Hematologic Tumors of the Bone: From Diagnosis to Prognosis

A special issue of Diagnostics (ISSN 2075-4418). This special issue belongs to the section "Clinical Diagnosis and Prognosis".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 462

Special Issue Editor


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Guest Editor
Hematology Unit, Department of Human Pathology in Adulthood and Childhood “Gaetano Barresi”, University of Messina, 98125 Messina, Italy
Interests: chronic myeloid leukemia; flow cytometry; multidrug resistance; BCR-ABL1 oncogene
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Special Issue Information

Dear Colleagues,

Hematologic tumors of the bone refer to blood-related cancers that either originate in the bone marrow or secondarily affect the bones. These tumors arise from hematopoietic tissues, primarily located in the bone marrow, and include multiple myeloma, leukemias, and lymphomas.

This Special Issue aims to highlight emerging topics in the field, spanning from classic morphology to modern molecular biology, as well as new diagnostic and prognostic tools, including those addressing novel drugs and targeted therapies.

Diagnostics is a well-known international, peer-reviewed, and open access journal by MDPI, ranked in Q1 (Medicine, General and Internal) and Q2 (Internal Medicine), with an IF of 3.3 (2024). I invite you to submit your scientific contributions related to bone hematologic malignancies.

Dr. Fabio Stagno
Guest Editor

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Keywords

  • bone marrow tumors
  • hematologic malignancies
  • diagnostic biomarkers
  • prognostic tools
  • targeted therapies

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Published Papers (1 paper)

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21 pages, 2178 KB  
Case Report
Bone Marrow Edema and Tyrosine Kinase Inhibitors Treatment in Chronic Myeloid Leukemia
by Sabina Russo, Manlio Fazio, Giuseppe Mirabile, Raffaele Sciaccotta, Fabio Stagno and Alessandro Allegra
Diagnostics 2025, 15(24), 3112; https://doi.org/10.3390/diagnostics15243112 - 8 Dec 2025
Viewed by 315
Abstract
Background and Clinical Significance: Tyrosine kinase inhibitors (TKIs) have transformed Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML) into a largely manageable chronic disease. However, off-target toxicities are increasingly recognized; rarer complications such as bone marrow edema (BME) remain underreported. BME is a [...] Read more.
Background and Clinical Significance: Tyrosine kinase inhibitors (TKIs) have transformed Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML) into a largely manageable chronic disease. However, off-target toxicities are increasingly recognized; rarer complications such as bone marrow edema (BME) remain underreported. BME is a radiological syndrome characterized by excess intramedullary fluid on fat-suppressed T2/STIR magnetic resonance imaging sequences and may progress to irreversible osteochondral damage if unrecognized. We report a case series of TKI-associated BME and propose a practical diagnostic-therapeutic framework. Case Presentation: We describe three patients with Ph+ CML who developed acute, MRI-confirmed BME of the lower limb during TKI therapy. Case 1 developed unilateral then bilateral knee BME, temporally associated first with dasatinib and subsequently with imatinib; symptoms improved after TKI interruption, bisphosphonate therapy, and supportive measures, and did not recur after switching to bosutinib. Case 2 presented with proximal femoral BME during long-term imatinib; imatinib was stopped, intravenous neridronate administered, and bosutinib initiated with clinical recovery and later near-complete radiological resolution. Case 3 experienced multifocal foot and ankle BME during imatinib; symptoms resolved after drug discontinuation and bisphosphonate therapy, and disease control was re-established with bosutinib without recurrence of BME. All patients underwent molecular monitoring and mutational analysis to guide safe therapeutic switching. Discussion: Temporal association across cases and the differential kinase profiles of implicated drugs suggest PDGFR (and to a lesser extent, c-KIT) inhibition as a plausible mechanistic driver of TKI-associated BME. PDGFR-β blockade may impair pericyte-mediated microvascular integrity, increase interstitial fluid extravasation, and alter osteoblast/osteoclast coupling, promoting intramedullary edema. Management combining MRI confirmation, temporary TKI suspension, bone-directed therapy (bisphosphonates, vitamin D/calcium), symptomatic care, and, when required, therapeutic switching to a PDGFR-sparing agent (bosutinib) led to clinical recovery and preservation of leukemia control in our series. Conclusions: BME is an underrecognized, potentially disabling, TKI-related adverse event in CML. Prompt recognition with targeted MRI and a multidisciplinary, stepwise approach that includes temporary TKI adjustment, bone-directed therapy, and consideration of PDGFR-sparing alternatives can mitigate morbidity while maintaining disease control. Prospective studies are needed to define incidence, risk factors, optimal prevention, and management strategies. Full article
(This article belongs to the Special Issue Hematologic Tumors of the Bone: From Diagnosis to Prognosis)
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