Sentences with phrase «by breast cancer cells»

Olaparib had no effect on tumors formed by breast cancer cells containing functional BRCA1 and BRCA2 genes.

Not exact matches

Cancer: Flaxseed may protect against breast cancer, prostate cancer, and colon cancer by inhibiting tumor growth and blocking enzymes that are involved in the spread of tumor Cancer: Flaxseed may protect against breast cancer, prostate cancer, and colon cancer by inhibiting tumor growth and blocking enzymes that are involved in the spread of tumor cancer, prostate cancer, and colon cancer by inhibiting tumor growth and blocking enzymes that are involved in the spread of tumor cancer, and colon cancer by inhibiting tumor growth and blocking enzymes that are involved in the spread of tumor cancer by inhibiting tumor growth and blocking enzymes that are involved in the spread of tumor cells.

The study, led by Dr Len Stephens and Dr Phill Hawkins and published today in the journal Molecular Cell, reveals why loss of the PTEN gene has such an impact on many people with prostate cancer, as well as in some breast cancers.

When researchers injected fresh breast cancer cells in the side opposite the original tumor site, the disease didn't recur in any of the mice, as the cancer was rejected by the immune system's memory.

In the Cell study, Dr. Massagué, with Fellow Manuel Valiente, PhD, and other team members, found that in mouse models of breast and lung cancer — two tumor types that often spread to the brain — many cancer cells that enter the brain are killed by astrocytes.

By hitting breast cancer cells with a targeted therapeutic immediately after chemotherapy, researchers from Brigham and Women's Hospital (BWH) were able to target cancer cells during a transitional stage when they were most vulnerable, killing cells and shrinking tumors in the lab and in pre-clinical models.

By hitting breast cancer cells with a targeted therapeutic immediately after chemotherapy, researchers were able to target cancer cells during a transitional stage when they were most vulnerable.

Lab testing showed that the plant - made virus particles, which naturally bind to receptors on cancer cells, were taken in by human breast cancer cells.

Still, how melanoma cells join into tumors — whether by individual cells coming together or small or large clusters of cells doing so — follows the same pattern as breast tissue cancer cells: Cables are extended to reel in other cells or clusters.

Extensive studies have found that 20 % to 30 % of breast cancers are characterized by over-expression of HER2, which makes the cancer cells grow and divide faster, leading to a cancer that's more aggressive and more likely to be resistant to the standard of care.

Johnson's team borrowed a technique from cancer biology, called the systematic evolution of ligands by exponential enrichment (SELEX), which creates a huge library of random, short chains of nucleotides, called aptamers, and then incubates them with a target of choice, such a specific breast cancer cell.

Women with the KRAS - variant are also more susceptible to triple - negative breast cancer, tumors whose growth is not fueled by the hormones estrogen and progesterone, or by the presence of a particular genetic mutation known as HER2, which promotes cancer cell growth.

Taken together, these findings suggest that BRCA2 mutations increase susceptibility to breast cancer by disrupting DNA repair and allowing cells to accumulate mutations, including those that foster cancer development.

To see whether cancer stem cell renewal involves a chain of events similar to that used by embryonic stem cells, and whether the process was affected by oxygen levels, Semenza and graduate student Chuanzhao Zhang focused their studies on two human breast cancer cell lines that responded to low oxygen by ramping up production of the protein ALKBH5, which removes methyl groups from mRNAs.

The researchers treated 63 cancer cell lines (26 breast, 14 colorectal and 23 ovarian) with low - dose 5 - azacitidine (AZA), an FDA - approved drug for myelodysplastic syndrome, that reverses epigenetic changes by stripping off the methyl group that silences the gene.

Previous work led by Charlotte Kuperwasser, principal investigator, determined that some common forms of breast cancer originate from luminal cells while some rarer forms of breast cancer originate from basal cells.

The time needed for breast cancer metastases (secondary lesions caused by cells that have escaped from the original tumour) to develop varies between patients, and little is known about the mechanisms that govern latency (the dormant state of cells that have already spread through the body).

The groundbreaking study identified a protein, known as cadherin - 22, as a potential factor in cancer metastasis, or spread, and showed that hindering it decreased the adhesion and invasion rate of breast and brain cancer cells by up to 90 per cent.

Researchers saw that injecting the miR - 34a mimic in mice could prevent the metastasis of breast and skin cancer cells specifically to bone, mainly by disarming the metastatic niche in bone.

«By understanding how stress accelerates invasion in aggressive breast tumor cells, this work will inform future studies into whether beta - blockers could be a useful adjuvant therapy in the treatment of some aggressive breast cancers.»

«Triple - negative breast cancers are cancer cells that lack three receptors targeted by current chemotherapy regimens.

Researchers from BUSM and the University of Cyprus compared the markers on the surface of the cancer cells to gene expression profile of breast tumors deposited by researchers in international public databases and found that a molecule named IL13RA2 (IL13R alpha2) was abundant in metastatic or late - stage BLBC.

The study, which will be published December 21 in the Journal of Cell Biology, suggests that the loss of these particular Numb proteins makes breast cancers more aggressive and resistant to chemotherapy, but points the way toward new therapeutic approaches that could improve patient outcome by preserving p53 levels.

This is a fascinating new field of thought in breast cancer research, especially given the team's findings that we might be able to stop cancer stem cells by blocking the molecule FAK.»

Researchers used IL - 15 to develop a whole tumor cell vaccine to target breast (TS / A) and prostate (TRAMP - C2) cancer cells in animal models; results showed that tumor cells stopped growing after the vaccine was introduced and that beneficial effects were enhanced further when IL - 15Rα was co-produced by the vaccine cells.

The researchers then exposed cells from each of these lines to a panel of 31 different drug treatments — including 23 chemotherapy compounds approved by the FDA for breast and ovarian cancers, six targeted cancer drugs, and two common drug combinations.

«Brain metastases are a secondary brain tumour, which means they are caused by cancer cells that escape from primary tumours like lung, breast or melanoma, and travel to the brain,» said Mohini Singh, the study's primary author and a PhD candidate in biochemistry at the Michael G. DeGroote School of Medicine at McMaster.

In tumors formed by human breast cancer cells, DNA damage (brown staining) is increased by simultaneous Olaparib treatment and PGAM1 suppression (right) when compared to either Olaparib treatment (left) or PGAM1 suppression (center) alone.

In this study, the researchers tested the effects of Olaparib on the tumors formed by human breast cancer cells injected into mice.

Dr Gillian Farnie, whose work at the University's Institute of Cancer Sciences was funded by a five - year # 500,000 Breast Cancer Campaign Scientific Fellowship, said: «We know that cancer stem cells are able to avoid or repair damage caused by treaCancer Sciences was funded by a five - year # 500,000 Breast Cancer Campaign Scientific Fellowship, said: «We know that cancer stem cells are able to avoid or repair damage caused by treaCancer Campaign Scientific Fellowship, said: «We know that cancer stem cells are able to avoid or repair damage caused by treacancer stem cells are able to avoid or repair damage caused by treatment.

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.

This research has the potential to rapidly reduce breast cancer mortality by mimicking these mechanisms with new drugs and improving prediction of when cancerous cells will grow or metastasize.

The Nature Communications paper covers lung cancer cells; a similar phenomenon of collective invasion led by distinctive cells has been observed in breast cancer, but different genes and biochemical pathways appear to be important in each system.

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 canceBy 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 canceby 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 canceby which normal cells turn malignant in mammary epithelial tissues, the tissues frequently involved in breast cancer.

Many breast cancers are marked by a lack of HOXA5 protein, a gene product known to control cell differentiation and death, and lower levels of the protein correspond to poorer outcomes for patients.

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.

The study, published by the journal Proceedings of the National Academy of Sciences, demonstrates that the Disney lab's compound, known as Targaprimir - 96, triggers breast cancer cells to kill themselves via programmed cell death by precisely targeting a specific RNA that ignites the cancer.

Affecting about one breast cancer patient in four, it is characterized by tumor cells overexpressing a signaling protein called HER2.

Previous in vitro studies conducted by researchers in other countries showed that this molecule was able to reduce the multiplication and increase the mortality of cells from melanoma, the most aggressive type of skin cancer, as well as breast cancer and neuroblastoma, a tumor that typically affects patients aged 15 or younger.

Professor Howell, based at the Genesis Breast Cancer Prevention Centre at University Hospital of South Manchester, and at The University of Manchester, said: said: «At least 50 per cent of cancer risk is genetic, but activated cell stress signalling could potentially be reduced by dietary or lifestyle interveCancer Prevention Centre at University Hospital of South Manchester, and at The University of Manchester, said: said: «At least 50 per cent of cancer risk is genetic, but activated cell stress signalling could potentially be reduced by dietary or lifestyle intervecancer risk is genetic, but activated cell stress signalling could potentially be reduced by dietary or lifestyle intervention.

Across multiple triple - negative breast cancer subtypes, inhibiting the androgen receptor greatly increased apoptosis (programmed cell death), inhibited growth and increased necrosis by 60 percent in animal models.

Scientists, led by Ottar Rolfssonat the University of Iceland, have built a mathematical model to examine the metabolism of breast epithelium — as the majority of breast cancers originate from these cells.

Researchers have built a model to investigate the metastasis of cancer by examining the metabolism of breast epithelial cells and look at the role of signaling.

When the Cornell team cultured human breast cancer cells on matrix deposited by fat - derived cells from obese mice, the cancer cells grew faster than they did on the matrix of cells from slimmer mice.

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.

The identification of patients with high - risk breast cancer is key to knowing whether a patient will require only the removal of the tumor by surgery or whether if she will need additional chemotherapy to make sure the removal of breast cancer cells.

«We note that there are two subgroups of breast tumors by epigenome: one which we have called Epi - Basal, characterized by loss of epigenetic marks causing breakage of chromosomes and the other that we have called Epi - Luminal B, that presents epigenetic inactivation of genes that should protect us from cancer and these altered cells can no longer do it.»

By contrast, in triple negative breast cancer cells, the researchers discovered that Myc reduces the expression of TXNIP.

A metabolic pathway that is up - regulated in certain breast cancers promotes the disease's progression by activating a cell signaling protein called Arf6, according to a paper published in the Journal of Cell Biolcell signaling protein called Arf6, according to a paper published in the Journal of Cell BiolCell Biology.

Cancer biologist Joan Massagué of the Memorial Sloan - Kettering Cancer Center in New York City uncovered the new clues by studying breast cancer metastasis, in which malignant cells tend to spread to the bones and Cancer biologist Joan Massagué of the Memorial Sloan - Kettering Cancer Center in New York City uncovered the new clues by studying breast cancer metastasis, in which malignant cells tend to spread to the bones and Cancer Center in New York City uncovered the new clues by studying breast cancer metastasis, in which malignant cells tend to spread to the bones and cancer metastasis, in which malignant cells tend to spread to the bones and lungs.