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Leukemias
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
The recognition of structural chromosomal and genetic abnormalities in the majority of lymphoblasts has contributed enormously to understanding the molecular pathogenesis and prognosis of ALL. These abnormalities include changes in chromosome numbers (aneuploidy) and chromosomal translocations and rearrangements, which probably constitute the initiating events, followed by somatic mutations and DNA copy number alterations.33 The ALL genome contains about 10–20 mutations at diagnosis. These mutations impact multiple cellular processes, including transcription, lymphoid development and differentiation, and cell-cycle regulation. Figure 28.6 depicts the unfolding cytogenetic and genomic landscape of ALL of both B- and T- lineages. About 10% of all ALL currently remains unclassifiable. Adolescents and adults have an usually high prevalence of poor-risk subtypes, such as BCR-ABL1 and MLL rearrangement, and a lower risk of the favorable subtypes, such as ETV6-RUNX1 and high hyperdiploidy.
Acquired Immunity
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
B lymphocytes are normally dormant in the lymphoid tissues. After exposure to an antigen, there is an interval of about 2 weeks before antibodies can be found in the blood. The invading antigen (microorganism) is first localized and phagocytosed by macrophages that present it to adjacent B lymphocytes. The antigen also activates helper T lymphocytes. The B lymphocytes then proliferate and differentiate into lymphoblasts that become plasma cells in the lymph gland. The plasma cells release antibodies into the lymph to be carried to the blood. These antibodies do not reach a high concentration and do not persist. This is the primary immune response (Figure 56.3). In the primary response, B lymphocytes produce IgM and then undergo the following changes: (i) class switching – changing, (ii) affinity maturation – antibody binds more tightly to antigen and (iii) memory cell formation.
Haematological malignancy
Published in Peter Hoskin, Peter Ostler, Clinical Oncology, 2020
Lymphoblastic leukaemia is characterized by the presence of large immature lymphoblasts throughout the reticuloendothelial system. These cells are distinguished from other cells such as myeloblasts by their staining, as presented in Table 17.1, although classification of leukaemias now has become much more sophisticated based on molecular profiling.
Therapy-related acute lymphoblastic leukemia following treatment for multiple myeloma – diagnostic and therapeutic dilemma
Published in Acta Oncologica, 2022
Alicja Sadowska-Klasa, Mary Abba, Justyna Gajkowska-Kulik, Jan Maciej Zaucha
Secondary acute leukemia refers to patients with either therapy-related or disease progressing from an antecedent hematologic disorder typically a myelodysplastic syndrome or a myeloproliferative neoplasm. Neither MM is considered a typical neoplasm that leads to secondary hematopoietic neoplasms nor ALL is a typical secondary hematopoietic malignancy. Lymphoblasts and plasmocytes are cells both originating from lymphopoiesis; however, their proliferating potential is very different. Plasma cells represent the final differentiation stage, nevertheless, there are hypotheses that somatic mutations occurring in younger precursors affect further stages of lymphopoiesis, and the final oncogenic events take place in secondary lymphoid organs [19,20]. The hereditary component of MM susceptibility was reported many years ago; however, increased risk for other B-cell originating neoplasms was also noticed in MM-risk families [1,8]. Interestingly tr-ALL, which accounts for up to 9% of all ALL, occurs mainly in women after chemotherapy for breast cancer [21]. Regardless, the second most common cause of tr-ALL is MM [22].
A Novel Compound Plumercine from Plumeria alba Exhibits Promising Anti-Leukemic Efficacies against B Cell Acute Lymphoblastic Leukemia
Published in Nutrition and Cancer, 2022
Aaheli Chatterjee, Amrita Pal, Santanu Paul
Leukemia, otherwise known as blood cancer is a type of haematological malignancy that is characterized by uncontrolled production of abnormal white blood cells (1). The increased percentage of the abnormal WBCs, in turn, reduces the ability of the bone marrow cells and cuts down the production of platelets and red blood cells leading to effects of cytopenia (2). Leukemia is mainly of two types: acute and chronic. Out of them, childhood acute lymphoblastic leukemia (ALL) is one of the first commonly diagnosed haematological malignant diseases that have been considered as a paradigm for cancer research for the last few decades by conducting wide-ranging therapeutic trials (3) ALL is a commonly diagnosed pediatric malignant hematologic disease that leads to uncontrolled proliferation of immature lymphoblast precursor cells (4). ALL are of two types, Precursor B cell Lymphoblastic Leukemia or B ALL and T cell Lymphoblastic Leukemia or T ALL (5).
Expanded NK cells from umbilical cord blood and adult peripheral blood combined with daratumumab are effective against tumor cells from multiple myeloma patients
Published in OncoImmunology, 2021
Chantal Reina-Ortiz, Michael Constantinides, Alexis Fayd-Herbe-de-Maudave, Jessy Présumey, Javier Hernandez, Guillaume Cartron, David Giraldos, Rosana Díez, Isabel Izquierdo, Gemma Azaceta, Luis Palomera, Isabel Marzo, Javier Naval, Alberto Anel, Martín Villalba
The present work demonstrates how the activation and expansion of allogeneic NK cells generates eNK cells that are active against MM cells. The activation and expansion were achieved in UCB and PB Nks by using LCL lymphoblasts as feeders in combination with IL-2 and IL-15. In both cases, the final eNK product exhibited CD16 expression on an important fraction of their population (more than 80%), which would allow for their combination with a variety of therapeutic mAbs directed against tumor antigens.7 This increase in cytotoxicity could be associated with increased expression of activation markers,7 and of the activating receptor NKp44.45 Moreover, in a similar study using a 5-d activation protocol, it was shown that the main change justifying the increase in cytotoxicity was the net increase in the level of granzyme B expression in activated NK cells.40