Takeda K, Hayakawa Y, Smyth MJ, Kayagaki N, Yamaguchi N, Kakuta S, Iwakura Y, Yagita H, Okumura K. Involvement of tumor necrosis factor - related apoptosis - inducing ligand in surveillance
of tumor metastasis by liver NK cells.
Despite this clinical importance, the exact pathologic process
of tumor metastasis is as yet poorly understood, and deciphering the exact molecular mechanism of this process is of paramount importance to identify specific therapeutic targets for this devastating disease.
The researchers also report that radiation sensitivity may be dependent on the anatomic location
of the tumor metastasis.
Not exact matches
According to Irving Weissman
of the Stanford University School
of Medicine in Palo Alto, California: «We showed that even after the
tumor has taken hold, the antibody can either cure the
tumor or slow its growth and prevent
metastasis.»
After adjusting for age,
tumor location, and stage, researchers from Cleveland Clinic's Dermatology & Plastic Surgery Institute discovered that women diagnosed with malignant melanoma during their pregnancy or within one year
of giving birth were 5.1 - times as likely to die, 6.9 - times as likely to experience
metastasis, and 9.2 - times more likely to have a recurrence.
«Once this novel
tumor - homing agent binds to the EphA2 receptor, the oncogene functions as a cancer - specific molecular Trojan horse for paclitaxel, carrying the drug inside the cancel cell, killing the cell, and thwarting
metastasis,» said Maurizio Pellecchia, a professor
of biomedical sciences at UCR's School
of Medicine who led the research.
Triple negative patients usually have shorter survival time after diagnosis
of brain
metastasis, suggesting that these
tumor cells adapt much more readily once they've moved to the brain.
Aside from the feat
of answering the longstanding question
of how the lymph system arises, understanding how it forms and develops can provide important insights into disease, from
metastasis to the abnormal accumulation
of lymph fluids, particularly in the wake
of surgery to remove cancerous
tumors.
Tumor metastasis is a leading cause
of patient morbidity and mortality, and no treatments are currently available that specifically target
metastasis formation.
But when their functioning is altered, as the UCL researchers observed in
tumor cells, the mitochondria can promote cell migration, thus leading to the formation
of metastasis.
Metastasis, the strategy adopted by
tumor cells to transform into an aggressive form
of cancer, are often associated with a gloomy prognosis.
The discovery
of a treatment capable
of blocking the mechanism responsible for the formation
of metastasis and the existence
of a family
of promising compounds, is encouragement for their future assessment in a clinical study that aims to validate a preventive treatment against
tumor metastasis.
According to Srikumar P. Chellappan, Ph.D., chair
of the Department
of Tumor Biology at Moffitt, «these cells can also contribute to the
metastasis of tumors as well as the reappearance
of tumors after they have been eliminated from the body.»
It is this overproduction
of superoxide that leads to the formation
of metastasis and, consequently, the growth
of a
tumor.
This is one
of the first research studies to highlight the importance
of the location
of the
metastasis as well as the location
of the original primary
tumor, in predicting response to radiation therapy.
According to Srikumar Chellappan, Ph.D., chair
of the Department
of Tumor Biology at Moffitt, «we expect that this study will lead to new therapeutic strategies to combat cancer
metastasis.
Excessive adipose or fat tissue, for example, raises circulating levels
of estrogen, which is associated with
tumor creation and
metastasis.
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.
«Given the devastating impact
of cancer
metastasis and the dire need for therapies to combat
tumor spread, we're highly encouraged by these findings and excited about the therapeutic possibilities they open up.»
Looking to target a key pathway in order to interfere with the processes that lead to
tumor spread, a research team led by Irwin H. Gelman, Ph.D.,
of Roswell Park Cancer Institute (RPCI) has identified a new suppressor
of cancer
metastasis that may point the way toward development
of more effective treatments for prostate cancers and other malignant solid
tumors.
The
tumor - cell survival factors uncovered by this study might one day be targeted with drugs to further diminish people's risk
of metastasis.
«What we may be looking at,» he adds, «is a future way to prevent
metastasis to many organs simultaneously» using drugs that make
tumor cells let go
of the blood vessels they cling to.
«This study has provided strong evidence demonstrating that the molecular signature
of metastasis exists prominently in the primary
tumor,» says Mary Hendrix, a cancer researcher at the University
of Iowa in Iowa City.
In recent years, atypical protein kinase C signaling has been found in the tissue invasion and
metastasis of multiple
tumors.
Runx2 has been linked to bone
metastasis in several solid
tumors, though researchers did not analyze the solid
tumors for expression
of bone - related genes.
Last fall, Bergö's group reported that ingestion
of extra antioxidants drove the
metastasis of melanoma in a mouse model, though they didn't have any effect on the primary
tumor.
With these in vitro test methods, the KU researchers have shown that anti-CD44s antibody can reduce pancreatic cancer cell growth,
metastasis and ability
of the
tumors to recur after radiation therapy.
Part
of the cytoskeleton, vimentin gives flexibility and structure to the cell, but it is also a marker
of epithelial - mesenchymal transition (EMT), which is considered a crucial event for
metastasis in epithelial
tumors.
Circulating
tumor cell (CTC) clusters — clumps
of from 2 to 50
tumor cells that break off a primary
tumor and are carried through the bloodstream — appear to be much more likely to cause
metastasis than are single CTCs, according to a study from investigators at the Massachusetts General Hospital (MGH) Cancer Center.
Their study, in the journal Oncotarget, is the most extensive analysis to date
of gene expression's role in ccRCC
tumor growth and
metastasis.
One application is the prognosis
of the melanoma: the authors show in
tumor biopsies that the amount
of RAB7 in a cutaneous
tumor defines the risk
of developing
metastasis.
In an article titled, «Allergen Induced Pulmonary Inflammation Enhances Mammary
Tumor Growth and
Metastasis: Role of CH13L1,» featured on the cover of the current issue of the Journal of Leukocyte Biology, this new research suggests inflammation raises the level of a known biomarker of cancer, called «chitinase -3-like-1» or «CHI3L1,» in the inflamed tissue, which leads to increased metastasis and faster cancer growth in th
Metastasis: Role
of CH13L1,» featured on the cover
of the current issue
of the Journal
of Leukocyte Biology, this new research suggests inflammation raises the level
of a known biomarker
of cancer, called «chitinase -3-like-1» or «CHI3L1,» in the inflamed tissue, which leads to increased
metastasis and faster cancer growth in th
metastasis and faster cancer growth in that tissue.
This blood vessel normalization results in an increased barrier function on the one hand — thereby blocking cancer cell dissemination and
metastasis - and in enhanced
tumor perfusion on the other hand, which increases the response
of the
tumor to chemotherapy.
According to Semenza, «Chemotherapy may kill more than 99 percent
of the cancer cells in a
tumor but fail to kill a small population
of cancer stem cells that are responsible for subsequent cancer relapse and
metastasis.»
Loss
of either GSTO1 or RYR1, the researchers report, decreased the number
of cancer stem cells in the primary
tumor, blocked
metastasis of cancer cells from the primary
tumor to the lungs, decreased the duration
of chemotherapy required to induce remission and increased the duration
of time after chemotherapy was stopped that the mice remained
tumor - free.
Where these three cells come in contact is where
tumor cells can enter blood vessels — a site called a
tumor microenvironment
of metastasis, or TMEM.
Treatment with an investigational CAR T - cell therapy induced complete remission
of a brain
metastasis of the difficult - to - treat
tumor diffuse large - B - cell lymphoma (DLBCL), which had become resistant to chemotherapy — the first report
of a response to CAR T - cells in a central nervous system lymphoma.
Investigators found that NPTX2 was expressed in all stages
of kidney cancer, especially
metastasis, which suggests it plays an important role in
tumor development and progression.
Metastasis, or cancer spread by the formation
of tumors at new sites, is generally what makes cancers deadly because surgery and other treatments are unlikely to find and destroy every cancer cell.
«If you can get a better handle on the biology
of the primary
tumor, and the elements
of the
tumor that may be more or less dangerous, then you don't need to worry about testing every single
metastasis for treatment decisions.»
The work also reinforces the importance
of finding
tumor cell clusters in the blood as a mechanism
of detecting cancer
metastasis earlier.
The research suggests that a cytokine produced by inflammatory cells near a prostate
tumor induces cancer cells to decrease production
of a protein that blocks
metastasis.
When the protein is present, these cells that start out round and stuck together in a pattern resembling cobblestones become irregularly shaped and tend to detach from the
tumor site in an uncoordinated way — hallmarks
of metastasis.
To test this idea, the researchers utilized two mouse models
of human breast cancer
metastasis and found dormant disseminated
tumor cells residing upon the membrane microvasculature
of lung, bone marrow and brain tissue.
«The result was an extensive inhibition
of tumor growth and prevention
of metastasis to the lung in HER2 - positive animal models
of breast cancer,» notes Navasona Krishnan, Ph.D., a postdoctoral investigator in the Tonks lab who performed many
of the experiments and is lead author on the paper reporting the results.
By identifying the cause
of this
metastasis — which often happens quickly in lung cancer and results in a bleak survival rate — Salk scientists are able to explain why some
tumors are more prone to spreading than others.
She is investigating the role
of glycosylated molecules in
tumor progression and
metastasis, tissue - and species - specific expression
of lectin receptors that play a role in regulating host innate immune responses and inflammation, and the immunological mechanisms underlying chronic inflammation and cancer development.
Surgeons use this procedure, known as «sentinel lymph node mapping,» to determine the extent
of cancer
metastasis after removing a
tumor.
Tumor metastasis is the primary cause
of mortality in cancer patients and remains the major challenge for cancer therapy.
Metastasis (the spread
of cancer from its primary site to other places in the body) to the ovaries can result in Krukenberg
tumors.