Dr. David Gilley's laboratory at the Indiana University School of Medicine in Indianapolis and Dr. Connie Eaves» laboratory at the BC Cancer Agency's Terry Fox Laboratory in Vancouver, Canada, collaborated to determine how telomeres are regulated in different types
of normal breast cells.
The research, using cells from the Breast Cancer Now Tissue Bank and due to be published in Nature Communications, also shows that the epigenetic changes are inherited as long as the cell divides, and that the team's manipulations permanently and negatively affected the biology
of a normal breast cell from a healthy individual.
Not exact matches
When the
breast is empty, the
cells of the alveoli return to their
normal shape and
breast milk production resumes.
Working with human
breast tissue, the new study's authors attempted to induce EMT in
normal cells; they figured they would just get fibroblasts, a type
of connective tissue that is important in wound healing.
In subsequent experiments, the Einstein team deciphered other parts
of the Rac1 signaling cascade during invasion and showed that this signaling mechanism is regulated differently in
normal breast epithelial
cells.
«Perhaps there are some mammary gland stem
cells that can be coaxed to have a slightly broader potential than
normal, but I very much doubt that embryonic - like
cells normally exist in the
breast,» says Robin Lovell - Badge
of the National Institute for Medical Research in London.
And because mouse embryo
cells with inactivated copies
of BRCA2 are more sensitive to ionizing radiation than
normal cells are, «it's a reasonable extrapolation» that
breast cancers with mutated copies
of the gene may be especially good candidates for radiation therapy.
Being obese or having a higher body mass index (BMI) while carrying a BRCA (
BReast CAncer gene) mutation is positively linked with higher levels of damage to the DNA in normal breast gland cells, new research sug
BReast CAncer gene) mutation is positively linked with higher levels
of damage to the DNA in
normal breast gland cells, new research sug
breast gland
cells, new research suggests.
Plakoglobin is a component
of two important structures involved in
cell - to -
cell adhesion, and the investigators found that suppressing its expression caused CTC clusters to fall apart, reducing their metastatic potential, and also disrupted
cell - to -
cell contact between
breast cancer
cells but not
normal breast tissue.
First author Adam Skibinski, M.D. / Ph.D., student at Tufts University School
of Medicine and the Sackler School
of Graduate Biomedical Sciences at Tufts University, said «We've known for a long time that
breast cells can lose their
normal identity when they become cancerous, but we are now realizing that
normal cells can change their characteristics as well in response to transcription factors like TAZ.
Breast cancer researchers have mapped early genetic alterations in
normal - looking
cells at various distances from primary tumours to show how changes along the lining
of mammary ducts can lead to disease.
By manipulating it in vitro, a team
of researchers led by Prof. David Mooney at Harvard SEAS have identified a possible mechanism by which
normal cells turn malignant in mammary epithelial tissues, the tissues frequently involved in
breast cancer.
Now, results
of a new study by Johns Hopkins Kimmel Cancer Center scientists suggests a powerful role for the protein in
normal breast cells, acting as a tumor suppressor that halts abnormal
cell growth.
They found that the protein seems to help maintain several traits in
normal breast cells, including the ability to adhere to other epithelial
cells, and the presence
of molecules marking the
cells as differentiated and not capable
of self - renewal like
breast stem
cells.
Since a protein called Rac1 is essential for
normal milk production, as well as phagocytosis in immune
cells, Nasreen Akhtar at the University
of Sheffield and her colleagues wondered whether it might also be involved in this
breast remodelling.
The 5E5 antibody recognized multiple types
of cancer
cells, including leukemia, ovarian,
breast, and pancreatic cancer
cells, but not
normal tissues.
Scientists discovered that a particular class
of normal breast precursor
cells have extremely short chromosome ends (known as telomeres).
They compared
normal, non-cancer-forming human
breast tissue
cells with cancerous
breast cells using both
of these treatments, contrasting them with
cells with unmanipulated mtDNA.
Their studies revealed that a subset
of normal breast precursor
cells, called luminal progenitors, have dangerously short telomeres and display a correspondingly high level DNA damage response localized at their chromosome ends.
The researchers inserted between 10,000 and 40,000
of these small RNAs at once into
breast cancer, colon cancer, and
normal human
cells in the lab.
Assistant Professor Camila dos Santos
of Cold Spring Harbor Laboratory (CSHL) is studying stem
cells in the
breast for clues about what changes occur when
normal breast cells become cancerous.
Quantification
of cellular volume and sub-cellular density fluctuations: comparison
of normal peripheral blood
cells and circulating tumor
cells identified in a
breast cancer patient.
It may explain why 77 percent
of breast cancers have a
normal p53 gene, and it further suggests a way that cancer
cells can use both to metastasize and survive the journey to organs where they set up a new home.
The team examined premalignant as well as cancer
cells from
breast and lung tumors and matched
normal and premalignant
breast cells from healthy women provided by scientists at the University
of California San Francisco.
It has been reported that human
breast CSCs and
normal human mammary stem / progenitor
cells showed decreased expression
of miR200c and other miR200 members and that restoring miR200c in
breast CSCs inhibits their ability to expand clonally and form tumors in vivo [38].
Cambridge, Mass. — June 16, 2014 — A team
of researchers led by David J. Mooney, Robert P. Pinkas Family Professor
of Bioengineering at the Harvard School
of Engineering and Applied Sciences (SEAS), have identified a possible mechanism by which
normal cells turn malignant in mammary epithelial tissues, the tissues frequently involved in
breast cancer.
Lauric Acid inhibited the viability
of both cancer
cell types without altering the growth
of MCF - 10A
normal breast epithelial
cells, thus suggesting its specific potential to trigger antiproliferative effects in malignant
cells.
Scientists were able to link the consumption
of fried meat with the amount
of DNA damage found within women's
breast tissue, the type
of damage that can potentially cause a
normal cell to mutate into a cancer
cell.
Nine years
of study have shown that a natural product called Ellagic acid is causing G - arrest within 48 hours (inhibiting and stopping mitosis - cancer
cell division), and apoptosis (
normal cell death) within 72 hours, for
breast, pancreas, esophageal, skin, colon and prostate cancer
cells.
:: Washington Post Bisphenol A can alter genes, study finds Bisphenol A, the widely used compound in polycarbonate plastic, has the ability to alter the activity
of genes in
normal breast cells in ways that resemble what is found in extremely dangerous
breast cancers, according to a new study.
A grade 1
breast cancer means that the cancer
cells look very like the
normal cells of the
breast.