Results 31 to 40 of about 183 (135)

The Role of “Adult‐Onset” Cancer Predisposition Genes in Pediatric Cancer: A Comprehensive Review

open access: yesPediatric Blood &Cancer, EarlyView.
ABSTRACT Current literature estimates that 10% of pediatric cancers are caused by pathogenic or likely pathogenic (P/LP) germline variants in cancer predisposition genes (CPGs). Variants in CPGs thought to increase cancer risk exclusively during adulthood are referred to as “adult‐onset” CPGs (aoCPGs).
Maria Rozo   +5 more
wiley   +1 more source

GABP is necessary for stem/progenitor cell maintenance and myeloid differentiation in human hematopoiesis and chronic myeloid leukemia

open access: yesStem Cell Research, 2016
Maintenance of hematopoietic stem cells and their potential to give rise to progenitors of differentiated lymphoid and myeloid cells are accomplished by a network of regulatory processes. As a part of this network, the heteromeric transcription factor GA-
Georgi Manukjan   +7 more
doaj   +1 more source

Neoantigens in Hematologic Malignancies

open access: yesFrontiers in Immunology, 2020
T cell cancer neoantigens are created from peptides derived from cancer-specific aberrant proteins, such as mutated and fusion proteins, presented in complex with human leukocyte antigens on the cancer cell surface.
Melinda A. Biernacki   +3 more
doaj   +1 more source

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

Farnesyltransferase inhibitor tipifarnib inhibits Rheb prenylation and stabilizes Bax in acute myelogenous leukemia cells

open access: yesHaematologica, 2014
Although farnesyltransferase inhibitors have shown promising activity in relapsed lymphoma and sporadic activity in acute myelogenous leukemia, their mechanism of cytotoxicity is incompletely understood, making development of predictive biomarkers ...
Husheng Ding   +14 more
doaj   +1 more source

Presence of the GFI1-36N single nucleotide polymorphism enhances the response of MLL-AF9 leukemic cells to CDK4/6 inhibition

open access: yesFrontiers in Oncology, 2022
The zinc finger protein Growth Factor Independence 1 (GFI1) acts as a transcriptional repressor regulating differentiation of myeloid and lymphoid cells. A single nucleotide polymorphism of GFI1, GFI1-36N, has a prevalence of 7% in healthy Caucasians and
Jan Vorwerk   +19 more
doaj   +1 more source

Chronobiology of Cancer: How Aging Fuels Oncogenesis at the Molecular Level

open access: yesAging and Cancer, EarlyView.
This graphical abstract illustrates the key biological pathways linking aging with cancer development and progression. In the upper left, cumulative exposure to ultraviolet radiation, toxins, and reactive oxygen species (ROS) causes DNA damage and genomic instability, whereas age‐related decline in repair mechanisms, such as ATM/ATR, BER, and NER ...
Anu Singh, Aroonima Misra, Sufian Zaheer
wiley   +1 more source

CCAAT/enhancer-binding protein alpha (CEBPA) gene haploinsufficiency does not alter hematopoiesis or induce leukemia in Lck-CALM/AF10 transgenic mice

open access: yesBrazilian Journal of Medical and Biological Research
Although rare, CALM/AF10 is a chromosomal rearrangement found in immature T-cell acute lymphoblastic leukemia (T-ALL), acute myeloid leukemia, and mixed phenotype acute leukemia of T/myeloid lineages with poor prognosis.
A.P. Lange   +7 more
doaj   +1 more source

Spectrum of Haematological malignancies managed at tertiary centre: A one-year retrospective review

open access: yesJournal of Society of Surgeons of Nepal, 2018
Introduction: Hematological malignancies are not uncommon and all ages and genders are affected. Hematological malignancies are a group of cancers that arise from a malignant transformation of cells of the bone marrow or lymphatic system.
Anjan Shrestha   +5 more
doaj   +1 more source

Genetic Ablation and Multi‐Omics Profiling Reveal CEP55 as a Key Driver of Tumorigenesis in Diverse Cancer Models

open access: yesAdvanced Science, EarlyView.
Genetic ablation of Cep55 in Pten‐deficient mouse models delays tumorigenesis. Integrated multi‐omics analyses (proteomics, phosphoproteomics, and spatial transcriptomics) reveal that CEP55 regulates oncogenic signaling (RAS/ERK, PI3K/AKT), integrin/FAK‐mediated adhesion, extracellular matrix (ECM) remodeling, and endocytosis.
Behnam Rashidieh   +22 more
wiley   +1 more source

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