 0.2 – 1.2 mg/dL The peripheral smear showed RBCs - Mild to moderate anisopoikilocytosis moderately hypochromic, a few microcytes and fragmented RBCs noticed About 17-18 nRBC s/100 leucocytes are noted . These normoblasts were of late and intermediate type of normoblast . No proerythroblast were noticed . WBC- Total count markedly increased on smear with eosinophilia. DLC- Blasts- 00% Promyelocyte- 00% Myelocyte- 04% Metamyelocyte- 06% Neutrophils + Band forms- 49% Monocytes- 03% Eosinophils and precursors - 37% Basophils and precursors - 02% Small lymphocytes - 01% Large lymphocytes - 04% No typical myeloblast or monoblast are seen . Platelets- On lower side of normal. A few giant platelets forms are seen . No haemoparasites seen as shown in table 2. Opinion - Hematomorphology is suggestive of leucoerythroblastic reaction with dominant eosinophil cell component as shown in figure 1,2,3. Table 2 shows peripheral smear findings showing marked eosinophilia with leukocytosis. Component Findings RBC Morphology Mild to moderate anisopoikilocytosis, moderately hypochromic, few microcytes, fragmented RBCs noted nRBCs 17–18 nucleated RBCs/100 WBCs (late and intermediate normoblasts; no proerythroblasts) WBC Total Count (Smear) Markedly increased DLC - Blasts 0% DLC - Promyelocytes 0% DLC - Myelocytes 4% DLC - Metamyelocytes 6% DLC - Neutrophils + Bands 49% DLC - Monocytes 3% DLC - Eosinophils + Precursors 37% DLC - Basophils + Precursors 2% DLC - Small Lymphocytes 1% DLC - Large Lymphocytes 4% Platelets Reduced; a few giant platelets seen Haemoparasites Not seen Bone marrow aspiration and biopsy revealed hypercellular marrow dominated by granulocytic hyperplasia with eosinophilic proliferation as shown in figure 4,5,6. Fluorescence in situ hybridization was done which was positive for BCR-FGFR 1 fusion. Discussion BCR-FGFR1 fusions are exceptionally rare. Because of this rarity, they are often difficult to recognize at first. Clinically, these neoplasms can look very much like chronic myeloid leukemia: patients may come in with high white blood cell counts and an enlarged spleen. [ 5 ]What often sets them apart, however, is the striking presence of eosinophilia—an overproduction of eosinophils in the blood—and, more alarmingly, their tendency to behave aggressively. Unlike chronic myeloid leukemia, which can often be managed for years, BCR-FGFR1–driven diseases typically transform into acute leukemia within just a few months of diagnosis. This rapid progression highlights how critical early recognition and molecular testing are for patients who might harbor these fusions.[ 6 ] A major challenge in managing these neoplasms is their resistance to the standard drugs we might otherwise use. For example, other eosinophilia-associated disorders, such as those caused by PDGFRA or PDGFRB rearrangements, respond dramatically to imatinib—a tyrosine kinase inhibitor that can essentially switch off the disease.[ 7 ] Unfortunately, FGFR1-driven cancers don’t respond in the same way. This resistance leaves physicians with very limited conventional treatment options. At present, the only intervention that offers a chance for cure is allogeneic hematopoietic stem cell transplantation (HSCT). For this reason, once the diagnosis is made, timely referral for transplant evaluation becomes a cornerstone of management, even if the patient is still clinically stable.[ 8 ] In recent years, however, a glimmer of hope has emerged. New drugs specifically designed to target FGFR pathways—such as pemigatinib, futibatinib, and erdafitinib—have begun to show promise.[ 9 ] In early case reports, some patients who were ineligible for HSCT achieved meaningful remissions, both hematologic and cytogenetic, with these agents. While it is too soon to know how durable these responses will be, the results point toward a future in which treatment is not solely reliant on transplantation. For patients and their families, these therapies offer not just new options, but also a sense of hope in the face of an otherwise devastating diagnosis.[ 10 ] Outcome The patient was initially treated with hydroxyurea for cytoreduction, which controlled leukocytosis and patient responded well to treatment. Patient was not started on pemigatinib or futibatinib because of non availability of these drugs as this patient was treated in a rural tertiary health care centre. Use of these drugs for treatment of eosinophilic myeloproliferative syndrome has been described by Freyer et al, in his case report[ 9 ]. Although most of these patients require allogeneic hematopoietic stem cell transplantation (HSCT) as the final treatment for remission this was not the case with our patient as she responded well to hydroxyurea. BCR-FGFR1–positive myeloproliferative neoplasm with eosinophilia represents a rare but profoundly aggressive hematologic disorder with a natural history marked by rapid disease progression and high risk of leukemic transformation. [ 11 ]For clinicians, maintaining a high index of suspicion is essential, as timely recognition and accurate molecular diagnosis can directly influence management decisions. Early referral for allogeneic stem cell transplantation remains the cornerstone of potentially curative therapy and offers the best chance for long-term survival.[ 12 ] At the same time, the therapeutic landscape is beginning to evolve. The emergence of novel FGFR inhibitors has introduced new hope, particularly for patients who are not candidates for transplant or who relapse after conventional therapy. These targeted agents, though still under investigation, may redefine treatment strategies in the years to come.[ 13 ] Conclusion This case underscores not only the aggressive biology of BCR-FGFR1–driven disease but also the urgent need for continued research and clinical awareness. Sharing such rare cases contributes to a growing collective understanding and, ultimately, to better outcomes for patients facing this challenging diagnosis. Declarations Ethical approval- The study protocol was approved by Datta Meghe Institue of Ethics committee, sawangi meghe,wardha in accordance with Helinski Declaration. Consent to Participate - Informed consent from all subjects for participation in an online open access publication was taken. Consent to publish- Informed consent from all subjects for publication of identifying information in an online open access publication was taken. Funding Statement No competing financial or non financial interest were there in relation to work. Data Availability The datasets used during current study are available from the corresponding author on reasonable request. Authors contribution statement All authors contributed equally for the work. Authorship The authors have read the journal policies and manuscript has been submitted in accordance with those policies. Clinical Trial Number not applicable for this manuscript. References Jackson CC, Medeiros LJ, Miranda RN. 8p11 myeloproliferative syndrome: a review. Hum Pathol. 2010;41(4):461 – 76. doi: 10.1016/j.humpath.2009.11.003. PMID: 20226962. Macdonald D, Aguiar RC, Mason PJ, Goldman JM, Cross NC. A new myeloproliferative disorder associated with chromosomal translocations involving 8p11: A review. Leukemia. 1995;9:1628–30. Fioretos T, Panagopoulos I, Lassen C, Swedin A, Billström R, Isaksson M, Strömbeck B, Olofsson T, Mitelman F, Johansson B. Fusion of the BCR and the fibroblast growth factor receptor-1 (FGFR1) genes as a result of t(8;22)(p11;q11) in a myeloproliferative disorder: The first fusion gene involving BCR but not ABL. Genes Chromosomes Cancer. 2001;32:302–10. Jackson CC, Medeiros LJ, Miranda RN. 8p11 myeloproliferative syndrome: A review. Hum Pathol. 2010;41:461–76. Li T, Zhang G, Zhang X, Lin H, Liu Q. The 8p11 myeloproliferative syndrome: Genotypic and phenotypic classification and targeted therapy. Front Oncol. 2022;12:1015792. Arber DA, Orazi A, Hasserjian R, Thiele J, Borowitz MJ, Le Beau MM, Bloomfield CD, Cazzola M, Vardiman JW. The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. Blood. 2016;127:2391–405. Abruzzo LV, Jaffe ES, Cotelingam JD, Whang-Peng J, Del Duca V Jr, Medeiros LJ. T-cell lymphoblastic lymphoma with eosinophilia associated with subsequent myeloid malignancy. Am J Surg Pathol. 1992;16:236–45. Urrea Pineda LY, Perilla O, Santiago–Pacheco V, Trujillo Montoya S. Myeloproliferative syndrome with eosinophilia associ– ated with translocation t(8; 13) and T–cell lymphoblastic lymphoma: A case report and review of the literature. Cureus. 2022;14:e22734. Freyer CW, Hughes ME, Carulli A, Bagg A, Hexner E. Pemigatinib for the treatment of myeloid/lymphoid neoplasms with FGFR1 rearrangement. Expert Rev Anticancer Ther. 2023;23(4):351–9. Epub 2023 Mar 29. PMID: 36927350. Buijs A, van Wijnen M, van den Blink D, van Gijn M, Klein SK. A ZMYM2–FGFR1 8p11 myeloproliferative neoplasm with a novel nonsense RUNX1 mutation and tumor lysis upon imatinib treatment. Cancer Genet. 2013;206:140–4. Chen J, Deangelo DJ, Kutok JL, Williams IR, Lee BH, Wadleigh M, Duclos N, Cohen S, Adelsperger J, Okabe R, et al. PKC412 inhibits the zinc finger 198–fibroblast growth factor receptor 1 fusion tyrosine kinase and is active in treatment of stem cell myeloproliferative disorder. Proc Natl Acad Sci USA. 2004;101:14479–84. Vizmanos JL, Hernández R, Vidal MJ, Larráyoz MJ, Odero MD, Marı́n J, Ardanaz MT, Calasanz MJ, Cross NC. Clinical vari– ability of patients with the t(6;8)(q27;p12) and FGFR1OP–FGFR1 fusion: Two further cases. Hematol J. 2004;5:534–7. Popovici C, Zhang B, G ŕ egoire MJ, Jonveaux P, Lafage–Pochitaloff M, Birnbaum D, Pébusque MJ. The t(6;8) (q27;p11) translocation in a stem cell myeloproliferative disorder fuses a novel gene, FOP, to fibroblast growth factor receptor 1. Blood. 1999;93:1381–9. Additional Declarations No competing interests reported. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7790354","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":545582945,"identity":"af93d019-ce09-4584-8fcb-c93570d94eb2","order_by":0,"name":"Sanchit 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01:14:12","extension":"png","order_by":27,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":369004,"visible":true,"origin":"","legend":"","description":"","filename":"Onlinefloatimage3.png","url":"https://assets-eu.researchsquare.com/files/rs-7790354/v1/b13f733385ad4d978a186ecf.png"},{"id":96454817,"identity":"7291a9b4-21ac-4157-b6ae-4ae6d921f004","added_by":"auto","created_at":"2025-11-21 10:03:09","extension":"png","order_by":28,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":390746,"visible":true,"origin":"","legend":"","description":"","filename":"Onlinefloatimage4.png","url":"https://assets-eu.researchsquare.com/files/rs-7790354/v1/fd513dc1a42282fca2bc68ac.png"},{"id":96423104,"identity":"76ce4a83-c78a-4383-844f-5e68bee55d72","added_by":"auto","created_at":"2025-11-21 01:14:13","extension":"png","order_by":29,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":388873,"visible":true,"origin":"","legend":"","description":"","filename":"Onlinefloatimage5.png","url":"https://assets-eu.researchsquare.com/files/rs-7790354/v1/ce1ce5dcfbeaad89b815f84b.png"},{"id":96423100,"identity":"d0a1ccac-e002-42a9-b6f7-8488797d9963","added_by":"auto","created_at":"2025-11-21 01:14:12","extension":"xml","order_by":30,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":60246,"visible":true,"origin":"","legend":"","description":"","filename":"ef378a1cf80d48fea084e8c756b3d5fb1structuring.xml","url":"https://assets-eu.researchsquare.com/files/rs-7790354/v1/46eb2866bc74f06d9b56856a.xml"},{"id":96454958,"identity":"6bb1ebf1-82df-4e2a-91dd-303baa33d66f","added_by":"auto","created_at":"2025-11-21 10:03:22","extension":"html","order_by":31,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":66027,"visible":true,"origin":"","legend":"","description":"","filename":"earlyproof.html","url":"https://assets-eu.researchsquare.com/files/rs-7790354/v1/dabd39f1052c3ec0310ceb25.html"},{"id":96454630,"identity":"2978c518-88d6-4b03-968d-d23c74e6e155","added_by":"auto","created_at":"2025-11-21 10:02:59","extension":"jpeg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":824280,"visible":true,"origin":"","legend":"\u003cp\u003eShowing promyelocyte in peripheral smear(black arrow) and RBC(red arrow).\u003c/p\u003e","description":"","filename":"3481ddc53b5143eea8f252ddbd0f2e9c.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7790354/v1/c3eb17994eec1a372931cbc3.jpeg"},{"id":96423074,"identity":"8ccac363-8971-4d61-82b1-a9029c8950e7","added_by":"auto","created_at":"2025-11-21 01:14:12","extension":"jpeg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":1520910,"visible":true,"origin":"","legend":"\u003cp\u003eShowing neutrophil(red arrow),myelocyte(blue arrow) and promyelocyte(black arrow) in peripheral smear.\u003c/p\u003e","description":"","filename":"e3fd366d0eab498894155dded8fa284f.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7790354/v1/5c610bf596f072dbc4217061.jpeg"},{"id":96454632,"identity":"ccad64dd-d1e7-4d5f-8e5a-4c0de1430ffa","added_by":"auto","created_at":"2025-11-21 10:02:59","extension":"jpeg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":912067,"visible":true,"origin":"","legend":"\u003cp\u003eShowing eosinophil(black arrow), promyelocyte(blue arrow), metamyelocyte(yellow arrow),lymphocyte(red arrow) in peripheral smear.\u003c/p\u003e","description":"","filename":"5686a9fa04734c9e87d23d614d7371c02.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7790354/v1/355ad78f9936fd32de6060bf.jpeg"},{"id":96423080,"identity":"ffd899b6-a47c-4930-b4e2-1ec26a8ee9db","added_by":"auto","created_at":"2025-11-21 01:14:12","extension":"jpeg","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":932527,"visible":true,"origin":"","legend":"\u003cp\u003eShowing promyelocyte(black arrow) and hyper segmented neutrophils(red arrow) in bone marrow.\u003c/p\u003e","description":"","filename":"7dbf2f1d33da4b11af1a4f778ddbd911.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7790354/v1/e975309dac09a3e8871559bc.jpeg"},{"id":96423083,"identity":"7909adc2-ab3e-4d79-afa9-3f00d4081670","added_by":"auto","created_at":"2025-11-21 01:14:12","extension":"jpeg","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":951591,"visible":true,"origin":"","legend":"\u003cp\u003eShowing eosinophil(black arrow) and blast cells(red arrow) in bone marrow.\u003c/p\u003e","description":"","filename":"b2b1dee3071c47469aa9ab9c988e307f.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-7790354/v1/d73193143b99632615851321.jpeg"},{"id":100238754,"identity":"6d957f54-2c1c-494a-9d85-f59e743acb15","added_by":"auto","created_at":"2026-01-14 12:55:43","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":5616647,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7790354/v1/54e0fe08-81bb-4acb-aca8-ce37ba0a2b38.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Myeloproliferative Neoplasm with BCR-FGFR1 Fusion Presenting as Eosinophilic Myeloproliferative Syndrome","fulltext":[{"header":"Introduction","content":"\u003cp\u003eMyeloproliferative neoplasms with eosinophilia and FGFR1 rearrangements represent a rare but distinct group of hematologic disorders, formally recognized as separate entities in the World Health Organization (WHO) classification. These neoplasms are unified by constitutive activation of the FGFR1 tyrosine kinase, which drives uncontrolled cellular proliferation and confers an aggressive clinical course.[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]\u003c/p\u003e\u003cp\u003eAmong the various FGFR1 fusion partners described, the \u003cb\u003eBCR-FGFR1 rearrangement\u003c/b\u003e, resulting from the translocation \u003cb\u003et(8;22)(p11;q11)\u003c/b\u003e, is particularly uncommon. Patients with this fusion often present with features resembling chronic myeloproliferative disorders, including leukocytosis, marked eosinophilia, and splenomegaly, but unlike more indolent conditions, these neoplasms frequently progress to acute leukemia\u0026mdash;most commonly acute myeloid leukemia or T-lymphoblastic lymphoma/leukemia\u0026mdash;within a short period of time.[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]\u003c/p\u003e\u003cp\u003eBecause of its rarity, BCR-FGFR1\u0026ndash;positive disease is often under-recognized, leading to delays in diagnosis and missed opportunities for timely intervention. Early identification is critical, as the natural history is aggressive and conventional therapies, including standard tyrosine kinase inhibitors such as imatinib, are ineffective. At present, \u003cb\u003eallogeneic hematopoietic stem cell transplantation\u003c/b\u003e remains the only curative strategy, although emerging FGFR inhibitors offer new hope for targeted treatment.[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]\u003c/p\u003e\u003cp\u003eHere, we report the case of a middle-aged woman with BCR-FGFR1\u0026ndash;positive myeloproliferative neoplasm presenting with eosinophilia, highlighting the diagnostic challenges, clinical course, and therapeutic considerations associated with this rare entity.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eA 37-year-old woman, previously healthy and working as a house wife, presented to the emergency department with a 7-day history of high-grade fever accompanied by chills and drenching night sweats. She had fatigue, generalized body aches, and a persistent dull pain in her lower back that worsened with movement. Over the past month, she had progressive loss of appetite, significant weight loss (around 5 kilograms), and increasing exhaustion that was beginning to interfere with her ability to work and perform daily activities.\u003c/p\u003e\n\u003cp\u003eOn arrival, she was febrile (temperature 39.1\u0026deg;C), had tachycardia (Pr-112 bpm), and was hypotensive (BP 92/60 mmHg). Her respiratory rate was increased, though she was not in distress. Physical examination revealed mild hepatosplenomegaly and localized tenderness in the lower lumbar region, but no focal signs of infection or neurological deficit.\u003c/p\u003e\n\u003cp\u003eInitial laboratory investigations revealed that she had total leukocyte count of 62600/mm\u0026sup3;. Platelet count was low \u0026nbsp;at 55,000/mm\u0026sup3;. \u0026nbsp; CRP(102) was significantly elevated, and procalcitonin(10) was raised, suggesting a severe inflammatory response. Liver and kidney functions were within normal limits as shown in table 1. Blood and urine cultures were drawn, and she was empirically started on broad-spectrum intravenous antibiotics and fluids for presumed sepsis.\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; Table 1 shows various initial laboratory investigations.\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"432\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eTest\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eValue\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eReference Range\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eTLC (Total Leukocyte Count)\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e62,600 /\u0026micro;L\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e4,000 \u0026ndash; 11,000 /\u0026micro;L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eNeutrophils\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e49%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e40 \u0026ndash; 75%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eEosinophils\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e37%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e1 \u0026ndash; 6%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eLymphocytes\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e4%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e20 \u0026ndash; 45%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003ePlatelet Count\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e55,000 /\u0026micro;L\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e150,000 \u0026ndash; 450,000 /\u0026micro;L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eCRP (C-Reactive Protein)\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e102 mg/L\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e\u0026lt;5 mg/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eProcalcitonin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e10 ng/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e\u0026lt;0.05 ng/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eUrea\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e20 mg/dL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e10 \u0026ndash; 50 mg/dL\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eCreatinine\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e1.0 mg/dL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e0.6 \u0026ndash; 1.2 mg/dL\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eSodium (Na⁺)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e132 mEq/L\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e135 \u0026ndash; 145 mEq/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003ePotassium (K⁺)\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e4.0 mEq/L\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e3.5 \u0026ndash; 5.0 mEq/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eSGOT (AST)\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e32 U/L\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eup to 40 U/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eSGPT (ALT)\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e30 U/L\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eup to 40 U/L\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eTotal Bilirubin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e0.6 mg/dL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e0.2 \u0026ndash; 1.2 mg/dL\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u0026nbsp;The peripheral smear showed RBCs - Mild to moderate anisopoikilocytosis moderately hypochromic, a few microcytes and fragmented RBCs noticed About 17-18 nRBC s/100 leucocytes are noted . These normoblasts were of late and intermediate type of normoblast . No proerythroblast were noticed . WBC- Total count markedly increased on smear with eosinophilia. DLC- Blasts- 00% Promyelocyte- 00% Myelocyte- 04% Metamyelocyte- 06% Neutrophils + Band forms- 49% Monocytes- 03% Eosinophils and precursors - 37% Basophils and precursors - 02% Small lymphocytes - 01% Large lymphocytes - 04% No typical myeloblast or monoblast are seen . Platelets- On lower side of normal. A few giant platelets forms are seen . No haemoparasites seen as shown in table 2. Opinion - Hematomorphology is suggestive of leucoerythroblastic reaction with dominant eosinophil cell component as shown in figure 1,2,3.\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;Table 2 shows peripheral smear findings showing marked eosinophilia with leukocytosis.\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eComponent\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eFindings\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eRBC Morphology\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eMild to moderate anisopoikilocytosis, moderately hypochromic, few microcytes, fragmented RBCs noted\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003enRBCs\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003e17\u0026ndash;18 nucleated RBCs/100 WBCs (late and intermediate normoblasts; no proerythroblasts)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eWBC Total Count (Smear)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eMarkedly increased\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eDLC - Blasts\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003e0%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eDLC - Promyelocytes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003e0%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eDLC - Myelocytes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003e4%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eDLC - Metamyelocytes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003e6%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eDLC - Neutrophils + Bands\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003e49%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eDLC - Monocytes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003e3%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eDLC - Eosinophils + Precursors\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003e37%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eDLC - Basophils + Precursors\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003e2%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eDLC - Small Lymphocytes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003e1%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eDLC - Large Lymphocytes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003e4%\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003ePlatelets\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eReduced; a few giant platelets seen\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eHaemoparasites\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 288px;\"\u003e\n \u003cp\u003eNot seen\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eBone marrow aspiration and biopsy revealed hypercellular marrow dominated by granulocytic hyperplasia with eosinophilic proliferation as shown in figure 4,5,6.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eFluorescence in situ hybridization was done which was positive for BCR-FGFR 1 fusion.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eBCR-FGFR1 fusions are exceptionally rare. Because of this rarity, they are often difficult to recognize at first. Clinically, these neoplasms can look very much like chronic myeloid leukemia: patients may come in with high white blood cell counts and an enlarged spleen. [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]What often sets them apart, however, is the striking presence of eosinophilia\u0026mdash;an overproduction of eosinophils in the blood\u0026mdash;and, more alarmingly, their tendency to behave aggressively. Unlike chronic myeloid leukemia, which can often be managed for years, BCR-FGFR1\u0026ndash;driven diseases typically transform into acute leukemia within just a few months of diagnosis. This rapid progression highlights how critical early recognition and molecular testing are for patients who might harbor these fusions.[\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]\u003c/p\u003e\u003cp\u003eA major challenge in managing these neoplasms is their resistance to the standard drugs we might otherwise use. For example, other eosinophilia-associated disorders, such as those caused by PDGFRA or PDGFRB rearrangements, respond dramatically to imatinib\u0026mdash;a tyrosine kinase inhibitor that can essentially switch off the disease.[\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e] Unfortunately, FGFR1-driven cancers don\u0026rsquo;t respond in the same way. This resistance leaves physicians with very limited conventional treatment options. At present, the only intervention that offers a chance for cure is allogeneic hematopoietic stem cell transplantation (HSCT). For this reason, once the diagnosis is made, timely referral for transplant evaluation becomes a cornerstone of management, even if the patient is still clinically stable.[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]\u003c/p\u003e\u003cp\u003eIn recent years, however, a glimmer of hope has emerged. New drugs specifically designed to target FGFR pathways\u0026mdash;such as pemigatinib, futibatinib, and erdafitinib\u0026mdash;have begun to show promise.[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e] In early case reports, some patients who were ineligible for HSCT achieved meaningful remissions, both hematologic and cytogenetic, with these agents. While it is too soon to know how durable these responses will be, the results point toward a future in which treatment is not solely reliant on transplantation. For patients and their families, these therapies offer not just new options, but also a sense of hope in the face of an otherwise devastating diagnosis.[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]\u003c/p\u003e\n\u003ch3\u003eOutcome\u003c/h3\u003e\n\u003cp\u003eThe patient was initially treated with \u003cb\u003ehydroxyurea\u003c/b\u003e for cytoreduction, which controlled leukocytosis and patient responded well to treatment. Patient was not started on pemigatinib or futibatinib because of non availability of these drugs as this patient was treated in a rural tertiary health care centre. Use of these drugs for treatment of eosinophilic myeloproliferative syndrome has been described by Freyer et al, in his case report[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. Although most of these patients require allogeneic hematopoietic stem cell transplantation (HSCT) as the final treatment for remission this was not the case with our patient as she responded well to hydroxyurea.\u003c/p\u003e\u003cp\u003eBCR-FGFR1\u0026ndash;positive myeloproliferative neoplasm with eosinophilia represents a rare but profoundly aggressive hematologic disorder with a natural history marked by rapid disease progression and high risk of leukemic transformation. [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]For clinicians, maintaining a high index of suspicion is essential, as timely recognition and accurate molecular diagnosis can directly influence management decisions. Early referral for \u003cb\u003eallogeneic stem cell transplantation\u003c/b\u003e remains the cornerstone of potentially curative therapy and offers the best chance for long-term survival.[\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]\u003c/p\u003e\u003cp\u003eAt the same time, the therapeutic landscape is beginning to evolve. The emergence of \u003cb\u003enovel FGFR inhibitors\u003c/b\u003e has introduced new hope, particularly for patients who are not candidates for transplant or who relapse after conventional therapy. These targeted agents, though still under investigation, may redefine treatment strategies in the years to come.[\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThis case underscores not only the aggressive biology of BCR-FGFR1\u0026ndash;driven disease but also the urgent need for continued research and clinical awareness. Sharing such rare cases contributes to a growing collective understanding and, ultimately, to better outcomes for patients facing this challenging diagnosis.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003eEthical approval- The study protocol was approved by Datta Meghe Institue of Ethics committee, sawangi meghe,wardha in accordance with Helinski Declaration.\u003c/p\u003e\n\u003cp\u003eConsent to Participate - Informed consent from all subjects for participation in an online open access publication was taken.\u003c/p\u003e\n\u003cp\u003eConsent to publish- Informed consent from all subjects for publication of identifying information in an online open access publication was taken.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding Statement\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNo competing financial or non financial interest were there in relation to work.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData Availability\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe datasets used during current study are available from the corresponding author on reasonable request.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors contribution statement\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll authors contributed equally for the work.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthorship\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors have read the journal policies and manuscript has been submitted in accordance with those policies.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical Trial Number not applicable for this manuscript.\u003c/strong\u003e\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eJackson CC, Medeiros LJ, Miranda RN. 8p11 myeloproliferative syndrome: a review. Hum Pathol. 2010;41(4):461\u0026thinsp;\u0026ndash;\u0026thinsp;76. doi: 10.1016/j.humpath.2009.11.003. PMID: 20226962.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eMacdonald D, Aguiar RC, Mason PJ, Goldman JM, Cross NC. A new myeloproliferative disorder associated with chromosomal translocations involving 8p11: A review. Leukemia. 1995;9:1628\u0026ndash;30.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eFioretos T, Panagopoulos I, Lassen C, Swedin A, Billstr\u0026ouml;m R, Isaksson M, Str\u0026ouml;mbeck B, Olofsson T, Mitelman F, Johansson B. Fusion of the BCR and the fibroblast growth factor receptor-1 (FGFR1) genes as a result of t(8;22)(p11;q11) in a myeloproliferative disorder: The first fusion gene involving BCR but not ABL. Genes Chromosomes Cancer. 2001;32:302\u0026ndash;10.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eJackson CC, Medeiros LJ, Miranda RN. 8p11 myeloproliferative syndrome: A review. Hum Pathol. 2010;41:461\u0026ndash;76.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eLi T, Zhang G, Zhang X, Lin H, Liu Q. The 8p11 myeloproliferative syndrome: Genotypic and phenotypic classification and targeted therapy. Front Oncol. 2022;12:1015792.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eArber DA, Orazi A, Hasserjian R, Thiele J, Borowitz MJ, Le Beau MM, Bloomfield CD, Cazzola M, Vardiman JW. The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. Blood. 2016;127:2391\u0026ndash;405.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAbruzzo LV, Jaffe ES, Cotelingam JD, Whang-Peng J, Del Duca V Jr, Medeiros LJ. T-cell lymphoblastic lymphoma with eosinophilia associated with subsequent myeloid malignancy. Am J Surg Pathol. 1992;16:236\u0026ndash;45.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eUrrea Pineda LY, Perilla O, Santiago\u0026ndash;Pacheco V, Trujillo Montoya S. Myeloproliferative syndrome with eosinophilia associ\u0026ndash; ated with translocation t(8; 13) and T\u0026ndash;cell lymphoblastic lymphoma: A case report and review of the literature. Cureus. 2022;14:e22734.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eFreyer CW, Hughes ME, Carulli A, Bagg A, Hexner E. Pemigatinib for the treatment of myeloid/lymphoid neoplasms with \u003cem\u003eFGFR1\u003c/em\u003erearrangement. Expert Rev Anticancer Ther. 2023;23(4):351\u0026ndash;9. Epub 2023 Mar 29. PMID: 36927350.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBuijs A, van Wijnen M, van den Blink D, van Gijn M, Klein SK. A ZMYM2\u0026ndash;FGFR1 8p11 myeloproliferative neoplasm with a novel nonsense RUNX1 mutation and tumor lysis upon imatinib treatment. Cancer Genet. 2013;206:140\u0026ndash;4.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eChen J, Deangelo DJ, Kutok JL, Williams IR, Lee BH, Wadleigh M, Duclos N, Cohen S, Adelsperger J, Okabe R, et al. PKC412 inhibits the zinc finger 198\u0026ndash;fibroblast growth factor receptor 1 fusion tyrosine kinase and is active in treatment of stem cell myeloproliferative disorder. Proc Natl Acad Sci USA. 2004;101:14479\u0026ndash;84.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eVizmanos JL, Hern\u0026aacute;ndez R, Vidal MJ, Larr\u0026aacute;yoz MJ, Odero MD, Marı́n J, Ardanaz MT, Calasanz MJ, Cross NC. Clinical vari\u0026ndash; ability of patients with the t(6;8)(q27;p12) and FGFR1OP\u0026ndash;FGFR1 fusion: Two further cases. Hematol J. 2004;5:534\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003ePopovici C, Zhang B, G ŕ egoire MJ, Jonveaux P, Lafage\u0026ndash;Pochitaloff M, Birnbaum D, P\u0026eacute;busque MJ. The t(6;8) (q27;p11) translocation in a stem cell myeloproliferative disorder fuses a novel gene, FOP, to fibroblast growth factor receptor 1. Blood. 1999;93:1381\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Myeloproliferative neoplasm, FGFR1 rearrangement, t(8;22)(p11;q11), Eosinophilia, 8p11 myeloproliferative syndrome","lastPublishedDoi":"10.21203/rs.3.rs-7790354/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7790354/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eMyeloproliferative neoplasms with FGFR1 rearrangements, historically described as the 8p11 myeloproliferative syndrome, represent a rare but highly aggressive group of hematologic disorders driven by constitutive activation of the FGFR1 tyrosine kinase. These neoplasms often manifest with striking eosinophilia and carry a significant risk of progression to acute leukemia. Among the different FGFR1 fusion partners, the \u003cb\u003eBCR-FGFR1\u003c/b\u003e rearrangement is particularly uncommon and portends a challenging clinical course.[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]\u003c/p\u003e\u003cp\u003eWe describe the case of a middle-aged woman who presented with fatigue, weight loss, and splenomegaly, accompanied by pronounced leukocytosis and eosinophilia. Cytogenetic analysis revealed a \u003cb\u003et(8;22)(p11;q11)\u003c/b\u003e translocation resulting in a BCR-FGFR1 fusion. Despite initial cytoreductive therapy, her disease evolved rapidly, underscoring the aggressive nature of this entity. She ultimately required intensive therapy and consideration for allogeneic stem cell transplantation.\u003c/p\u003e\u003cp\u003eThis case highlights the diagnostic and therapeutic challenges of BCR-FGFR1\u0026ndash;positive neoplasms and emphasizes the importance of early recognition, molecular testing, and timely referral for potentially curative interventions. In the era of emerging FGFR inhibitors, documenting such cases adds valuable insight into the natural history and management strategies for this rare and devastating disorder.\u003c/p\u003e","manuscriptTitle":"Myeloproliferative Neoplasm with BCR-FGFR1 Fusion Presenting as Eosinophilic Myeloproliferative Syndrome","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-11-21 01:14:07","doi":"10.21203/rs.3.rs-7790354/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"6155adf0-29d1-4c13-9036-aad5e56b38a6","owner":[],"postedDate":"November 21st, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-01-14T12:55:32+00:00","versionOfRecord":[],"versionCreatedAt":"2025-11-21 01:14:07","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-7790354","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-7790354","identity":"rs-7790354","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}