Using a comprehensive integration of genomic and molecular approaches we will determine the biochemical context in which AR signaling drives breast
cancer tumorigenesis.
Not exact matches
«This novel technique,» they said, «should help distinguish and monitor
cancer stages and progression, aid in elucidation of basic mechanisms underlying
tumorigenesis, and facilitate analyses of processes related to early detection of
cancer, screening and / or
cancer risk assessment.»
«We found that AIM2 inhibits
tumorigenesis in multiple animal models of colorectal
cancer by restricting the pro-survival signaling molecule, Akt, which is commonly hyperactive in many human
cancers.»
As a doctoral student in the lab of Drs. Margaret Wheelock and Keith Johnson at the University of Toledo, Dr. Islam focused on identifying a link between cadherins (a family of cell adhesion proteins) and
tumorigenesis (start of
cancer cell formation).
IBD is known to promote colon
tumorigenesis and gave rise to the term «colitis - associated
cancer.»
Deletion of Sox9 prevents skin
cancer formation demonstrating the essential role of Sox9 during
tumorigenesis and leads to the progressive disappearance of the oncogene expressing cells.
Identification and functional validation of proteins involved in
tumorigenesis are essential steps toward advancing
cancer precision medicine.
Since proliferation is a hallmark of
cancer cells, the researchers analyzed the involvement of tRNA halves in
tumorigenesis.
We have found that the initiation of pancreatic
cancer does not follow the classic paradigm seen in colon
cancer where loss of a tumor suppressor gene initiates
tumorigenesis and then acquisition of an oncogene promotes tumor formation.
The
tumorigenesis mechanisms of colorectal
cancer have been widely studied at a molecular level.
GPCRs and their downstream signaling are involved in
cancer growth and development by controlling many features of
tumorigenesis, including immune cell - mediated functions, proliferation, invasion and survival at the secondary site.
Blebbishields, the emergency program for
cancer stem cells: sphere formation and
tumorigenesis after apoptosis.
These findings reinforce many things that we already know: that mutations acquire gradually with age, that most of the mutations in AML (and likely other tumors) are random background events not contributing to
tumorigenesis, and that subsequent mutation and evolution can give rise to subclones that ultimately determine
cancer progression and response to therapy.
Cancer studies have increasingly focused on chromatin — the intertwined proteins and DNA that are packaged into chromosomes — because of its ability to regulate genes important for either activating or inhibiting
tumorigenesis.
Dr. Harris is a renowned expert on the role of COX - 2 in chronic inflammation and in promoting
tumorigenesis and angiogenesis, and has authored numerous papers in peer - reviewed journals and book chapters on the use of NSAIDS and selective COX - 2 inhibitors in the chemoprevention of various
cancer types.
With the help of
cancer biologists, these data will be leveraged to better understand the genes, proteins, and pathways underlying
tumorigenesis.
Disruption of a Quorum Sensing mechanism triggers
tumorigenesis: a simple discrete model corroborated by experiments in mammary
cancer stem cells
Bench and mouse studies have shown that the Notch1 gene is a crucial contributor to
tumorigenesis in non — small - cell lung
cancer (NSCLC).
Although driver mutations were the main focus of
cancer research for a long time, passenger mutational signatures, the imprints of DNA damage and DNA repair processes that have been operative during
tumorigenesis, are also biologically illuminating.
In preclinical trials, the effect of chloroquine and hydroxychloroquine on
tumorigenesis has been extensively investigated in mouse
cancer models, including genetic and xenograft models (summarized in Table 2).
Interestingly, BRCA1 is not a haploid - insufficient tumor suppressor gene; therefore monoallelic deletion may not affect its function or affect
tumorigenesis of those breast
cancers bearing deletions.
The paper, Redundant Innate and Adaptive Sources of IL17 Production Drive Colon
Tumorigenesis, http://cancerres.aacrjournals.org/content/76/8/2115, April 2016 found that colorectal
cancers associated with B. fragilis could be suppressed, not just by eradicating the microorganism, BUT ALSO BY REDUCING INFLAMMATION.
Evidence exists that chronically elevated blood glucose, insulin and IGF1 levels facilitate
tumorigenesis and worsen the outcome in
cancer patients.