Sentences with phrase «p53 is a tumor»

P53 is a tumor suppressor gene, a protein that regulates cell growth, and it is the most frequently mutated suppressor gene in cancer.

Not exact matches

Pregnancy's cancer - fighting effects may be due to a famous tumor inhibitor, p53.

Hence, a major goal of cancer scientists has been to develop drugs that prevent Mdm2 from binding to p53, and to thereby activate p53 to kill the tumor cell.

Using tumor samples from the Women's Healthy Eating and Living clinical trial, researchers identified stem - like tumor cells as being characterized by low levels of the molecule p53 upregulated modulator of apoptosis (PUMA).

Spalax naturally have a variant in the p53 gene (a transcription factor and known tumor suppressor), which is identical to a cancer - related mutation in humans, Band said.

Moreover, this approach was effective in treating mice with malignant colorectal cancer tumors containing Kras and p53 mutations, which are found in about half of colorectal tumors in humans.

One protein that keeps healthy cells from behaving this way is a tumor suppressor named p53.

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.

In this mouse model, mutations in Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different colors.

«These findings show that miR - 486 serves a tumor - suppressor function in lung cancer, and that miR - 486 action is partially dependent on p53.»

Importantly, it's secretion from normal cells can be induced by activating p53 so that Par - 4 enters circulation, thereby potentially targeting tumor cells at distant sites.

This switch is driven by p53, the well - documented tumor - suppressing protein.

These effects are partly mediated by tumor suppressor p53, which is frequently mutated in human cancers.

In a retrospective case study involving published data on p53, an important tumor suppressor protein, the team showed that this new resource called the Knowledge Integration Toolkit (KnIT) is an important first step in that direction, accurately predicting the existence of proteins that modify p53 — proteins that were subsequently found to do just that.

Because it more effectively induces cancer cell apoptosis in p53 - deficient tumors, FL118 is especially effective against late - stage cancers, which usually lose functional p53 and are resistant to DNA - damage drugs.

But mutations, which are found in 96 percent of patients with high - grade serous ovarian tumors, can cause p53 to form clumps, or «aggregates,» which impair the protein's normal function.

«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.

The scientists are planning further study of HOXA5's role in breast cancer, following up on this work and a study published by Sukumar's lab in 2000 that showed a connection between low levels of HOXA5 and the well - known tumor suppressor protein p53.

Pten is the most prominent human tumor suppressor after p53.

«Ninety percent of human tumors have chromosome abnormalities, and we know that many of these are made possible by mutations in p53,» says Holland.

Importantly, about 70 percent of LFS families have a mutation in their version of the gene TP53, which is the blueprint for protein p53, well known by the nickname «the tumor suppressor.»

«Most other tumors have a mutant p53, but in these testicular cell tumors, the p53 is functioning properly, and the drugs used for testicular cancer appear to work in concert with p53's tumor suppression function to kill the cancer cells.»

«This model, when combined with a rare genetic disease, revealed for the first time how a protein known to prevent tumor growth in most cases, p53, may instead drive bone cancer when genetic changes cause too much of it to be made in the wrong place.»

«Through further functional studies we found that myosin IIa is also required for activation of the main guardian of the genome — a tumor suppressor protein called p53.»

Mice that are unable to fully activate the powerful tumor suppressor p53 are resistant to high doses of radiation.

«If our predictions hold true, tumor cells with intact p53 may show the best response to therapy targeting the IGF - 1R signal; however, when p53 is not functioning normally, response to this therapy may not be as expected,» said Greenberg, the study's corresponding author.

«Restoring the tumor suppressor ability of p53 with a drug is paramount in anti-cancer drug development,» notes Carpizo, who is an associate professor of surgery and pharmacology at Rutgers Robert Wood Johnson Medical School.

The product of the p53 tumor suppressor gene is discovered independently by several groups: Lionel Crawford and David Lane; Albert Deleo and Lloyd Old; and Arnold Levine.

As such, tumors that retain normal p53 are more likely to respond to treatment while tumors carrying a defective p53 pathway are often less responsive,» says Wahl.

But when14 ARF was reintroduced in cells, p53 began functioning again and Onyx - 015 was no longer able to replicate in the tumor cells.

p53 (aka tumor protein 53) is a transcription factor whose inactivation can trigger the onset of cancer.

Although persistent loss of IGF - 1R expression ultimately induced cell stasis and death, both of these processes are regulated by the tumor suppressor gene p53 that is commonly mutated in human prostate cancers.

His team identified a factor that may be important for clinical trial design: progesterone was not toxic to all glioblastoma cell lines, and its toxicity may depend on whether the tumor suppressor gene p53 is mutated.

This could explain why, in about half of the breast tumors, including premalignant lesions, that the team studied at both UC San Francisco and at Sanford Burnham Medical Research Institute, when TGF - β1 signaling was highly activated, the levels of p53 were reduced, and vice versa - if the TGF - β1 pathway was reduced, there were high levels of p53.

This phenotype is reminiscent of the rich spectrum of spontaneous tumors developed by p53 - null and by p19ARF - null mice (36, 37, 38, 42, 43), albeit with a longer latency.

The tumor suppressor p53 is critical in the protection of cells against radiation - induced carcinogenesis, most likely through its ability to trigger apoptosis of radiation - damaged cells (45).

Efforts to combat the mutated p53 tumor suppressor gene with targeted drugs, for example, have so far been unsuccessful.

Therefore, mutation (s) in alternate reading frame protein dysregulate p53 function and play a role in tumor immune evasion.

It can be proposed that p21 contributes to mediate p53 - dependent tumor suppression in some tumor types, which would include histiocytic sarcomas, hemangiomas, B - cell lymphomas, and lung carcinomas, but not in other tumor types, particularly spontaneous or radiation - induced T - cell lymphomas.

Interestingly, p21 - deficient mice did not develop T - cell lymphomas, which is one of the most common tumor types in p53 - null mice (36, 37, 38).

However, says Korn, the new finding raises the possibility that the tumors in which p53 remained intact might have been defective in p14 ARF, and were, therefore, responding to Onyx - 015.

P21 is closely related to the tumor suppressor gene P53: cancer suppression and enhanced regeneration are frequently found to be opposite sides of the same coin.

«Our work supports the idea of exploring the use of Onyx - 015 in tumors that we presumed would be immune to the drug because they were thought to frequently have p53 genes, such as such as melanoma and glioblastoma [a form of brain cancer].

Because researchers later determined that the response to the combination therapy occurred both in tumors in which p53 was mutated and in which it was in tact, the finding left open the possibility that chemotherapy was the critical factor in the shrinking of tumors.

We conclude that p21 plays a significant role in tumor suppression, which is more important than that of Bax but weaker than that of p53 or its upstream regulators ATM and p19ARF.

Alternate reading frame protein (ARF) complexes with mouse double minute 2 homolog 2 (MDM2), an E3 ubiquitin ligase that regulates the stability of p53 and therefore suppressing tumor growth, it is also involved in the immune response, by modulating the tumor environment [46].

It is interesting to note that p21 - deficient mice did not develop T - cell lymphomas, which is one of the most common tumor types in p53 - null and p19ARF - null mice (36, 37, 38, 42, 43).

Another protein, P53 is a known tumor suppressor.

She chose the dynamics and function of the tumor suppressor protein p53, which plays a key role in cancer and is widely studied.

Several factors have been reported to induce the expression of p21waf1 / cip1 and the most important one is the tumor suppressor p53 (16).