Results 51 to 60 of about 157,947 (291)

Significance of Inactivated Genes in Leukemia: Pathogenesis and Prognosis

open access: yesCell Journal, 2017
Epigenetic and genetic alterations are two mechanisms participating in leukemia, which can inactivate genes involved in leukemia pathogenesis or progression.
Nazanin Heidari   +5 more
doaj   +1 more source

A comprehensive microarray-based DNA methylation study of 367 hematological neoplasms [PDF]

open access: yes, 2011
Background: Alterations in the DNA methylation pattern are a hallmark of leukemias and lymphomas. However, most epigenetic studies in hematologic neoplasms (HNs) have focused either on the analysis of few candidate genes or many genes and few HN entities,
Agirre, Xabier   +34 more
core  

Notch and NF-kB: Coach and Players of Regulatory T-Cell Resposnse in Cancer [PDF]

open access: yes, 2018
The Notch signaling pathway plays multiple roles in driving T-cell fate decisions, proliferation, and aberrant growth. NF-kB is a cell-context key player interconnected with Notch signaling either in physiological or in pathological conditions.
Bellavia, Diana   +5 more
core   +2 more sources

CDK4/6 Inhibition Induces CD8+ T Cell Antitumor Immunity via MIF‐Induced Functional Orchestration of Tumor‐Associated Macrophages

open access: yesAdvanced Science, EarlyView.
CDK4/6 inhibition promotes CD8+ T cell expansion through tumor‐macrophage crosstalk by activating HIF‐1α and enhancing MIF‐CD44/CD74 signaling. This reprograms TAMs to boost MHC‐I antigen presentation, and CDK4/6 inhibitor‐trained M1 TAM supernatant therapy synergizes with low‐dose PD‐1 blockade to restore antitumor immunity.
Lin He   +17 more
wiley   +1 more source

A rare presentation of chronic myeloid leukemia blast crisis

open access: yesIraqi Journal of Hematology, 2020
Chronic myeloid leukemia (CML), as the name suggests, is a chronic disorder in which granulocytes undergo dysregulated production and uncontrolled proliferation. Majority of CML patients present during the chronic phase (CP) of the disease.
P S Shruthi   +3 more
doaj   +1 more source

Protein stabilization explains the gag requirement for transformation of lymphoid cells by Abelson murine leukemia virus [PDF]

open access: yes, 1985
The single protein encoded by Abelson murine leukemia virus is a fusion of sequence from the retroviral gag genes with the v-abl sequence. Deletion of most of the gag region from the transforming protein results in a virus capable of transforming ...
Baltimore, David   +3 more
core  

Novel strategy for rapid functional in vivo validation of oncogenic drivers in haematological malignancies [PDF]

open access: yes, 2019
In cancer research, it remains challenging to functionally validate putative novel oncogenic drivers and to establish relevant preclinical models for evaluation of novel therapeutic strategies.
Berx, Geert   +16 more
core   +2 more sources

Loss of SOCS1 in Donor T Cells Exacerbates Intestinal GVHD by Driving a Chemokine‐Dependent Pro‐Inflammatory Immune Microenvironment

open access: yesAdvanced Science, EarlyView.
T cell‐specific Socs1 knockout leads to inflammatory differentiation of CD8+ T cells, prompting the STAT1/2 complex to drive the activation of Ccl5, Ccr5, and Cxcr3, and promoting the skewing of monocytes toward a pro‐inflammatory M1 macrophage lineage.
Zhigui Wu   +14 more
wiley   +1 more source

Long-term cultures of murine fetal liver retain very early B lymphoid phenotype. [PDF]

open access: yes, 1984
Long-term cultures of murine fetal liver have been successfully established using a modification of our in vitro bone marrow culture system (14, 15).
Denis, KA   +3 more
core  

Invariant NKT cells contribute to chronic lymphocytic leukemia surveillance and prognosis [PDF]

open access: yes, 2017
Chronic lymphocytic leukemia (CLL) is characterized by the expansion of malignant CD5(+) B lymphocytes in blood, bone marrow and lymphoid organs. CD1d-restricted invariant Natural Killer T (iNKT) cells are innate-like T lymphocytes strongly implicated in
Azzimonti, Laura   +17 more
core   +1 more source

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