«The technology could also greatly improve our ability to study how
tumor cells change in response to treatment and could help answer important biological questions about how treatment resistance arises.»
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?
The introduction of infant formula to babies» diets
changes the infants» gut microbiome, thus affecting the response of the infant immune system to pathogens.47 - 51 A greater amount of natural - killer
cells, suggesting a more mature immune system, have been found in breastfed infants than in formula - fed infants.52 In addition, pH level in the stomach of breastfed children is better for the promotion of the protein - lipid α - lactalbumin (termed HAMLET), which induces apoptosislike death in
tumor cells.51, 53
A successful test would therefore require isolating enough of these scarce
cells to make statistically valid inferences about the
tumor, often at a stage when the
tumor itself is growing and
changing rapidly.
«Current therapies in clinical trials are focused on targeting genetic
changes in
tumors and helping to boost one's immune system to fight the cancer
cells.
Bowel cancer, also called colorectal cancer, results from a series of genetic
changes (mutations) that cause healthy
cells to become progressively cancerous, first forming early
tumors called polyps that can eventually become malignant.
The researchers demonstrated that blocking the PGD enzyme genetically or with a pharmacologic inhibitor reversed the epigenetic reprogramming and malignant gene expression
changes detected in distant metastases, and also strongly inhibited their
tumor - forming capacity, with no effect on normal
cells or peritoneal pancreatic cancer controls.
The Campàs lab is studying several of these questions, including how limbs are built and how mechanical
changes in
tumors affect the behavior of malignant
cells and the growth of the
tumor.
Wistar scientists have previously shown that age - related
changes in the
tumor microenvironment — or the surrounding area where
tumor cells crosstalk with normal and immune
cells — can drive melanoma progression and therapy resistance.
Although
changes in treatment methodology still have to be studied, Dr. Cripe believes it may be that the timing of various treatments is what matters, and that perhaps initially suppressing immunity could allow the virus to infect a large number of
tumor cells before relieving the immunosuppression to allow the body's own T
cells to fight off the
tumor.
«In the past, we've thought the resistance was caused by genetic
changes in
tumor cells.
A multicenter team of researchers reports that a full genomic analysis of
tumor samples from a small number of people who died of pancreatic cancer suggests that chemical
changes to DNA that do not affect the DNA sequence itself yet control how it operates confer survival advantages on subsets of pancreatic cancer
cells.
To see if PGD and the pentose phosphate pathway were tied to the epigenetic
changes the researchers had detected in distant metastases, they treated
tumor cells from different sites in a single patient with the drug 6 - aminonicotinamide (6AN), which is known to inhibit PGD but is not used in humans because of its severe side effects.
But the
cells also
changed shape and other properties in the absence of the protein in ways that reduced the likelihood that they would travel away from the
tumor — a sign that myoferlin not only
changes genes in cancer
cells, but also alters the
cells» mechanical properties.
Aware that cancers rewire their metabolism in ways that could
change the epigenome and that distant metastases in pancreatic cancer naturally spread to organs fed by a sugar - rich blood supply, the researchers wondered if the
tumor cells had altered the way they use the basic form of sugar, glucose.
«Beta blockers may lead to new novel triple negative breast cancer treatments: New research suggests that adrenaline can act on
tumor cells via a
cell surface receptor called the beta2 - adrenoceptor and that
changes in signaling within the
cell make it highly invasive.»
«The finding that certain
cell signaling lipids
change the activity of an oncogenic Ras protein, suggests that we might be able to interfere with
tumor progression by inhibiting the enzymes which make the specific
cell signaling lipid in
cells,» Buck said.
«We know very little about how gene mutations in
tumor cells can
change how a
tumor might respond or not to certain chemotherapy drugs.
«These were delivered directly to the
tumor site to
change the molecular signature of the cancer
cells, rendering the
tumor dormant or eradicating it altogether.
And IL - 22 helped
tumor cells express stem -
cell genes through epigenetic
changes to these genes.
The results suggest the simultaneous activation of certain molecular pathways — actions among molecules in a
cell that can lead to
change — in particular the MAPK and PI3K cellular pathways, triggered
tumor initiation and produced increasingly dense low - grade gliomas that quickly progressed to glioblastoma multiforme (GBM).
Furthermore, the normal ductal
cells that are able to develop into pancreatic cancer represent about 10 percent of the
cells in the pancreas, complicating efforts to pinpoint the
changes that occur as the
tumor develops.
Steinmetz points out that other cervical
tumors have massive rearrangements on chromosome 11, so the
changes in the HeLa
cell may have contributed to Lacks»
tumor.
They found that, by using math models to understand the complex dynamics within cancers, they could use small
changes in the environment to promote the growth of
cells that are less aggressive and thereby decrease
tumor growth.
The
cell changes, known as an epithelial to mesenchymal transition, or EMT, are normal and helpful during wound healing, but problematic when cancer
cells spread from the primary
tumor site to other sites in the body.
The researchers used computer models to predict that small
changes of the pH within the
tumor could tip the balance, decreasing the survival advantage of the invasive
cells in favor of the non-invasive
cells.
«
Tumor cells can
change or evolve,» Vanapalli said.
In 2010, Herlyn and his colleagues published findings that
changed the way scientists look at
tumor cells.
Their recent study, which appears as the cover article in the May issue of Cancer Research, shows that mathematical models can be used to predict how different
tumor cell populations interact with each other and respond to a
changing environment.
Furthermore, only those fusion - derived IEC - 6
cell clones that had undergone the
changes in cellular growth indicative of neoplastic transformation produced
tumors in mice.
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.
Already the German biochemist and Nobel Prize laureate Otto H. Warburg observed in the 1920s that
tumor cells radically
change their metabolism.
Approximately half of all metastatic melanoma patients»
tumors have a BRAF mutation, an abnormal
change that can enable melanoma
tumor cells to grow and spread.
They used the gene - editing CRISPR / Cas9 technique to sift the genomes of melanoma
cells for
changes that made
tumors resistant to being killed by immune T
cells, which are the main actors in the immune system response against infections and cancer
cells.
She also noted the targeting Msi in primary
tumors significantly
changed «the trajectory of progression by halting pancreatic cancer growth and improving survival,» inhibiting both cancer stem
cells and other
tumor cells.
A doctor treating a patient with a potentially fatal metastatic breast
tumor would be very pleased to find, after administering a round of treatment, that the primary
tumor had undergone a
change in character — from aggressive to static, and no longer shedding
cells that can colonize distant organs of the body.
Overall, including all genomic variations present in most if not all
tumor cells (clonal) as well as those present only in subsets of the cancer
cells (subclonal) from
tumor tissue, the researchers detected a total of 864 genetic
changes in tissue samples across the three
tumor types, and 627 (73 %) of those were also found in the blood.
«The apparent ability to
change immunosuppressive T
cells within the
tumor into T
cell types that are more active and potentially helpful against cancer was a really exciting finding, and one that we're continuing to investigate,» says Poznansky, who is an associate professor of Medicine at Harvard Medical School (HMS).
While the colorectal and breast cancer patients had no unusual CNVs, 7 % of those with early - onset testicular germ
cell tumors — which are the vast majority of all testicular cancer cases — had a CNV that had developed de novo, that is not inherited directly from their parents but the result of a
change to a sperm or egg
cell.
Tumor cells metastasized to bone modify the activity of these
cells and, depending on the type of cancer, cause osteoblastic or osteolytic
changes.
Together, the
changes promote
tumor progress and cancer -
cell survival.
Tumor cells circulating through the body in the bloodstream then take advantage of these cellular and molecular
changes to lodge in the liver and form metastases.
A major component of the study was a comprehensive analysis of the «phosphoproteome» of prostate cancer
tumors and
cells, revealing
changes in the phosphorylation states of cellular proteins.
The study has important implications for human health, and is particularly useful for understanding the
changes that occur in
cells during the development of the
tumors that underlie cancers.
The assembly and analysis of human
tumor cell genomes, many of which contain chromosome deletions, duplications and insertions, as well as single nucleotide
changes, requires immense data storage capacity and high - speed computation.
«To check this hypothesis, we searched the
tumor cells for molecular
changes that are indicative of the tendency to spread early,» Hoheisel explained.
Four years ago, during a magnetic resonance experiment with
tumor cells, TUM physicist Dr. Franz Schilling found signals from a molecule that was highly sensitive towards pH
changes.
In these cases, drug exposure caused significant
changes in
tumor cells» gene expression profile but had no lasting physical effect.
For a
tumor to develop,
cells must undergo a series of genetic
changes, or mutations, that cause them to proliferate uncontrollably.
The researchers have shown that this marker protein
changes myoepithelial
cells in breast tissue to promote
tumor cell invasion in vitro and enhances mammary
tumor growth in vivo.