Different Types of Leukemias, Lymphomas, and Myelomas
Tariq I Mughal, John M Goldman, Sabena T Mughal in Understanding Leukemias, Lymphomas, and Myelomas, 2017
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.
Treating the cardio-oncology patient
Susan F. Dent in 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).
Leukemias
Pat Price, Karol Sikora in Treatment of Cancer, 2020
The 2016 WHO revised classification recognizes myeloproliferative neoplasms (MPNs) to comprise seven subtypes: chronic myeloid leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET), primary myelofibrosis (PMF), chronic neutrophilic leukemia (CNL), chronic eosinophilic leukemia, not otherwise specified (CEL), and myeloproliferative neoplasm, unclassifiable (MPN-U). In addition, the WHO 2016 classification recognizes myeloid/lymphoid neoplasms with eosinophilia and rearrangements of PDGFRA, PDGFRB, FGFR1, or PCM-JAK2 (a provisional entity), and mastocytosis (see Table 28.2). CML, PV, ET, and PMF are often referred to collectively as “classic” MPNs and includes patients who transform to myelofibrosis (MF) from PV (post-PV MF) or ET (post-ET MF); in contrast, CNL, CEL, and MPN-U are referred to as “non-classic” or atypical MPNs. The classic MPNs are in turn often divided into BCR-ABL1-positive (CML) and -negative (PV, ET, and PMF).
Frequency of JAK2V617F, MPL and CALR driver mutations and associated clinical characteristics in a Norwegian patient cohort with myeloproliferative neoplasms
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2023
Susanne Lilleskare, Marta Vorland, Anh Khoi Vo, Aasne K. Aarsand, Håkon Reikvam
In the period 2014–2019, a total of 2407 patient samples were referred to Haukeland University Hospital due to suspected myeloproliferative neoplasm. Following filtering of results from duplicate analyses, and exclusion of patients not consenting to participate in the study or where clinical records were not available, the study population consisted of 820 patients (Figure 1). A Philadelphia chromosome-negative myeloproliferative neoplasm was diagnosed in 182 of these patients. In 129 cases, the JAK2V617F-mutation was identified, in 28 cases CALR exon 9 frameshift variants, and in two cases MPLW515K/L. In 23 patients with a diagnosed myeloproliferative neoplasm, none of these mutations were detected (Figure 2). From a total of 63 cases with polycythemia vera, 51 patients had JAK2V617F (Figure 2).
Tagraxofusp as treatment for patients with blastic plasmacytoid dendritic cell neoplasm
Published in Expert Review of Anticancer Therapy, 2020
Sophia S. Lee, Deborah McCue, Naveen Pemmaraju
Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive hematologic malignancy [1,2]. The incidence of BPDCN has not been systematically studied, owing to the multiple name changes and rarity of this disease, but studies have reported an extremely low incidence of 0.44% in all hematologic malignancies and 0.7% of cutaneous lymphomas [3,4]. BPDCN predominantly affects men, with a male to female ratio of 3:1, up to 5:1 in some series. The median age at diagnosis is in the seventh decade of life [3–5]. There are no well-established environmental or hereditary risk factors, although, approximately 10–20% of patients have a prior or concomitant (PCHM) myeloid hematologic malignancy including myelodysplastic syndrome (MDS), myeloproliferative neoplasm, chronic myelomonocytic leukemia (CMML), and/or acute myeloid leukemia (AML) [6,7].
Thrombosis and hemorrhage in myeloproliferative neoplasms: The platelet perspective
Published in Platelets, 2022
Yiming Feng, Yue Zhang, Jialan Shi
Classical myeloproliferative neoplasm (MPN), also known as BCR-ABL-negative MPN, is a clonal disease characterized by abnormal expansion of hematopoietic stem cells [1]. Essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF) are the main subtypes of MPN [2]. Mutations in Janus-activated kinase 2 (JAK2), calreticulin (CALR), and myeloproliferative leukemia virus (MPL) genes are commonly observed in patients with MPN [3]. All these gene mutations induce MPN via the excessive activation of the JAK-STAT signaling pathway [4].
Related Knowledge Centers
- Calreticulin
- White Blood Cell
- Platelet
- Bone Marrow
- Neoplasm
- Red Blood Cell
- Janus Kinase 2
- Primary Myelofibrosis
- Acute Myeloid Leukemia
- Malignancy