«In this case, the pathway involved the loss of a protein called MBD3 that
allows tumor cells to become more like stem cells and persist,» said first author on the study Rakesh Verma, a postdoctoral associate in hematology.
After more than six years of research, the research team led by María Soengas, head of CNIO's Melanoma Group, showed that RAB7 acts as an orchestra director, determining the fate of melanoma cells: at high concentrations of RAB7, cellular autodigestion is very active, and
this allows tumor cells to obtain energy, prevent the accumulation of toxic components and thus divide and proliferate; when RAB7 is reduced, cells use endosomes to recycle metastatic proteins, favouring their dispersal throughout the body.
That allowed tumor cells to survive gemcitabine treatment in lab dishes and mouse studies, Leore Geller of the Weizmann Institute of Science in Rehovot, Israel, and colleagues discovered.
CCL5 attracts tumor cells to the lungs and lymph nodes, and VEGF increases the number of blood vessels and makes them more porous,
allowing tumor cells to metastasize and infiltrate the lungs.
Not exact matches
Breast cancer
tumors can fuse with blood vessel
cells,
allowing clumps of cancer
cells to break away from the main
tumor and ride the bloodstream to other locations in the body, suggests preliminary research.
EphA2 spreads cancer by
allowing malignant
cells to migrate from the primary
tumor into circulation and eventually to adhere to other tissues.
Overexpression of ZNF217 provides an advantage to
tumor cells by
allowing cells to infinitely proliferate and turning down pathways that typically tell
cells to mature into functional
cells (bone, blood, skin
cells).
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.
These findings support that
tumor cells prefer pre-formed tunnels because they
allow the
cells to move easier.
Pembrolizumab, or pembro, an immunotherapy drug that unmasks cancer
cells and
allows the body's own immune system to help destroy
tumors, appears to be safe in treating lung cancers, according to a study by Cancer Treatment Centers of America ® (CTCA) at Western Regional Medical Center (Western) in Goodyear, Arizona.
If we can boost the immune system and
allow microglia to do their job and control brain
tumor stem
cells, it would be like removing the seed from the soil — stopping the
tumor growth before it starts to get out of control.»
When the scientists inserted human colorectal cancer
cells into zebrafish embryos and
allowed them to grow for 4 days, the resulting
tumors showed three hallmarks of human solid
tumors: rapid
cell division, formation of blood vessels to supply nutrients, and the ability to spread to other locations in the body.
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.
Another version, the CTC - iChip, rapidly isolates CTCs in a way that does not rely on preidentified
tumor antigens,
allowing capture of
cells with gene expression patterns that may be missed by the antibodies used in the HBCTC - Chip.
The class of medications that he conceived, known as immune checkpoint inhibitors, works counterintuitively: By turning off one of the immune system's built - in safeguards, the inhibitors
allow T
cells — the system's foot soldiers — to attack
tumors more effectively.
New technologies are coming to the fore that
allow interrogation of the types of
cells interacting with
tumors, in particular providing intelligence on the broad variety of complex associations between
tumor cells and the immune system.
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.
Conversely, high levels of Bmal1 overtook the UPR, thereby
allowing protein synthesis to continue, which was toxic to
tumor cells.
Numb therefore stabilizes p53 and
allows this
tumor suppressor protein to limit stem
cell proliferation.
The massive recruitment of NK
cells allows killing cancer
cells and lets the
tumors shrink.
«New computer program can help uncover hidden genomic alterations that drive cancers: Tested on large
tumor genomics database, REVEALER method
allows researchers to connect genomics to
cell function.»
Once it «parked,» an enzyme present in pancreatic cancer caused the carrier to biodegrade,
allowing the therapeutic cargo to be released at the correct address — the
tumor cells.»
The number of extracted
tumor cells allows conclusions to be drawn with respect to the success of therapy and the future course of the disease.
The resulting «map» of gene - drug interactions
allowed the researchers to accurately predict the responses of multiple human cancer
cell lines to different chemotherapy agents based on the
cell lines» genetic profiles and also revealed new genetic factors that appear to determine the response of breast and ovarian
tumor cells to common classes of chemotherapy treatment.
Partnering with the U.S. Food and Drug Administration
allowed Doebele and colleagues to access clinical trial data describing initial
tumor response, PFS and OS for 305 patients with stage IIIb or IV non-small
cell lung cancer on trials of ALK inhibitors and 355 similar patients on trials of immunotherapies directed at PD - 1.
By performing a genome - wide screen in breast cancer
cells, Dr. Oesterreich and her colleagues identified a gene called HOXC10 as one that the cancer seems to modify to
allow continued
tumor growth in patients whose cancer becomes resistant to traditional therapies.
«SynNotch receptors essentially
allow us to confine the T
cell response at the site of disease with the goal of enhancing the ability of the T
cell to, for example, overcome the inhospitable microenvironment of a solid
tumor.
The findings made by IMBA scientists now provide evidence that one can find key molecular brakes in innate immune
cells that, when modified,
allow such
cells to seek out and destroy metastatic
tumors.
«Understanding the molecular mechanism that leads to CD8 T
cell exhaustion brings us a step closer to developing strategies to induce optimal T
cell responses that can successfully clear infections and kill
tumor cells,» explains postdoctoral researcher and co-lead author Renata M. Pereira, Ph.D. «Conversely, it may
allow us to interfere with autoimmune responses that paradoxically depend on the same protein.»
UCLA scientists have unlocked an important mechanism that
allows chemotherapy - carrying nanoparticles — extremely small objects between 1 and 100 nanometers (a billionth of a meter)-- to directly access pancreatic cancer
tumors, thereby improving the ability to kill cancer
cells and hence leading to more effective treatment outcome of the disease.
Finally, they equipped the nanoparticles with polyethylene glycol molecules, which
allow them to resist the internal defenses of a
tumor cell.
For example, cancer
cells floated above denser blood
cells, which could
allow clinicians to spot rare circulating
tumor cells in a patient sample.
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.
That is, they contained multiple populations of
cells, including the so - called JARID1B
cells, which their research suggested was responsible for
allowing tumors to survive drug therapy.
HM - SNS
allows researchers to sequence the genomes of single
tumor cells and study multiple
cells simultaneously, both lowering the cost and boosting data analysis for such studies.
The National Institutes of Health today announced in Nature that it has reached an understanding with the family of the late Henrietta Lacks to
allow biomedical researchers controlled access to the whole genome data of
cells derived from her
tumor, commonly known as HeLa
cells.
«The diabetes drug puts the brakes on the
cells that would otherwise repopulate the
tumor, thus
allowing the anticancer drug to be more effective.»
This
allows cells within the cancerous
tumors to be successfully treated even at an advanced stage.
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.
A University of Colorado Cancer Center study published in the journal Oncogene used next - generation sequencing technologies to perform the most detailed DNA - based analysis to date of 25 commonly used bladder cancer
cell lines,
allowing researchers to match patient
tumors with their closest genetic
cell line match, and demonstrated genetic alterations that may make
cells more or less sensitive to common therapies.
When the animals» immune systems identify a cancer
cell, a genetic tweak
allows their bodies to launch a massive attack of white blood
cells that kills the budding
tumor.
Now, researchers reporting in the
Cell Press journal Chemistry & Biology have developed a new method that
allows investigators to label and track single
tumor cells circulating in the blood.
Researchers have for the first time developed a technique that coats anticancer drugs in membranes made from a patient's own platelets,
allowing the drugs to last longer in the body and attack both primary cancer
tumors and the circulating
tumor cells that can cause a cancer to metastasize.
«Our combined analysis of
cell - free DNA and white blood
cell DNA
allows for identification of
tumor DNA with much higher sensitivity, and deep sequencing also helps us find those rare
tumor DNA fragments.»
Instead, we administer a combination therapy to
allow immune
cells, which are capable of killing
tumors, to see
tumors that were previously invisible to the immune system.»
This would stop the
tumor cells from gaining the flexibility to revert back to stem
cells and
allow doctors to wipe them out once and for all.
Another possibility is attaching the contrast agent to immune
cells engineered to attack a patient's
tumor,
allowing the
cells to be tracked inside the body.
This in turn
allows accumulation of this fat in
tumor cells.
The concept should
allow more accurate surgical removal of solid
tumors at the same time it eradicates any remaining cancer
cells.