These cancer cells break away from the initial tumor and spread to other parts of the body.
More specifically, the Warburg effect describes the reality that
cancer cells break down sugars more rapidly than most other types of cells.
Metastasis is a life - threatening condition in which
cancer cells break away from the site where they formed to other areas of the body.
Cells suspended in a stiff matrix were more likely to work their way through the matrix to other side of a serum gradient, analogous to how metastasizing
cancer cells break free from their tumors.
Then tiny clumps of
cancer cells broke away from the tumor and floated away in the fluid flowing through the capillary.
Not exact matches
Even in winter, the sun's damaging ultraviolet rays can dry your skin, make it look older,
break down
cells and even cause
cancer.
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.
Cancer cells can
break away from a primary tumor, penetrate into lymphatic and blood vessels, circulate through the bloodstream, and grow in a distant focus (metastasize) in normal tissues elsewhere in the body.
A late
breaking subanalysis of the phase III CONVERT trial presented at the European Lung
Cancer Conference (ELCC) shows that white blood cell boosting drugs are safe during concurrent chemo - radiotherapy of small cell lung cancer (
Cancer Conference (ELCC) shows that white blood
cell boosting drugs are safe during concurrent chemo - radiotherapy of small
cell lung
cancer (
cancer (SCLC).
In contrast, the
cancer cells often had subsets of miRNAs that were not connected to the rest of the network — rogue groups that had
broken free.
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.
In
cancer cells, the protein networks that control the behavior are changed in such a way as to cause the
cells to lose control and
break away — a mutated skin
cell, for instance, might then migrate into the bloodstream.
To migrate from a primary tumor, a
cancer cell must first
break through surrounding connective tissue known as the extracellular matrix (ECM).
Metastatic
cancer cells have the ability to
break free from tissue, circulate in the blood stream, and form tumors all over the body, in a way acting like blood
cells.
ON THE ROAD Breast
cancer cells may
break away from the main tumor in clumps, already bearing most of the mutations that will drive
cancer recurrence, a study suggests.
Previous studies of genetic alterations in lymphoma and lung
cancer have found that certain genetic mutations — specifically when part of a gene
breaks off and gets fused to another — can inappropriately switch on ALK, driving
cancer cells to grow and divide.
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.
Batimastat does not work this way: instead, it is designed to keep
cancers in check by preventing malignant
cells breaking away and forming secondary tumours elsewhere in the body.
«We're seeing now that the mechanics are going to drive whether
cancer cells can migrate faster or slower or
break away or not.
In these vesicles, we saw the EGFR and HER2 receptors being
broken down, but we also saw our negative control receptor, c - MET,» said Dent, who is the Universal Corporation Chair in
Cancer Cell Signaling and a member of the
Cancer Cell Signaling research program at Massey.
The research suggests that reducing production of the protein, called myoferlin, affects
cancer cells in two primary ways: by changing the activation of many genes involved in metastasis in favor of normal
cell behavior, and by altering mechanical properties of
cancer cells — including their shape and ability to invade — so they are more likely to remain nested together rather than
breaking away to travel to other tissues.
Importantly, like
cancer cells with other mutations in the HR repair pathway, CHD1 - depleted prostate
cancer cells proved to be hypersensitive to chemotherapeutic drugs causing DNA
breaks, such as Mitomycin C, Irinotecan and PARP inhibitors.
Min Huang, Jian Ding, and colleagues at the Shanghai Institute of Materia Medica, Chinese Academy of Sciences, discovered that inhibiting PGAM1 made
cancer cells more sensitive to drugs that induce
breaks in both strands of the
cells» DNA.
Now, a research team led by the Georgia Institute of Technology has developed a new treatment to thwart it by, in a sense,
breaking cancer cells» legs.
Now researchers have discovered a mutation that fixes a key protein that's often
broken in
cancer cells.
Breast
cancer cells that spread to other parts of the body
break off and leave the primary tumour at late stages of disease development, scientists from the Wellcome Trust Sanger Institute and their collaborators have found.
L1CAM protein (brown in top panel) resides in
cells poised to
break from the
cancer's bulk (
cells with b - catenin are brown in bottom panel) and invade other tissues.
«This work ties together the study of
cell metabolism and
cancer chronotherapy — If
cells don't have to «rest,» they may replicate all the time, with no
breaks at all.»
«
Breaking down
cancer cell defenses: Inhibiting membrane enzyme may make some
cancer cells more vulnerable to chemotherapy.»
The
cancer originated in some unfortunate clam somewhere and has persisted ever since as those cancerous
cells divide,
break free, and make their way to other clams.
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.
Cell phones can not cause
cancer, because they do not emit enough energy to
break the molecular bonds inside
cells.
A key question in
cancer research has been how
cancer cells are able to survive once they
break away from a tumour to spread around the body.
Turning off the pathway can trigger
cancer cells to self - destruct because the machinery used to untangle the DNA fails, meaning it is torn apart as the
cell divides — ravaging and causing huge
breaks in the code which lead to the
cancer cells» demise.
The study of human astrocytes has faced issues related to access (samples of living tissue must be obtained from brain
cancer or epilepsy surgeries or fetal tissue) and purification (
breaking apart astrocytes away from other
cells often killed them and many experiments ended in failure).
The study, published in Nature Communications, examined the changes that occur in
cancer cells as they
break away from tumours in
cell cultures, zebrafish and mice.
The acidic environment inside the
cancer cell then begins to
break apart the pseudo-platelet — freeing the Dox to attack the
cancer cell's nucleus.
Although this research was conducted on ovarian
cancer cells, the ground -
breaking results are applicable to a wider range of
cancers.
«This paper shows that an increase in physical mobility of DNA strands is something that happens inside mammalian
cells every time there is a
break in the DNA,» says de Lange, who is also American
Cancer Society Professor, and Director of the Anderson Center for
Cancer Research at Rockefeller.
These tumors might yield to a new kind of drug known as a PARP inhibitor that kills
cancer cells by hijacking the
cell's ability to mend DNA
breaks.
One treatment is a vaccine that targets a structure on the outside of
cancer cells, while the other is an altered enzyme that
breaks apart RNA and causes the
cell to commit suicide.
As described in a study posted online May 21 by Science magazine, the strategy uses tumor
cells» own protein - chopping machinery to
break down and dispose of proteins that drive
cancer growth.
Like most machinery, the mitotic spindle can malfunction, and when it does, DNA can be
broken or unevenly divided, errors implicated in the uncontrolled
cell division of
cancer.
One tragic feature of osteosarcoma is the rapid, error - prone production of weaker bone by cancerous bone - making
cells, where a young person surprisingly
breaks a bone to reveal undiagnosed, advanced
cancer.
Then, they showed that when the
cancer cells didn't make enough ATRX, the
cells couldn't join together the two ends of a
broken DNA strand.
«We found that these new - generation paradox -
breaking BRAF inhibitors did not promote or accelerate the growth in the colorectal
cancer cells and may therefore, pending the results from ongoing clinical trials, be a safer alternative to be used alone or in combination in melanoma patients,» Dr Behren said.
A small molecule inhibitor of monoubiquitinated proliferating
cell nuclear antigen (PCNA) inhibits repair of interstrand DNA cross-link, enhances DNA double strand
break, and sensitizes
cancer cells to cisplatin.
Dr Behren said the «paradox
breaking» compounds were tested on BRAF melanoma
cells for their potential to inhibit their growth and, after being seen to successfully target these
cells, were then tested for their growth - promoting effects on various colorectal
cancer cells in comparison to the classical drugs.
The
cancer cells placed protective membrane «sacks» round
cell waste, and filled them with chemicals to
break up and recycle the contents.
A Small Molecule Inhibitor of Monoubiquitinated Proliferating
Cell Nuclear Antigen (PCNA) inhibits Repair of Interstrand DNA Crosslink, enhances DNA Double - strand
Break, and sensitizes
Cancer Cells to Cisplatin.