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Topic Review
FRA-1 as a Regulator in Breast Cancer
Among FOS-related components of the dimeric AP-1 transcription factor, the oncoprotein FRA-1 (encoded by FOSL1) is a key regulator of invasion and metastasis. The well-established FRA-1 pro-invasive activity in breast cancer, in which FOSL1 is overexpressed in the TNBC (Triple Negative Breast Cancer)/basal subtypes, correlates with the FRA-1-dependent transcriptional regulation of EMT (Epithelial-to-Mesenchymal Transition).
  • 281
  • 21 Jun 2023
Topic Review
CGF Biomolecules
Concentrated Growth Factors (CGF) represent new autologous (blood-derived biomaterial), attracting growing interest in the field of regenerative medicine. 
  • 279
  • 24 Jan 2022
Topic Review
ATRX/DAXX and ALT
ATRX is named for its causal role in ATR-X syndrome (α-thalassemia with mental impairment, X-linked), an X-linked disorder characterized by developmental delays, urogenital abnormalities, distinctive craniofacial features, and α-thalassemia caused by insufficient α-globin expression. Because of the central role of decreased α-globin mRNA expression in the ATR-X phenotype, research on ATRX initially focused on its potential as a transcriptional regulator. In fact, ATRX in concert with DAXX play wide-ranging roles in maintaining chromatin and reckoning with problematic DNA repeat sequences, with downstream effects on gene expression that have critical impacts in development. Proliferating cells must enact a telomere maintenance mechanism to ensure genomic stability. In a subset of tumors, telomeres are maintained not by telomerase, but through a homologous recombination-based mechanism termed Alternative Lengthening of Telomeres or ALT. The ALT process is linked to mutations in the ATRX/DAXX/H3.3 histone chaperone complex. This complex is responsible for depositing non-replicative histone variant H3.3 at pericentric and telomeric heterochromatin but has also been found to have roles in ameliorating replication in repeat sequences and in promoting DNA repair.
  • 279
  • 17 Apr 2023
Topic Review
Potential Use of MitoEVs as Diagnostic Markers
Similar to other subtypes of EVs (extracellular vesicles), MitoEVs (mitochondrial extracellular vesicles) are altered in several diseases, including cancer, neurodegenerative disorders, and cardiovascular disease. MitoEVs contain a variety of molecular components from releasing cells, including proteins, lipids, and nucleic acids, which may serve as indicators of disease status.
  • 279
  • 27 Apr 2023
Topic Review
Tumor Angiogenesis and Vasculogenesis
Cancer cells exploit blood vessels to survive and diffuse in the body, metastasizing distant organs. During tumor expansion, the neoplastic mass progressively induces modifications in the microenvironment due to its uncontrolled growth, generating a hypoxic and low pH milieu with high fluid pressure and low nutrient concentration.
  • 279
  • 01 Jun 2023
Topic Review
Direct and Indirect Myc Regulation by Mitotic Kinases
c-Myc and the other protein family members (i.e., N-Myc and L-Myc), collectively known as “Myc”, are ubiquitous basic helix–loop–helix–leucine zipper (bHLH-LZ) transcription factors that are critical for several cellular processes during cancer genesis and progression. The importance of kinases in Myc regulation goes beyond their ability to phosphorylate the protein. Some kinases can also indirectly affect Myc protein stability by inducing the degradation of the ubiquitin ligase (PLK1 and PKA). Additionally, some kinases physically interact with Myc, protecting it from proteasomal degradation, such as Aurora-A in neuroblastoma.
  • 278
  • 08 Mar 2023
Topic Review
Autophagy in Crohn’s Disease
Crohn’s disease (CD) is a chronic inflammatory bowel disease marked by relapsing, transmural intestinal inflammation driven by innate and adaptive immune responses. Autophagy is a multi-step process that plays a critical role in maintaining cellular homeostasis by degrading intracellular components, such as damaged organelles and invading bacteria. Dysregulation of autophagy in CD is revealed by the identification of several susceptibility genes, including ATG16L1, IRGM, NOD2, LRRK2, ULK1, ATG4, and TCF4, that are involved in autophagy.
  • 278
  • 13 Jul 2023
Topic Review
Endoplasmic Reticulum Stress and Cancer
Unfolded protein response (UPR) is an adaptive response which is used for re-establishing protein homeostasis, and it is triggered by endoplasmic reticulum (ER) stress. Specific ER proteins mediate UPR activation, after dissociation from chaperone Glucose-Regulated Protein 78 (GRP78). UPR can decrease ER stress, producing an ER adaptive response, block UPR if ER homeostasis is restored, or regulate apoptosis. 
  • 277
  • 13 Feb 2023
Topic Review
Krüppel-like Factors 4 and 5 in Colorectal Tumorigenesis
Krüppel-like factors (KLFs) are transcription factors regulating various biological processes such as proliferation, differentiation, migration, invasion, and homeostasis. Importantly, they participate in disease development and progression. KLFs are expressed in multiple tissues, and their role is tissue- and context-dependent. KLF4 and KLF5 are two fascinating members of this family that regulate crucial stages of cellular identity from embryogenesis through differentiation and, finally, during tumorigenesis. They maintain homeostasis of various tissues and regulate inflammation, response to injury, regeneration, and development and progression of multiple cancers such as colorectal, breast, ovarian, pancreatic, lung, and prostate, to name a few.
  • 277
  • 12 Sep 2023
Topic Review
Inflammasome-Mediated Cytokines
Liver cancer is one of the most lethal malignancies and is commonly diagnosed as hepatocellular carcinoma (HCC), a tumor type that affects about 90% of patients. Non-alcoholic steatohepatitis (NASH) and obesity are both risk factors for this disease. HCC initiation and progression are deeply linked with changes in the hepatic microenvironment, with cytokines playing key roles. The understanding of the pathogenic pathways that connect these disorders to liver cancer remains poor.
  • 276
  • 07 Feb 2023
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