Anil Belur Nagaraj (Bornhäuser, TUD)-- «Understanding the regulation of
tumor cell cycle to identify and characterize factors that negatively regulate the tumor phenotype.»
Not exact matches
In this special section of Science, expert contributors retrace the long and tortuous path leading to the mapping and identification of the BRCA1 gene; discuss the ways in which BRCA mutation status has been integrated into the clinical management of patients in high - risk families; and highlight the role of the BRCA proteins in preserving the structural and numerical integrity of chromosomes throughout the
cell cycle, a function that may explain their
tumor suppressor activity.
In cancer, these switches inappropriately activate or silence important genes, such as those that regulate
cell growth and life
cycle, ultimately leading to
tumors.
There are as many as 14, but the scientists found that cyclin D adds just a single phosphate at one, and only one, of the 14 locations during the early G1 phase of
cell cycle progression, essentially make 14 different versions of the Rb
tumor suppressor.
Lee's study results, which appear in the July 16, 2015 issue of Nature Communications, revealed new understanding about how 14 -3-3 sigma — a
cell cycle «controller» - regulates cancer metabolic programming, thus protecting healthy
cells from turning into
tumor - producing factories.
In healthy human
cells, the p53 protein helps prevent
tumors by putting the brakes on the
cell cycle to give an ailing
cell time to fix itself — or die — rather than spawning more corrupted
cells.
In addition, they found that epithelial - derived MMP9 suppresses
tumors in CAC by activating the MMP9 - Notch1 - ARF - p53 axis pathway, which increases apoptosis, initiates
cell cycle arrest and keeps a check on DNA damage.
In fact, KLF4 blocks senescence and apoptosis by repressing transcription of P53, whereas it can activate P21 - dependent
cell -
cycle arrest, and therefore, KLF4 can function both as a
tumor suppressor and an oncogene (33, 34).
«The CDK4 and 6 proteins are critical drivers of the
cell - division
cycle and are required for the formation and growth of various types of solid
tumors,» says Dana - Farber's Shom Goel, MD, PhD, co-first author of the study with Molly DeCristo of the Hematology Division at BWH.
The
cell cycle regulator p21 mediates the ability of the
tumor suppressor p53 to arrest cellular proliferation.
This
cell cycle arrest in the G0 phase requires the retinoblastoma
tumor suppressor protein (Rb).
Limiting dilution
tumor formation of parental, hypoxia - exposed adherent, and
cycling hypoxia - selected breast cancer
cells in vivo
In
tumors, the clockwork genetic mechanisms that control the life
cycle of
cells are entirely disrupted, a fact that may hold the key to defeating cancer.
Growth curves of primary
tumors generated from the parental
cell lines and
cycling hypoxia - selected subpopulations.
Title:
Tumor - initiating cells are not enriched in cisplatin - surviving BRCA1; p53 - deficient mammary tumor cells in vivo Authors: Pajic M, Kersbergen A, van Diepen F, Pfauth A, Jonkers J, Borst P, Rottenberg S Date: 2010 Publication Details: Cell C
Tumor - initiating
cells are not enriched in cisplatin - surviving BRCA1; p53 - deficient mammary
tumor cells in vivo Authors: Pajic M, Kersbergen A, van Diepen F, Pfauth A, Jonkers J, Borst P, Rottenberg S Date: 2010 Publication Details: Cell C
tumor cells in vivo Authors: Pajic M, Kersbergen A, van Diepen F, Pfauth A, Jonkers J, Borst P, Rottenberg S Date: 2010 Publication Details:
Cell Cycle.
The restriction of cellular growth by p53 has been reported to result in
cell cycle arrest or apoptosis [6], and targeting p53 and restoring p53 function to limit
tumor growth has been intensively researched for cancer therapy [7].
The
tumor suppressor p53 connects ribosome biogenesis to
cell cycle control: a double - edged sword.
In response to cellular stress such as DNA damage, oncogene activation, transcriptional inhibition, and hypoxia,
tumor suppressor p53 is activated and expressed, and acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair,
cell cycle, apoptosis, senescence, and angiogenesis [2 - 4].
TGFβ inhibits
tumor initiation and progression by inducing
cell cycle arrest and apoptosis; however epithelial tumorigenesis may escape this common antitumor mechanism by inducing aberrations in TGFβ signaling resulting in enhanced development and progression of human carcinomas.
CBX2 overexpression in breast
tumors was associated with the upregulation of genes involved in
cell cycle progression and is associated with poorer 5 - year survival.
All CM members have research interests in basic cancer mechanisms, including the normal functions of oncogenes and
tumor suppressor genes; regulators of
cell cycle and apoptosis; regulators of angiogenesis and metastasis; and stem
cells and blood formation.
In
cells from certain brain
tumors, in stomach cancer, and in colorectal cancer lines, vitamin K halts the reproductive
cell cycle and induces apoptosis.
https://www.nature.com/articles/nm.3804 Lee, Changhan et al. «Fasting
Cycles Retard Growth of
Tumors and Sensitize a Range of Cancer
Cell Types to Chemotherapy.»
Possible reduction in certain types of cancer: «It appears to work primarily by blocking the growth and metastatic spread of
tumors, controlling the
cell cycle, and by reducing inflammation.»
Removing the ovaries by spaying the dog before the first heat
cycle prevents the release of hormones, thus leaving the breast tissue as a hostile environment for the
tumor cells.