Sentences with phrase «finds tumor gene»

«Machine learning finds tumor gene variants and sensitivity to drugs in The Cancer Genome Atlas.»

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However, the impact of the two methylation - regulating enzymes was still seen at 10 to 15 months, when scientists found decreased expression of hundreds of genes — many of which are key tumor suppressor genes such as BMP3, SFRP2 and GATA4 — in the smoke - exposed cells and a five - or - more-fold increase in the signaling of the KRAS oncogene that is known to be mutated in smoking - related lung cancers.

However, no mutations were found in the KRAS gene itself or the tumor suppressor genes during the 15 - month period of cigarette smoke exposure.

After EZH2 enzymes rise, their levels taper off, and then, the scientists found two to three-fold increases in a protein called DNMT1, which maintains DNA methylation in the «start» location of a variety of tumor suppressor genes that normally suppress cell growth.

Teixeira and his team also found that a malfunctioning tumor - suppressing gene that's associated with certain cancers, such as colon and pancreatic, and is known as Stk11, additionally influenced the development of BPH.

«Combination therapy strengthens T cells in melanoma pre-clinical study: Findings have implications for treating tumors lacking tumor suppressor gene PTEN.»

Their analysis of more than 4,000 individual tumor cells, the largest effort to date in brain tumors, finds three developmental categories of cancer cells — one resembling neural stem cells and two characterized by sets of genes indicting paths towards differentiation.

She and her colleagues sequenced genomic DNA in the tumor samples but did not find any new driver gene mutations in the metastatic samples compared to the primary tumor samples, said McDonald, who completed clinical training under Iacobuzio - Donahue at Johns Hopkins.

«Genes may cause tumor aggressiveness, drug resistance in African - American prostate cancer: Research found many targeted therapies for prostate cancer may not be effective against tumors in African - American men.»

Now, researchers studying mice have found one of the most powerful tumor suppressor genes yet — animals lacking it have a startling 50 % chance of developing cancer.

Mutations in the gene BRAF are the most common mutation found in melanoma, with up to 50 percent of tumors testing positive for the mutations.

The findings provide proof of principle that restoring the function of a single tumor suppressor gene can cause tumor regression and suggest future avenues for developing effective cancer treatments.

PTEN prevents tumor cells from growing uncontrollably, and mutations in the gene encoding this protein are commonly found in many different types of cancer.

However, cancer cells may instead be coaxed to turn back into normal tissue simply by reactivating a single gene, according to a study that found that restoring normal levels of a human colorectal cancer gene in mice stopped tumor growth and re-established normal intestinal function within only 4 days.

Another found gene is linked to angiogenesis, the production of new blood vessels to support a tumor.

For example, if scientists can find a way to turn down overexpression of these genes in cancer, we could disrupt cancer growth and prevent tumor progression.

«These findings underscore the significance of Gcn5 - regulated gene expression coupled with the metabolic enzyme alpha - KGDH in tumor cell proliferation and formation.»

Scientists knew Apc was involved in stifling tumor formation because most colon cancers find a way to turn the gene off.

The researchers conducted genetic tests and found that many of the tumor cells had a mutation in a gene called PPM1D, which causes cells to proliferate and avoid natural death.

Gene therapy researchers have found that a popular viral vector used to insert disease - curing genes into mice has a dangerous down side: it can apparently trigger liver tumors.

A study published in Molecular Cancer Research reveals that a tumor suppressor gene p16 is turned off by a histone mutation (H3.3 K27M), which is found in up to 70 percent of childhood brain tumors called diffuse intrinsic pontine glioma (DIPG).

The researchers further found that miR - 486 is itself regulated by the tumor - suppressor gene p53, the most frequently altered gene in human cancers, and that activity of miR - 486 is partially dependent upon functional p53.

Upon sequencing the DNA, they found that DNA fragments containing mutated genes — markers of tumors — were typically smaller than healthy versions of the gene from within the same patient.

If such an indel is found in this gene, Ding and her colleagues suggest a patient may benefit from an EFGR inhibitor, such as erlotinib, regardless of the tumor type.

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.

Using a fluorescent protein to detect Rgs16 expression, the investigators found that this gene is induced by pancreatic tumor formation starting from its earliest manifestation as ductal neoplasm all the way to advanced solid tumor in a spatially and temporally coincidental manner.

H3.3 has been found attached to chromatin sections containing tumor growth - promoting genes, or oncogenes, suggesting it helps suppress their activity.

To validate their findings, the scientists injected the novel nanoparticles into pancreatic tumor - bearing mice and observed that by balancing these two targets — bringing them to a normal level by increasing their expression or blocking the gene responsible for their expression — they significantly prolonged the survival of the mice.

All the fish had the human cancer mutation BRAFV600E — found in most benign moles — and had also lost the tumor suppressor gene p53.

In recent studies of cancer patients who received a bone marrow transplant, genes from the marrow's white blood cells were found in the patient's tumor cells.

They found that ONC201 alters the gene expression of cancer stem cell markers and signaling pathways prior to killing the tumor cells, providing pharmacodynamic biomarkers of response.

A new method has been found for identifying therapeutic targets in cancers lacking specific key tumor suppressor genes.

The finding warrants research into adding drugs that could prevent the cancer from hijacking patients» repressive gene regulatory machinery, which might allow the original therapy to work long enough to eradicate the tumor, the researchers report in their National Institutes of Health - funded study, published in the current issue of Science Translational Medicine.

For example, drugs that target a specific BRAF gene mutation commonly found in melanoma shrink tumors in about half of patients with the mutation.

Both Tsigelny and Kurzrock agreed that this finding is an excellent example of the power of collaboration between SDSC and the Moores Cancer Center, and that such modeling needed to be studied across tumors and with multiple different genes involved in cancer.

The new findings could help physicians prescribe the most effective treatments for each patient based on how genes are activated in the individual tumor.

«These findings raise the possibility that by determining the gene expression profile of a patient's tumor, physicians may be able to identify aggressive disease at the outset of diagnosis and start treatment earlier,» said Sungyong You, PhD, an instructor in the Cedars - Sinai Department of Surgery and the first author of the study.

A significant finding by the team was that either the mutant KRAS gene or another cancer gene is amplified, depending on which tumor suppressor gene is affected and to what degree its function is impaired.

Surprisingly, they found that although the patterns of gene expression — as shown by the RNA sequencing — differed between the hepatocellular carcinomas and the liver cancers with biliary phenotype and depended on the histological type, the overall pattern of mutations in the cells was actually similar between the tumors — of either type — that had emerged in patients who had had infections with either hepatitis C or B, and were different in patients without such infections.

A comprehensive genomic analysis of Wilms tumor — the most common kidney cancer in children — found genetic mutations involving a large number of genes that fall into two major categories.

«While we expected to find some mutations in stem cell lines, we were surprised to find that about five percent of the stem cell lines we analyzed had acquired mutations in a tumor - suppressing gene called p53,» said Merkle.

Another key finding was observing the inhibitor effect on tumor models with a gene PTEN deficiency as a biomarker — of huge interest because PTEN, a tumor suppressor, is known to be defective in as many as half of all advanced solid tumor cancers.

Researchers at The Rockefeller University have shown that a new technique using RNA interference is able to find genes that cause epidermal tumor growth in months rather than the decades it may take using traditional methods employing specially bred, genetically altered mice.

Furthermore, higher levels of LAPTM4B, a gene that has been found in liver, lung, breast, ovarian and gastric cancers, were found in airways closer to tumors.

Knocking down the expression of either the fruit fly version of the FOXD1 gene or the fruit fly version of ALDH1A3 blocks the formation of brain tumors in a brain cancer model of the fruit fly species Drosophila melanogaster, the researchers found.

«And we found all three types of «gain - of - function» mutations in the estrogen receptor gene ESR1 in the tumor samples.»

It is known that the genes that accumulate the most mutations are linked to the tumor type, and we found this too, however we showed that the mutational spectrum of a tumor is determined by breed type,» says Dr. Ingegerd Elvers, a researcher with Professor Kerstin Lindblad - Toh at both Uppsala University and Broad Institute.

Researchers found the gene therapy approach had stronger results when used in combination with either depletion of immunosuppressive cells from the tumor mass or with immune checkpoint blockade.

In the Oncogene study, the research team found key distinctions in how these mutated genes give rise to PLGGs, a varied group of cancers that collectively account for the most common brain tumor in children.

After sequencing the tumor samples, the authors found that the JAK2 gene was more frequently amplified in chemotherapy - treated TNBC than in tumors before treatment.