Along with the study's co-first authors, Drs. Aayoung Hong and Gatien Moriceau, Lo hypothesized that if they could identify the key
tumor cell processes triggered by withdrawal of MAPK inhibitors, then scientists can exploit these process with existing or investigational drugs to trigger the maximal levels of tumor cell death immediately following cessation of the initial therapy.
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?
«Used in cancer therapy, this
process could increase the impact of a treatment by heating the cancer
cells while introducing the drug compound into the
tumor.»
Cancer stem
cells can reproduce themselves through a
process called self - renewal and sustain the growth of a
tumor.
Dr. Llovet and colleagues demonstrated that the expression of mutant IDH in the adult liver of genetically engineered mice impairs liver
cell development and liver regeneration — a
process in which the liver responds to injury — and increases the number of
cells to form a
tumor.
Metastasis, the
process that allows some cancer
cells to break off from their
tumor of origin and take root in a different tissue, is the most common reason people die from cancer.
Several studies have used
cell - surface markers — proteins found on the outer membranes of
tumor cells — to identify glioblastoma stem
cells; but the specific markers used have been controversial and can not reflect molecular
processes going on within
tumor cells.
«If we can identify the point at which
tumor cells acquire the characteristics of stem
cells, it will be possible to look for ways to interrupt the
process and avoid progression of the disease.»
According to the head of the research group of chemoresistance and Predictors of
tumor response and stromal environment ICO - IDIBELL, Alberto Villanueva, «
tumor exosomes contain certain proteins (Dicer, TRBP and Ago2) able to
process microRNAs that can alter the around the
tumor cells transforming them into tumoral
cells.»
The
process enables some viruses to insert their genetic material into the DNA of healthy human
cells, which can lead to
tumors and other diseases.
The scientists went through the same
process using
tumor - derived
cells that continuously multiply.
The vaccine harnesses the natural
process of T -
cell immunity to
tumors, but enhances it to help overcome
tumors» formidable defenses.
Drugs that enhance a
process called oxidative stress were found to kill rhabdomyosarcoma
tumor cells growing in the laboratory and possibly bolstered the effectiveness of chemotherapy against this aggressive
tumor of muscle and other soft tissue.
Endosomes are machinery that
tumor cells, via a
process called endocytosis, can use to incorporate components into their environment and obtain energy by degrading them via autodigestion or autophagy.
A mutation that helps make
cells immortal is critical to the development of a
tumor, but new research at the University of California, Berkeley suggests that becoming immortal is a more complicated
process than originally thought.
Cheng and colleagues did experiments using human
cells and identified hnRNPM's role in controlling the
processes linked to
tumor metastasis.
Any deviation in these
processes could lead to
cells that do not have the proper number of chromosomes, which could accelerate
tumor initiation and progression.
«But mounting evidence confirming angiotropism and EVMM has revolutionized the knowledge of how cancer spreads through the body to the point that other scientists have confirmed the
process in other solid
tumor cell types such as pancreatic cancer.»
They found that if autophagy — the intracellular recycling
process — is blocked in
tumor cells, they produce cytokines that attract NK
cells.
Autophagy — an essential
process cancer
cells need to fuel their growth — is a key troublemaker spurring
tumor growth.
In a bid to progress beyond the shotgun approach to fighting cancer — blasting malignant
cells with toxic chemicals or radiation, which kills surrounding healthy
cells in the
process — researchers at the Harvard - MIT Division of Health Sciences and Technology (HST) are using nanotechnology to develop seek - and - destroy models to zero in on and dismantle
tumors without damaging nearby normal tissue.
Glioblastoma is the most lethal form of primary brain
tumor and leads to death in patients by invading the brain tissue in a
process that allows single
cells to move through normal brain tissue, which makes complete surgical removal of the
tumor impossible.
A combination of hypoxia and messages from the
tumor cells initiates a
process whereby the newly arrived macrophages assume their bad - boy identity as
tumor promoters.
How
cell division occurs and is coordinated with organismal development is a subject of intense research interest, as is how this
process malfunctions in the development of
tumors.
Understanding how cancer
cells are able to metastasize — migrate from the primary
tumor to distant sites in the body — and developing therapies to inhibit this
process are the focus of many laboratories around the country.
Another view is that
tumors can become resistant to therapy by a
process called
cell fate decision, by which some
tumor cells are killed by therapy and others become cancer stem
cells.
Metastasis is the
process in which
cells from a primary
tumor break - off, enter the blood stream and create new
tumors elsewhere in the body.
This allows cancer
cells to break off from
tumors, spread throughout the body (in blood or other fluid) and form new
tumors at distant sites — a
process called metastasis.
The software allowed them to cluster genes into groups associated with specific molecular
processes and see which
processes in
tumors and blood
cells were associated with each other.
Because diseases such as cancer tend to evade detection by T -
cells» receptors, allowing a
tumor to grow unchecked, scientists have long sought «intel» on this
process as a means of developing therapies that target malignant
cells, but leave healthy
cells alone.
This
process requires a fundamental change in the character of
cells within the primary
tumor, insofar as members of a localized
cell mass must be converted into actively migrating
cells that invade into the surrounding tissue and blood vessels, and finally settle in distant tissues.
However, an overactive stimulation of mTOR in response to nutrients and growth factors — metabolic
processes that are crucial in
tumor biology — leads to an increase in
cell growth and proliferation.
In the
process they induce inflammation; the
cells also secrete other inflammatory chemicals, like interleukin - 6 and
tumor necrosis factor - alpha, which are known to adhere to the endothelium of the blood vessels, an early event in atherosclerosis.
The discovery of
cells» ultra-sensitivity for mechanical property of their environment is crucial to understanding basic physiological
processes that underlie embryo development,
tumor metastasis, wound healing and many other aspects of human health and disease.
Knowing how
cells exert force and sense mechanical feedback in their microenvironment is crucial to understanding how they activate a wide range of cellular functions, such as
cell reproduction, differentiation and adhesion — basic physiological
processes that underlie embryo development,
tumor metastasis, wound healing and many other aspects of human health and disease.
As the cost of DNA sequencing continues to plummet, the lab will move ever closer to a once - elusive goal: economically
processing every patient's complete genome in both
tumors and healthy
cells.
Myc cancer gene empowers
tumor cells to relentlessly divide but simultaneously, provokes a
cell suicide
process called apoptosis.
The system can help scientists determine more about how a
cell reacts to its immediate environment, Bissell says, and how that
process goes wrong in growing or spreading
tumors, in which
cells lose their ability to read signals from their environment that would prevent them from dividing.
Half to 90 percent of glioblastoma
cells use this cellular
process so indoximod helps a patient's own immune system to find and attack their
tumors.
Researchers knew at the time that
tumors can induce normal endothelial
cells to form new blood vessels, a
process called angiogenesis.
«Why premature
cell division promotes cancers: Researchers have discovered how genes responsible for
cell division, when mutated, disrupt the replication
process of the genome and promote
tumor formation.»
The Ludwig Center at the University of Chicago --- under the direction of Ralph Weichselbaum, MD, the Daniel K. Ludwig Professor and Chair of the Department of Radiation and Cellular Oncology, and Geoffrey Greene, PhD, the Daniel K. Ludwig Professor in the Ben May Cancer Research Institute at the University of Chicago — will focus on metastasis, the
process by which cancer
cells migrate from a primary
tumor to multiple distant sites.
Leakage outside the
tumor cells would mean that the heated particles could potentially fry healthy
cells in the
process.
«Our results show that not only do exosomes enhance the phenomenon of the «Warburg effect» in
tumors, but exosomes also contain «off - the - shelf» metabolites within their cargo that cancer
cells use directly in their metabolic
processes,» Zhao said.
Metastatic colonization is a highly inefficient
process that only a small subset of disseminated
tumor cells accomplish (Nguyen et al., 2009).
More importantly, Zhang and his team for the first time found that treating the pancreatic
tumor cells with MIR506 induced autophagy, a
process that occurs as a normal and controlled part of an organism's growth or development and that could promote cancer
cell death.
In cancer, however, this
process can produce invasive and mobile
cells that can pass through membranes and travel to distant sites, where they seed new
tumors.
This technique allows us to capture images of biological
processes, for instance to trace individual
tumor cells in mice for several weeks at subcellular resolution.
More recently, the
process of EMT was associated with the ability of
cells to initiate experimental
tumors — a key - trait ascribed to «cancer stem
cells».
Alex Huang and Drew Pardoll, with Elizabeth Jaffee and Hyam Levitsky at Johns Hopkins School of Medicine demonstrate
tumor - associated antigen
processing and presentation to CD8 + T
cell by bone marrow - derived professional antigen presenting
cells via «cross-priming.»