The new study led by Thomas Helleday at Karolinska Institutet / SciLifeLab, reveals that castration therapy decreases the amounts of proteins essential for DNA -
repair in cancer cells.
Absence of TRF2 resulted in increased DSB sites which led us to conclude that TRF2 is indispensable for efficient DSB
repair in cancer cells.
The promising results of this experimental study are based on a combination of the drug temozolomid and other extant drugs that inhibit an enzyme instrumental in DNA
repair in cancer cells.
Their findings in the study «Phosphoglycerate mutase 1 regulates dNTP pool and promotes homologous recombination
repair in cancer cells,» which has been published in The Journal of Cell Biology, suggest that this FDA - approved ovarian cancer medicine has the potential to treat a wider range of cancer types than currently indicated.
Not exact matches
A type of immune therapy known as PD - 1 blockade controlled
cancer in 77 percent of patients with defects
in DNA mismatch
repair — the system
cells use to spell - check and fix errors
in DNA (SN Online: 10/7/15).
The study found that carfilzomib and irinotecan have a potential synergistic effect
in SCLC and other Irinotecan - sensitive
cancers by allowing normal DNA damage
repair and enabling normal
cell - cycle death.
Once stem
cells can be grown and differentiated
in a controlled way to replace degenerated
cells and
repair tissues, medical science may then be able to diagnose and cure many intractable diseases at their earliest stages, such as type 1 diabetes, Parkinson's disease, various cardiovascular diseases, liver disease, and
cancer.
Now, results described
in tomorrow's issue of Nature suggest that BRCA2 mutations could lead to
cancer by interfering with
cells» ability to
repair damaged DNA.
Olaparib is good at killing
cancer cells that have errors
in genes that have a role
in repairing damaged DNA such as BRCA1 or BRCA2.
They found that
cancer cells had acquired new genetic changes that cancelled out the original errors
in DNA
repair — particularly
in the genes BRCA2 and PALB2 — that had made the
cancer susceptible to olaparib
in the first place.
«DNA
repair helps thwart
cancer and keep the
cell in top shape — it is usually all
in a day's work within each
cell,» Dr. Durocher adds.
In previous research, this team of University of Alberta researchers found that PRC1 complex helps to repair DNA damage in cancer cell
In previous research, this team of University of Alberta researchers found that PRC1 complex helps to
repair DNA damage
in cancer cell
in cancer cells.
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.
In particular, it has been shown that cells with other HR repair pathway defects, such as BRCA mutations frequently found in breast and ovarian cancer, are sensitive to inhibition of the enzyme PARP, and the PARP inhibitor Olaparib has been approved for treatment of BRCA - mutated ovarian cancer
In particular, it has been shown that
cells with other HR
repair pathway defects, such as BRCA mutations frequently found
in breast and ovarian cancer, are sensitive to inhibition of the enzyme PARP, and the PARP inhibitor Olaparib has been approved for treatment of BRCA - mutated ovarian cancer
in breast and ovarian
cancer, are sensitive to inhibition of the enzyme PARP, and the PARP inhibitor Olaparib has been approved for treatment of BRCA - mutated ovarian
cancers.
Moreover,
in some cases, pancreatic
cancer cells can even
repair damage to their DNA caused by the chemotherapy drugs that do get into the tumor, further protecting themselves.
Now his lab has found that Set2 is also a major player
in DNA
repair, a complicated and crucial process that can lead to the development of
cancer cells if the
repair goes wrong.
They work particularly well if the
cancer cells they attack already have defects
in the corresponding DNA
repair pathways, as it frequently occurs
in breast
cancer and other tumors.
And researchers at the «Seattle project», an effort funded by the National
Cancer Institute to find new anticancer drugs, are mutating genes in yeast cells — such as the ATM gene or the mismatch repair genes — that often lead to cancer in h
Cancer Institute to find new anticancer drugs, are mutating genes
in yeast
cells — such as the ATM gene or the mismatch
repair genes — that often lead to
cancer in h
cancer in humans.
To date, yeast has taught scientists a lot about
cell division and DNA
repair, processes that go wrong
in cancer.
In normal cells, this is a part of the wound repair process when PGE2 induces tissues stem cells to regrow; in cancer PGE2 ironically induces regrowth of more cancer stem cells in between chemotherapy cycles, Kurtova and Xiao sai
In normal
cells, this is a part of the wound
repair process when PGE2 induces tissues stem
cells to regrow;
in cancer PGE2 ironically induces regrowth of more cancer stem cells in between chemotherapy cycles, Kurtova and Xiao sai
in cancer PGE2 ironically induces regrowth of more
cancer stem
cells in between chemotherapy cycles, Kurtova and Xiao sai
in between chemotherapy cycles, Kurtova and Xiao said.
The ERK pathway plays a critical role
in embryonic development and tissue
repair because it instructs
cells to multiply and start dividing, but when over activated
cancer growth occurs.
Last week, Lin Zhang, MD, an associate professor of Obstetrics and Gynecology, described
in Science Translational Medicine, how his team treated therapy resistant
cancer cells to renew their sensitivity to PARP inhibitors, a class of drugs that, when effective, prevent
cancer cells from keeping up with DNA
repair, causing them to eventually die.
The stem
cells that proliferate the most
in response to damage caused by cigarette smoke
repair their DNA using a process prone to errors, setting the stage for lung
cancer, according to a study publishing January 26, 2017
in the open - access journal PLOS Biology by Marie - Liesse Asselin - Labat and her team of the Walter and Eliza hall Institute of Medical Research, Australia.
In a new study, Yale
Cancer Center researchers identified a novel genetic defect that prevents brain tumor
cells from
repairing damaged DNA.
However the team from the Krebs Institute for Nucleic Acids at the University of Sheffield found that the key to preventing resistance to a common class of chemotherapy used to treat breast and colon
cancer is to change the speed
in which the
cancer cells repair damage to their DNA that is introduced by chemotherapy.
A report
in the 15 February issue of the Proceedings of the National Academy of Sciences suggests that a lotion containing an algal protein can ward off sunburns — often the first step on the road to skin
cancer — by
repairing part of the damage to skin
cells» chromosomes.
When researchers at Johns Hopkins University
in Baltimore, Maryland, examined tumor tissue from the original man with colon
cancer who responded to a PD - 1 inhibitor, they found a clue: His tumor had mutations
in «mismatch
repair» genes, so - called because their encoded proteins fix errors
in DNA bases when
cells replicate their DNA.
«Our researchers were able to identify a change
in a specific mark
in the proteins that wrap the DNA — called histones —
in such a way that makes
repair much faster
in cancer cells, increasing their resistance to therapy.»
In healthy individuals, MDSCs regulate immune responses and tissue
repair, and the population of these
cells rapidly expands during inflammation, infection and
cancer.
Professor Sherif El - Khamisy, who led the research, said: «If we can find a way to hijack the
cancer's fix and
repair toolkit and make it less efficient, then we can tip the scale
in favour of
cancer cell death instead of survival and prevent resistance to chemotherapy.
«Hail Mary» mechanism can rescue
cells with severely damaged chromosomes: Understanding the mechanisms involved
in chromosome
repair, and how they can fail, may lead to new strategies to combat
cancer.»
Although these
cells play an essential role
in wound healing and injury
repair, they may also promote
cancer incidence
in tissues.
This is because faults
in the gene mean the
cell can not properly
repair its DNA, causing genetic damage to build up, leading to
cancer.
Olaparib targets a molecule called PARP, and exploits weaknesses
in cancer cells» ability to
repair damage to their DNA.
To our knowledge, this is the first direct report of efficient DSB
repair in cancer stem
cell clonospheres.
Cancer stem cell markers are enriched in normal tissue adjacent to triple negative breast cancer and inversely correlated with DNA repair defic
Cancer stem
cell markers are enriched
in normal tissue adjacent to triple negative breast
cancer and inversely correlated with DNA repair defic
cancer and inversely correlated with DNA
repair deficiency.
Cancer researchers at Columbia have discovered three genes that undermine the DNA
repair process and promote tumor formation
in cells with BRCA mutations.
We report a role of TRF2
in cancer stem
cell maintenance and efficient DNA
repair in the clonospheric sub-population of HCT 116
cell line.
The films are «Killing
Cancer: Cytotoxic T -
Cells on Patrol» by Alex Ritter, NIH Oxford - Cambridge Scholars Program; «Companions
in Discovery» by Amy Gladfelter, Dartmouth; and «
Cell Repair» by Bill Bement, University of Wisconsin, Madison.
Research Paper Role of TRF2
in efficient DNA
repair, spheroid formation and
Cancer Stem
Cell maintenance Arka Saha, SwatiShree Padhi, Madhabananda Kar, Shomereeta Roy, Prasanta Maiti, Birendranath Banerjee Oncomedicine 2017; 2: 71 - 79.
Because the insertion can be placed so that it interrupts a protein's function, the insertion and
repair system may be useful for producing certain pharmaceuticals or protein products, such as
cancer drugs,
in culture, which would otherwise kill the
cell.
The problem is that GFI1 is often overexpressed
in cancer cells:
in these cases, GFI1 can help them resist certain treatments, since GFI1 helps to
repair DNA breaks caused by radiotherapy or chemotherapy.
2010 — We discover how a gene that normally plays a role
in nerve
cell repair can also help some nerve
cancers spread.
«Rhode Island Hospital hosts three separate National Institutes of Health COBREs — for stem
cell biology, skeletal health
repair, and for
cancer discoveries,» Timothy J. Babineau, CEO of parent company Lifespan, said
in a statement.
Our laboratory is particularly interested
in studying alternative DNA
repair mechanisms, such as the alternative end joining (alt - EJ) pathway, that take place
in cancer cells to compensate for the loss of homologous recombination (HR) activity (Figure 2A).
In cancer cells, the damage is not
repaired.
«One of the big problems that people worry about
in the use of stem
cells for the
repair of body parts, is whether or not you are going to be creating
cancer,» said Kosik.
Many mechanisms of MDR have been described, such as the overexpression of MDR1 (also known as P - glycoprotein or ABCB1) or other ATP - dependent transporters that pump drugs out of the
cancer cells, amplification of drug - inactivating enzymes, mutations or modifications of drug targets, alterations
in DNA
repair machinery, and increased resistance to apoptosis (1 — 3).
As I explain
in my new book, Mind Over Medicine: Scientific Proof That You Can Heal Yourself, the body is equipped with natural self -
repair mechanisms that can kill stray
cancer cells, fight infections, and even slow the aging process.
Along with other brassica vegetables, kale is also a source of Indole -3-carbinol, a chemical which boosts DNA
repair in cells and appears to block the growth of
cancer cells.