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Interleukin-6 and the Lung
Published in Jason Kelley, Cytokines of the Lung, 2022
Ralph J. Zitnik, Jack A. Elias
These authors suggested that an interaction between myeloblasts and stromal cells resulted in a dysregulated cytokine network within the bone marrow. Support for this concept came from studies by Oster et al. (1989) showing that blast cells produce IL-6, IL-1, and TNF. Additionally, many blast cells also constitutively produced G-CSF and GM-CSF and those that did not were able to induce G-CSF and GM-CSF production by endothelial cells. Thus, in AML interactions between myeloblasts, endothelial cells, and stromal cells may play an important role in maintaining the leukemic phenotype, and dysregulated IL-6 production appears to be involved in this process.
Immunotoxin-Mediated Depletion of CD5+ T Cells from Bone Marrow for Graft-vs.-Host Disease Prophylaxis
Published in Adrian P. Gee, BONE MARROW PROCESSING and PURGING, 2020
Joseph H. Antin, Howard J. Weinstein, Cyril Bouloux, Barbara E. Bierer
Loss of the GvL is another problem associated with T cell depletion.8 We hoped, by intensifying the conditioning regimen and leaving some NK cells and alloreactive T cells in the marrow, that the leukemic relapse rate would not be affected. Only 1/13 (8%) patients with AML in first remission has relapsed (actuarial disease-free survival 72%), suggesting that loss of GvL may not be a concern in AML. As noted above, the conditioning regimen used in this study is extremely toxic to leukemic myeloblasts.38 In patients with stable phase CML, 6/14 (43%) patients have relapsed (actuarial disease-free survival 37%). Small numbers of patients in each group were studied, and a reliable estimate of the antileukemic effect will depend on studies of a larger cohort; however, these results are consistent with previous observations in CML.8
Leukemias
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Most patients with AML present with signs and symptoms arising from bone marrow failure and organ infiltration by leukemic cells. Pallor, lethargy, dyspnea, infections, and bleeding manifestations are all common. Patients with monocytic or myelo-monocytic lineage AML might present with striking gingival hyperplasia (Figure 28.1). Occasionally, patients present as a consequence of hyperleukostasis. The diagnosis of AML is often made when more than 20% leukemic blast cells (myeloblasts) are found in the bone marrow or peripheral blood, with the exception of a small minority of patients with specific cytogenetic abnormalities, such as t(8;12)(q22;q22), inv(16)(p12q22), or t(15;17)(q22;q12) (Figure 28.2).
Isolated intracranial myeloid sarcoma: report of a case and review of the literature
Published in British Journal of Neurosurgery, 2023
Francesca Romana Barbieri, Adolfo De Luna, Laura Moschettoni, Pierpaolo Lunardi
Unexpectedly, histological examination revealed the presence of proliferating myeloblasts. B-cell antigens CD20 and 79a, T-cell antigen CD3 and monocytic antigen CD68 were not detectable. Staining for neutrophilic elastase with the antibody Ki-My2p as well as for CD45 was strongly positive. Chloroacetate esterase staining showed positivity in approximately 15% of blasts. Therefore, a diagnosis of MS (Figure 3) was made, so the patient was referred to the Department of Hematology/Oncology to complete tumor staging. Peripheral blood, chemistry laboratory exams and bone marrow histology and cytology did not demonstrate any myeloproliferative disease. Similarly a whole-body 18-fluorodeoxyglucose-positron emission tomography (FDG-PET) CT scan did not reveal any extra-cranial localization, confirming the diagnosis of isolated intracranial MS. After one month the patient underwent one course of chemotherapy (3 days of daunorubicin and 7 days of cytarabine and subsequent post-induction therapy with cytarabine 3 g/m2 on days 1, 3, and 5 for four courses), with no complications.
Combining the past and present to advance immuno-radiotherapy of cancer
Published in International Reviews of Immunology, 2023
Ioannis M. Koukourakis, Michael I. Koukourakis
Interesting results have also been obtained in patients with hematological malignancies treated with ASI. In 1976, Bakesi et al reported an interesting clinical study in patients with myelocytic leukemia [81]. Following experimental studies in mice, where neuraminidase pretreated leukemia cells induced strong immunity and neutralized tumorigenicity, authors treated a group of patients with myelocytic leukemia, with neuraminidase treated allogeneic myeloblasts, once they had achieved complete remission with chemotherapy. Patients remained in remission for 79-132 weeks vs. 19 weeks of patients treated with chemotherapy alone. Powles et al. treated 52 patients with myelogenous leukemia with chemotherapy, while 30 of them also received immunotherapy with irradiated allogeneic myeloblastic leukemia cells. The medium survival was increased from 39 weeks to 74 weeks [82].
Philadelphia-positive acute lymphoblastic leukemia in a case of MPL p.(W515L) variant essential thrombocythemia: case report and literature review
Published in Platelets, 2022
Jiale Ma, Shan Chen, Yanqing Huang, Jie Zi, Jinlong Ma, Zheng Ge
Although a relatively indolent disorder, there exists a potential for ET to progress to post-ET myelofibrosis and a low propensity to transform to acute leukemia, less than 1% in the first 10 years of the disease [7]. Advanced age, extreme thrombocytosis, anemia, leukocytosis, and sequence variants/mutations involving TP53 and EZH2 have been reported the risk factors for ET [10]. The nature of the leukemic transformation in myeloproliferative disorders is generally considered to be a variant of acute myeloblastic leukemia (AML), and when patients with MPN develop terminal leukemia, it is invariably non-lymphoblastic [11]. Acute lymphoblastic leukemia (ALL) transformation in MPN is infrequent but have been as yet reported in PV [12–14], ET [15,16] and PMF [17,18]. Whether all these cases represent a true clonal evolution of MPN or are the manifestation of two separate diseases remains uncertain. The impact of MPL mutations on myelofibrotic and leukemic transformation is less well defined. Of note, lymphoproliferative neoplasm (LPN), such as lymphoid neoplasms, chronic lymphocytic leukemia (CLL) and non-Hodgkin lymphoma (NHL), has been reported more in MPN patients compared to the general population [19], suggesting a pathophysiological link between the two diseases [19,20]. Besides, a specific microenvironment generated by MPN such as mutations in epigenetic regulators, chronic inflammation and myelofibrosis may potentiate to the existence and progression of an aberrant clone [21,22].