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Treating the cardio-oncology patient
Published in Susan F. Dent, Practical Cardio-Oncology, 2019
Pulmonary hypertension has several causes in cancer patients. It may be a sign of cancer progression, such as a progressive myeloproliferative disease (57). It may also be caused by cancer therapy (58). For instance, dasatinib therapy, used to treat chronic myelogenous leukemia and acute lymphoblastic leukemia, has been associated with pulmonary hypertension; dasatinib-related pulmonary hypertension can be treated with sildenafil (59,60). The veno-occlusive form of pulmonary hypertension may be associated with alkylating agents, but medical management of this form of pulmonary hypertension is usually unsatisfactory (61). Chronic thromboembolic pulmonary hypertension may be observed in cancer patients and must be distinguished from pulmonary hypertension associated with HF or lung diseases (62).
Different Types of Leukemias, Lymphomas, and Myelomas
Published in Tariq I Mughal, John M Goldman, Sabena T Mughal, Understanding Leukemias, Lymphomas, and Myelomas, 2017
Tariq I Mughal, John M Goldman, Sabena T Mughal
CMML is a chronic myeloproliferative disease (MPD) that was included in the FAB categorization of MDSs (discussed below). It is now classified by the WHO as a myelodysplastic/myeloproliferative disease. It affects predominantly the middleaged and there is a slight male preponderance. Patients often have splenomegaly but the degree of splenic enlargement is less than in CML. The peripheral blood shows an absolute neutrophilia and monocytosis. The absence of immature granulocytes in the blood film also distinguishes CMML from CML (Fig. 4.20). The bone marrow is hypercellular with immature monocytes recognizable. The natural history of CMML is variable. In some patients, the leukemia appears to remain in a stable phase for some years, while in others there is a progression to a picture resembling an acute leukemia within one year of diagnosis.
Haematology
Published in Fazal-I-Akbar Danish, Essential Lists of Differential Diagnoses for MRCP with diagnostic hints, 2017
Hyposplenism:1 Congenital asplenism/splenectomy.2 Sickle-cell anaemia.3 GI diseases (e.g. coeliac disease, IBD).4 Myeloproliferative disease.5 Amyloidosis.
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.
Chronic myelomonocytic leukemia - a review
Published in Expert Review of Hematology, 2021
Thomas P. Thomopoulos, Anthi Bouhla, Sotirios G. Papageorgiou, Vasiliki Pappa
Although, great advancements have been made in the understanding of the CMML genetic landscape, the exact disease pathogenesis remains elusive. It has been suggested that age-induced DNA damage to the adult hematopoietic stem cell (HSC) predisposes to the emergence of a clone with evolutionary advantage, harboring mutations in genes implicating in epigenetic regulation, most commonly TET2 [38]. Mutations of ASXL1 might also initiate a clonal evolution toward CMML, through upregulation of HOXA genes and IRF8 [24]. Subsequently, the initial clone acquires secondary mutations in genes involved in the assembly of spliceosomes, most commonly SRSF2 that allow evolution to full-blown malignancy [38,39]. Presence of the SRSF2 mutation, otherwise disadvantageous in a TET2 wild clone, confers an evolutionary clonal advantage and promotes the expansion of the myelomonocytic compartment accompanied by erythroid and megakaryocytic dysplasia [40]. Other mutations, such as those involved in cell-signaling may be considered as secondary lesions, as well, and if present, may contribute to the myeloproliferative disease phenotype (MP-CMML) [34].
Expression profile analysis reveals hub genes that are associated with immune system dysregulation in primary myelofibrosis
Published in Hematology, 2021
Haotian Ma, Jincen Liu, Zilong Li, Huaye Xiong, Yulei Zhang, Yanping Song, Jianghua Lai
Primary myelofibrosis (PMF) is a chronic myeloproliferative disease (Ph-negative) that is a myeloproliferative neoplasm (MPN) with the main characteristics of a significantly enlarged spleen, enhanced oxidative stress, advanced bone marrow fibrosis and extramedullary haematopoiesis [1]. PMF usually occurs in middle-aged and elderly individuals, and the median age is approximately 67 [2]; its annual incidence is approximately 0.6∼1.3/100,000. Although PMF is uncommon, the median survival time of intermediate-risk patients is only approximately 5 years, and there is still a lack of specific treatments. The most important factors related to the prognosis of PMF are complications, such as thrombosis, haemorrhage, and infection [2–4]. Among them, infections are one of the main causes of unfavorable prognosis in myelofibrosis, representing the cause of death in approximately 10% of cases [6,7]. Autoimmune symptoms are a main characteristic of patients with PMF [5].