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Myeloid blast crisis of chronic myeloid leukemia (CML-MBC) is rarely seen at presentation and has a poor prognosis. There is no standard therapy for CML-MBC. It is often difficult to distinguish CML-MBC from acute myeloid leukemia expressing the Philadelphia chromosome (Ph+ AML). We present a case in which CML-MBC was seen at the initial presentation in a 75-year-old male. He was treated with conventional AML-directed chemotherapy followed by imatinib mesylate monotherapy, which failed to induce response. However, he achieved long-term complete molecular response after combination therapy involving dasatinib, a second-generation tyrosine kinase inhibitor, and conventional chemotherapy.

Ferritin is an iron-storage protein composed of different ratios of 24 light (L) and heavy (H) subunits. The serum level of ferritin is a clinical marker of the body's iron level. Transferrin receptor (TFR)1 is the receptor not only for transferrin but also for H-ferritin, but how it binds two different ligands and the blood cell types that preferentially incorporate H-ferritin remain unknown. To address these questions, we investigated hematopoietic cell-specific ferritin uptake by flow cytometry. Alexa Fluor 488-labeled H-ferritin was preferentially incorporated by erythroid cells among various hematopoietic cell lines examined, and was almost exclusively incorporated by bone marrow erythroblasts among human primary hematopoietic cells of various lineages. H-ferritin uptake by erythroid cells was strongly inhibited by unlabeled H-ferritin but was only partially inhibited by a large excess of holo-transferrin. On the other hand, internalization of labeled holo-transferrin by these cells was not inhibited by H-ferritin. Chinese hamster ovary cells lacking functional endogenous TFR1 but expressing human TFR1 with a mutated RGD sequence, which is required for transferrin binding, efficiently incorporated H-ferritin, indicating that TFR1 has distinct binding sites for H-ferritin and holo-transferrin. H-ferritin uptake by these cells required a threshold level of cell surface TFR1 expression, whereas there was no threshold for holo-transferrin uptake. The requirement for a threshold level of TFR1 expression can explain why among primary human hematopoietic cells, only erythroblasts efficiently take up H-ferritin.

Background: Primary extranodal marginal zone mucosa-associated lymphoid tissue-type B-cell lymphoma (EMZMBCL), which presents as a dural mass, is a rare intracranial tumor that mimics a subdural hematoma or meningioma. Case Description: A 49-year-old woman presented to our hospital with transient right upper limb paresis, dysarthria for 10 min, and ongoing right upper-limb numbness. Computed tomography (CT) of the head revealed extra-axial lesions in the left frontal and parietal lobes. Based on the initial CT findings in the emergency room, an acute subdural hematoma was suspected. However, meningiomas and other intracranial tumors were also listed as differential diagnoses because there was no history of head trauma or coagulation abnormalities on blood examination, and further imaging studies were performed. Imaging findings suggested a subdural neoplastic lesion. A partial resection was performed for the lesion. Based on histopathological and immunohistochemical examinations, the patient was diagnosed with EMZMBCL. Whole-brain and intensity-modulated radiation therapies were administered as adjuvant therapies. The patient was discharged without neurological deficits. Conclusion: EMZMBCL is a rare disease that should be considered in the differential diagnosis of subdural lesions, especially when there is no history of trauma or abnormalities in the coagulation system. The patient had a favorable outcome after selecting radiotherapy as the adjuvant therapy. [ABSTRACT FROM AUTHOR]