Not exact matches
As a
cancer researcher, do you think the
mechanisms of tumor
growth are somehow changing to come into line with your perceptions, or is it possible that the process
of our learning more about DNA mutations and cell architecture and nutrient exchange and epigenetic effects make it possible for us to inch ever closer to understanding that which is already going on under our noses?
Similar to capsaicin, tumor necrosis factor is suspected to both induce and reduce
cancer cell
growth, and was shown to commit cells to survival when stimulating EGFR transactivation
mechanisms, indicating that EGFR could act as a molecular switch determining the antiapoptotic effect
of tumor necrosis factor (50).
A new study by researchers at The Ohio State University Comprehensive
Cancer Center — Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC — James) has identified a mechanism by which cancer cells develop resistance to a class of drugs called fibroblast growth factor receptor (FGFR) inhib
Cancer Center — Arthur G. James
Cancer Hospital and Richard J. Solove Research Institute (OSUCCC — James) has identified a mechanism by which cancer cells develop resistance to a class of drugs called fibroblast growth factor receptor (FGFR) inhib
Cancer Hospital and Richard J. Solove Research Institute (OSUCCC — James) has identified a
mechanism by which
cancer cells develop resistance to a class of drugs called fibroblast growth factor receptor (FGFR) inhib
cancer cells develop resistance to a class
of drugs called fibroblast
growth factor receptor (FGFR) inhibitors.
Metastatic melanoma is the deadliest
of the skin
cancers and the
mechanisms that govern early metastatic
growth and interactions
of metastatic cells with the brain microenvironment remain shrouded in mystery.
«Next steps are to further explore this possibility in human trials in order to assess if it will help patients, but these two drugs make sense from a variety
of studies and we find that they act together through multiple
mechanisms to control
cancer growth in the laboratory.»
Until now, little was known in preclinical models about the
mechanisms that allow breast
cancer cells to leave the latent state and even less is known in patients,» explains Roger Gomis, head of the Growth Control and Cancer Metastasi
cancer cells to leave the latent state and even less is known in patients,» explains Roger Gomis, head
of the
Growth Control and
Cancer Metastasi
Cancer Metastasis Lab.
Researchers at the San Diego Supercomputer Center (SDSC) and the Moores
Cancer Center at the University of California, San Diego, have described for the first time the molecular mechanism of cancer development caused by well - known «resistance» mutations in the gene called epidermal growth factor receptor (
Cancer Center at the University
of California, San Diego, have described for the first time the molecular
mechanism of cancer development caused by well - known «resistance» mutations in the gene called epidermal growth factor receptor (
cancer development caused by well - known «resistance» mutations in the gene called epidermal
growth factor receptor (EGFR).
The phenomenon, known as Warburg effect, is typical for
cancer cells and the
mechanism behind is believed to benefit
cancer cells by switching biochemical engines from energy manufacturing reactions to anabolic reactions, which primarily support
growth of the cell size and proliferation.
A breast
cancer therapy that blocks estrogen synthesis to activate cancer - killing genes sometimes loses its effectiveness because the cancer takes over epigenetic mechanisms, including permanent DNA modifications in the patient's tumor, once again allowing tumor growth, according to an international team headed by the University of Pittsburgh Cancer Institute (
cancer therapy that blocks estrogen synthesis to activate
cancer - killing genes sometimes loses its effectiveness because the cancer takes over epigenetic mechanisms, including permanent DNA modifications in the patient's tumor, once again allowing tumor growth, according to an international team headed by the University of Pittsburgh Cancer Institute (
cancer - killing genes sometimes loses its effectiveness because the
cancer takes over epigenetic mechanisms, including permanent DNA modifications in the patient's tumor, once again allowing tumor growth, according to an international team headed by the University of Pittsburgh Cancer Institute (
cancer takes over epigenetic
mechanisms, including permanent DNA modifications in the patient's tumor, once again allowing tumor
growth, according to an international team headed by the University
of Pittsburgh
Cancer Institute (
Cancer Institute (UPCI).
The study, called «Molecular Determinants
of Drug - Specific Sensitivity for Epidermal
Growth Factor Receptor (EGFR) Exon 19 and 20 Mutants in Non-Small Cell Lung
Cancer,» and published online in the journal Oncotarget, demonstrates how computer modeling of EGFR mutations found in lung cancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat pat
Cancer,» and published online in the journal Oncotarget, demonstrates how computer modeling
of EGFR mutations found in lung
cancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat pat
cancer can elucidate their molecular
mechanism of action and consequently optimize the selection
of therapeutic agents to treat patients.
«We challenged a current dogma in the field that emphasized PLK1's role in mitosis (cell division) as a primary
mechanism for
cancer growth,» says Zheng Fu, Ph.D., lead investigator on the study, member of the Cancer Molecular Genetics research program at VCU Massey Cancer Center and assistant professor in the Department of Human and Molecular Genetics at the VCU School of Med
cancer growth,» says Zheng Fu, Ph.D., lead investigator on the study, member
of the
Cancer Molecular Genetics research program at VCU Massey Cancer Center and assistant professor in the Department of Human and Molecular Genetics at the VCU School of Med
Cancer Molecular Genetics research program at VCU Massey
Cancer Center and assistant professor in the Department of Human and Molecular Genetics at the VCU School of Med
Cancer Center and assistant professor in the Department
of Human and Molecular Genetics at the VCU School
of Medicine.
While further research is needed to understand the effectiveness
of H1.0 protein in preventing the spread
of cancer growth, this research advances significantly the study
of the
mechanisms of cancer stem cells and the relatively new epigenetic approach to
cancer research.
Further investigations could pave the way to a more complete understanding
of the genetics and metabolomics
of cell
growth in yeast and the underlying
mechanisms relevant to other settings in which cells face challenging conditions, such as
cancer progression and the evolution
of drug resistance.
Are there any other ways to strike at the fundamental
mechanisms that trigger
growth of cancer cells?
In particular, he wanted to study the genomes
of marbled crayfish to uncover basic
mechanisms underlying epigenetics, the binding
of molecules to DNA that can drive tumor
growth and help
cancer spread.
She says they can now identify the
mechanisms that cause tumor
growth in half
of all adenocarcinomas, a family
of cancer that affects skin and other tissue, including the lungs.
Biochemist Valerie Weaver
of the University
of California, San Francisco, who led previous studies linking tissue stiffness and breast
cancer growth, calls the paper «very important» because it finds a novel
mechanism linking obesity with breast
cancer.
The researchers, including scientists from pharmaceutical company AstraZeneca, report in an advanced online publication in Nature Medicine on May 4, that their findings indicate «an underappreciated genomic heterogeneity» in
mechanisms of resistance to tyrosine kinase inhibitor (TKI) drugs that target the Epidermal
Growth Factor Receptor (EGFR) mutation that drive some cases
of non-small cell lung
cancer (NSCLC).
«Researchers inhibit tumor
growth in new subtype
of lung
cancer: Insight into tumor suppressing and tumor promoting
mechanisms offers potential for new treatments.»
Zhang's laboratory now seeks to understand the
mechanisms of the tissue - environment influence, opening the possibility that the environment could be altered in a way that fights
cancer by preventing tumor cell
growth.
These include, for example, the
mechanisms behind stem - cell development and what happens when normal cellular
growth spirals out
of control, such as in
cancer.
Published in the May 1 edition
of Cancer Research, the study supports a critical role for IGF - 1R signaling in prostate - tumor development and identifies an important IGF - 1R - dependent
growth control
mechanism, according to the authors.
Many
cancers are still difficult to treat and development
of drugs exploiting new pathways and
mechanisms involved in tumor initiation and malignant
growth is
of high priority [1].
Early observations suggesting that the virus might attack
cancer in part by damaging blood vessels that feed tumor
growth led the SillaJen team to strike up a collaboration with McDonald, an expert in tumor vasculature, to investigate the virus's
mechanism of action in animal models.
Through its various targets, MMP1 promotes not only tumor invasion but also breast
cancer colonization to bone by
mechanisms that include the release
of membrane - bound EGF - like
growth factors from tumor cells, leading to activation
of EGF receptor signaling and suppression
of OPG expression in osteoblasts, which in turn promotes the differentiation and activation
of osteoclasts required for bone destruction and enhanced tumor
growth in the bone microenvironment (32).
The acquisition
of growth signal self - sufficiency is one
of the hallmarks
of cancer.28 In this paper, we show that a broad spectrum
of spontaneous mutations in one
of the endogenous JAK1 alleles is the main
mechanism that confers to BaF3 cells cytokine - independent
growth capability in vitro and full tumorigenicity in vivo (Online Supplementary Figure S5), secondary to the upregulation
of the JAK1 transcript.
Specifically, my research proposal addresses the
mechanisms by which the kinase 3 - phosphoinoside dependent protein kinase - 1 (PDK1) mediates resistance to cell cycle related CDK4 / 6 inhibition in ER + breast
cancer and explores the in vivo effects
of inhibiting PDK1 in combination with CDK4 / 6 inhibitors toward ER + breast
cancer growth.
It's considered that this is a component
of the
mechanism driving out
of control cell division and
cancer growth.
A number
of the
mechanisms which help prevent abnormal cell
growth are avoided in
cancer cells.
What is the
mechanism by which our diet can affect our levels
of this
cancer - promoting
growth hormone IGF - 1?
http://nutritionfacts.org/video/animal-protein-compared-cigarette-smoking/ If you watch the series
of videos on NutritionFacts about IGF - 1, you will learn one
mechanism on how / why animal based proteins contribute to
cancer growth..
Researchers were able to demonstrate the
mechanism by which a plant - based diet and exercise could suppress the
growth of breast and prostate
cancer cells and protect against prostate enlargement (more on prostate problems in Some Prostates are Larger Than Others and Prostate Versus Plants).
Avocado helps prevents the
growth of cancer while supporting the body's natural defense
mechanisms.
EPA has potent anti-inflammatory properties, helps thin blood, and prevent the
growth of new blood vessels (one
mechanism of how
cancer spreads).
Viewing
cancer as a metabolic disease — opposed to a disease
of damaged DNA, which is a downstream effect
of mitochondrial dysfunction — gives us the power to control this dysfunction by carefully choosing foods and nutrients and employing strategies that help optimize the biochemical pathways that suppress
cancer growth while simultaneously stimulating
mechanisms to push it into remission.
While the exact
mechanisms are still unknown, vitamin D has been shown to lower blood pressure, increase flexibility
of blood vessels, inhibit
cancer cell
growth and reduce whole - body inflammation.
Polyunsaturated fats such as corn oil and soybean oil are highly unstable and vulnerable to oxidation — and oxidation, in turn, is linked to
cancer — while the omega - 6 fatty acids that predominate in vegetable oils have been shown to accelerate the
growth of tumor cells.6 As Fallon and Enig explain, 4 excessive consumption
of toxic polyunsaturated oils — not red meat — represents a known
mechanism for colon
cancer: «Colon
cancer occurs when high levels
of dietary vegetable oils and hydrogenated fats, along with certain carcinogens, are acted on by certain enzymes in the cells lining the colon, leading to tumor formation» [Emphasis added].
As such, another
mechanism for the ketogenic diet working within brain
cancer is the ability
of the ketone bodies to enhance the protection
of healthy central nervous system (CNS) from
cancer growth (11).
That is, simple adjustment
of dietary protein (casein) within very normal ranges
of protein intake controlled
cancer growth and it worked not by one
mechanism but by a large array
of mechanisms.