Different mechanisms are responsible for oncogene activation in human mammary neoplasia

1988 ◽  
pp. 49-66 ◽  
Author(s):  
Matthias H. Kraus ◽  
Pier Paolo Di Fiore ◽  
Jacalyn H. Pierce ◽  
Stuart A. Aaronson
Keyword(s):  
Oncogene Activation ◽  
Mammary Neoplasia

scholarly journals Induction and transmission of oncogene-induced senescence

2020 ◽  
Author(s):  
Nattaphong Rattanavirotkul ◽  
Kristina Kirschner ◽  
Tamir Chandra
Keyword(s):  
Stress Response ◽  
Single Cell ◽  
Cellular Stress ◽  
Cellular Stress Response ◽  
End Points ◽  
Oncogene Activation ◽  
Suppressor Mechanism ◽  
Bona Fide ◽  
Organ Level ◽  
Complex Scenario

Abstract Senescence is a cellular stress response triggered by diverse stressors, including oncogene activation, where it serves as a bona-fide tumour suppressor mechanism. Senescence can be transmitted to neighbouring cells, known as paracrine secondary senescence. Secondary senescence was initially described as a paracrine mechanism, but recent evidence suggests a more complex scenario involving juxtacrine communication between cells. In addition, single-cell studies described differences between primary and secondary senescent end-points, which have thus far not been considered functionally distinct. Here we discuss emerging concepts in senescence transmission and heterogeneity in primary and secondary senescence on a cellular and organ level.

Role of oncogene activation in human thyroid carcinomas

1990 ◽  
Vol 14 ◽  
pp. 22
Author(s):  
A FUSCO ◽  
M GRIECO ◽  
M SANTORO ◽  
R MELILLO ◽  
C BATTAGLIA ◽  
...  
Keyword(s):  
Human Thyroid ◽  
Thyroid Carcinomas ◽  
Oncogene Activation

Mammary Neoplasia in the Female Rat After Neonatal and/or Adult 7,12-Dimethylbenz(a) Anthracene Administration

1973 ◽  
Vol 144 (1) ◽  
pp. 96-98
Author(s):  
R. D. Brown ◽  
A. R. Rao ◽  
C. J. Shellabarger
Keyword(s):  
Female Rat ◽  
Mammary Neoplasia

Oncogene Activation in Multistage Carcinogenesis

1989 ◽  
Vol 8 (2) ◽  
pp. 241-243
Author(s):  
Seymour J. Garte
Keyword(s):  
Protease Inhibitors ◽  
In Vitro Studies ◽  
Ras Oncogene ◽  
Multistage Carcinogenesis ◽  
Oncogene Activation ◽  
Shed Light

Oncogene activation in multistage carcinogenesis is discussed. Results from a number of in vitro studies are cited. An understanding of the mechanisms that suppress activated ras oncogene-induced transformation by protease inhibitors is expected to shed light on the process of multistage carcinogenesis.

scholarly journals “Cell Membrane Theory of Senescence” and the Role of Bioactive Lipids in Aging, and Aging Associated Diseases and Their Therapeutic Implications

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 241
Author(s):  
Undurti N. Das
Keyword(s):  
Fatty Acids ◽  
Cell Membrane ◽  
Linolenic Acid ◽  
Genomic Stability ◽  
Bioactive Lipids ◽  
Camp Content ◽  
Associated Diseases ◽  
Epa And Dha ◽  
Oncogene Activation ◽  
Anti Inflammatory

Lipids are an essential constituent of the cell membrane of which polyunsaturated fatty acids (PUFAs) are the most important component. Activation of phospholipase A2 (PLA2) induces the release of PUFAs from the cell membrane that form precursors to both pro- and ant-inflammatory bioactive lipids that participate in several cellular processes. PUFAs GLA (gamma-linolenic acid), DGLA (dihomo-GLA), AA (arachidonic acid), EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) are derived from dietary linoleic acid (LA) and alpha-linolenic acid (ALA) by the action of desaturases whose activity declines with age. Consequently, aged cells are deficient in GLA, DGLA, AA, AA, EPA and DHA and their metabolites. LA, ALA, AA, EPA and DHA can also be obtained direct from diet and their deficiency (fatty acids) may indicate malnutrition and deficiency of several minerals, trace elements and vitamins some of which are also much needed co-factors for the normal activity of desaturases. In many instances (patients) the plasma and tissue levels of GLA, DGLA, AA, EPA and DHA are low (as seen in patients with hypertension, type 2 diabetes mellitus) but they do not have deficiency of other nutrients. Hence, it is reasonable to consider that the deficiency of GLA, DGLA, AA, EPA and DHA noted in these conditions are due to the decreased activity of desaturases and elongases. PUFAs stimulate SIRT1 through protein kinase A-dependent activation of SIRT1-PGC1α complex and thus, increase rates of fatty acid oxidation and prevent lipid dysregulation associated with aging. SIRT1 activation prevents aging. Of all the SIRTs, SIRT6 is critical for intermediary metabolism and genomic stability. SIRT6-deficient mice show shortened lifespan, defects in DNA repair and have a high incidence of cancer due to oncogene activation. SIRT6 overexpression lowers LDL and triglyceride level, improves glucose tolerance, and increases lifespan of mice in addition to its anti-inflammatory effects at the transcriptional level. PUFAs and their anti-inflammatory metabolites influence the activity of SIRT6 and other SIRTs and thus, bring about their actions on metabolism, inflammation, and genome maintenance. GLA, DGLA, AA, EPA and DHA and prostaglandin E2 (PGE2), lipoxin A4 (LXA4) (pro- and anti-inflammatory metabolites of AA respectively) activate/suppress various SIRTs (SIRt1 SIRT2, SIRT3, SIRT4, SIRT5, SIRT6), PPAR-γ, PARP, p53, SREBP1, intracellular cAMP content, PKA activity and peroxisome proliferator-activated receptor γ coactivator 1-α (PGC1-α). This implies that changes in the metabolism of bioactive lipids as a result of altered activities of desaturases, COX-2 and 5-, 12-, 15-LOX (cyclo-oxygenase and lipoxygenases respectively) may have a critical role in determining cell age and development of several aging associated diseases and genomic stability and gene and oncogene activation. Thus, methods designed to maintain homeostasis of bioactive lipids (GLA, DGLA, AA, EPA, DHA, PGE2, LXA4) may arrest aging process and associated metabolic abnormalities.

scholarly journals Oncogene Activation in Pituitary Tumors

2006 ◽  
Vol 11 (3) ◽  
pp. 328-341 ◽  
Author(s):  
Run Yu ◽  
Shlomo Melmed
Keyword(s):  
Pituitary Tumors ◽  
Oncogene Activation

Oncogene Activation by Chromosome Translocation in Human Malignancy

1987 ◽  
Vol 21 (1) ◽  
pp. 321-345 ◽  
Author(s):  
F G Haluska ◽  
Y Tsujimoto ◽  
C M Croce
Keyword(s):  
Chromosome Translocation ◽  
Human Malignancy ◽  
Oncogene Activation

High Frequency of ras Oncogene Activation in Benign and Malignant Human Thyroid Tumours

ras Oncogenes ◽  
1989 ◽  
pp. 29-36 ◽  
Author(s):  
Nick R. Lemoine ◽  
Edward S. Mayall ◽  
Fiona S. Wyllie ◽  
David Wynford-Thomas
Keyword(s):  
High Frequency ◽  
Human Thyroid ◽  
Ras Oncogene ◽  
Oncogene Activation
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