Aromatase Inhibitors May Increase Risk of Heart Disease

Aromatase inhibitors—hormonal therapy drugs commonly used in the treatment of postmenopausal breast cancer—may increase the risk of heart disease. These results were presented at the 2010 San Antonio Breast Cancer Symposium.

Tamoxifen and aromatase inhibitors are hormonal therapy drugs that are commonly used in the treatment of hormone receptor-positive breast cancer. Both types of drugs slow or stop breast cancer growth by reducing the effects of estrogen on the breast.

Aromatase inhibitors include ArimidexR (anastrozole), FemaraR (letrozole), and AromasinR (exemestane). In studies that compared aromatase inhibitors to tamoxifen in postmenopausal women, aromatase inhibitors tended to be more effective against breast cancer recurrence. As a result, treatment guidelines recommend that postmenopausal women with hormone receptor-positive breast cancer consider using an aromatase inhibitor at some point in their course of treatment.[1]

Adverse effects of tamoxifen and aromatase inhibitors differ. Blood clots and endometrial (uterine) cancer are more common with tamoxifen, and bone loss is more common with aromatase inhibitors. Previous studies have also raised questions about the effects of aromatase inhibitors on the heart.

To further evaluate the issue of heart problems, researchers collected information from seven large clinical trials that compared tamoxifen with an aromatase inhibitor among postmenopausal breast cancer patients.[2]

Compared with tamoxifen, use of an aromatase inhibitor was linked with a 26% increase in risk of heart disease. This is not a large increase in risk, but the researchers speculated that the risk may be greater for women who have other risk factors for heart disease. In a second study conducted using data from health insurance plans, there did not appear to be an increased risk of cardiac disease among women taking aromatase inhibitors. ?

Unfortunately, it is not possible to determine at this time if aromatase inhibitors truly increase the risk of heart problems. ?Women are encouraged to discuss potential risks and benefits of all treatments with their physicians.

References:

[1] Burstein HJ, Prestrud AA, Seidenfeld J et al. American Society of Clinical Oncology Clinical Practice Guidelines: Update on adjuvant endocrine therapy for women with hormone receptor-positive breast cancer. Journal of Clinical Oncology. 2010; 28: 3784-3796.

[2] Amir E, Ocana A, Niraula S, Carlsson L, Seruga B. Toxicity of adjuvant endocrine therapy in postmenopausal breast cancer patients. Presented at the 33rd annual San Antonio Breast Cancer Symposium, December 8-12, 2010. Abstract S2-7.

View the original article here

Bladder Cancer Deserves Urgent Attention

Main Category: Urology / Nephrology
Also Included In: Cancer / Oncology
Article Date: 09 May 2013 - 2:00 PDT Current ratings for:
Bladder Cancer Deserves Urgent Attention

It is the 4th most common cancer in men[1] (and 11th in women), but bladder cancer remains an extremely low priority in the UK. Action on Bladder Cancer[2] (ABC) reports that almost half (45%) of the UK public do not know that even just one episode of blood in the urine, the most common warning sign, could mean bladder cancer. Smoking is the most common cause of bladder cancer and yet 95% of people are not aware of this. ABC calls for much stronger recognition of bladder cancer amongst the general public and the medical profession in order to prevent avoidable deaths.

ABC welcomes a recent paper[3] which highlights the paucity of clinical studies in bladder cancer compared with other cancers with a similar incidence. Well-designed randomised controlled trials usually provide the strongest evidence possible regarding the efficacy of new diagnostic tools or interventions and yet studies into bladder cancer are comparatively few and those that have been performed are under-utilised.

Dr Alison Birtle, Honorary Clinical Senior Lecturer & Consultant Oncologist, Preston; ABC Trustee and Chair of the NCRI Clinical Sub Group on Bladder Cancer says, "Bladder cancer is not just one disease. As our medical understanding is growing, we need to be tailoring information accordingly for patients, so that they receive sufficient information on their condition to be involved in making informed choices about their care options. The type of information that someone with low risk bladder cancer will need is very different from someone who has been diagnosed with very late stage disease."

A more robust framework of support is needed for all patients and ABC is supporting new initiatives to improve the lives of people with bladder cancer. One example is a new group being set up by NHS Lothian in South East Scotland with Maggies, Macmillan and SCAN (South East Scotland Cancer Network).

Mr Param Mariappan, Consultant Urologist, NHS Lothian and Regional Advisor to ABC says, "The focus of the South East Scotland Support Group is an 'out of hospital' service for those affected by bladder cancer to share and learn from others with similar experiences. Supplementing the care provided within the healthcare setting, this group is being established around a 'buddying system' and workshops specifically tailored to different states of the disease. Over and above what we do as Clinicians, extended care is critical for a patient with cancer. I term this CIS (Communication, Information and Support) - Our Support Group looks to bring individuals together who can help others likely to go through a similar experience of care."

Mr Brian Sibbald O.B.E. who has been affected by bladder cancer and involved in the beginnings of the Group says, "At the moment, because of my treatment, I don't have cancer, but I feel I am still on a journey. To me, it is important to find ways, such as a dedicated support group to share and reassure others who are more recently diagnosed with bladder cancer."

Over 10,000 people are diagnosed every year in the UK and ABC, the only UK charity dedicated to bladder cancer, wants to encourage more people to understand more about the disease. Up to date information on the disease and advice on how people can help raise awareness is available through the ABC website. The work of ABC supports the Be Clear on Cancer Campaign run by the Department of Health as well as Bladder Cancer initiatives organised throughout the US during May-July 2013.

Mr Colin Bunce, Chair of ABC and Consultant Urologist in Barnet says: "The profile of bladder cancer and, as a result, the care of patients can be significantly improved by asking the public and healthcare professionals and providers to become involved in our dedicated Charity, ABC - we want to work together".

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our urology / nephrology section for the latest news on this subject. 1) Cancer Research UK, Cancer Stats Key Facts, Bladder Cancer

2) GfK NOP Survey on bladder cancer for Action on Bladder Cancer, April 2012

3) Bassel et al. (2013). Demographic analysis of randomized controlled trials in bladder cancer. BJU International 111:3;419-426

Source: Action Bladder Cancer

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

ABC. "Bladder Cancer Deserves Urgent Attention." Medical News Today. MediLexicon, Intl., 9 May. 2013. Web.
13 May. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Bladder Cancer Deserves Urgent Attention'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

BRCA1-2 Mutations Increase Risk of Cancer in Opposite Breast

Among women with breast cancer, those with a BRCA1 or BRCA2 gene mutation are much more likely than other women to develop a second breast cancer in the opposite breast. These results were published in the Journal of Clinical Oncology.

Some women who have been diagnosed with breast cancer will eventually develop a second breast cancer in the opposite breast. This is referred to as a contralateral breast cancer. The risk of a second breast cancer among women who have already had breast cancer is higher than the risk of a first breast cancer among women in the general population.

A factor that may influence the risk of contralateral breast cancer is the presence of BRCA1 or BRCA2 gene mutations. Inherited mutations in these genes—which can be passed down through either the mother’s or the father’s side of the family—have been found to greatly increase the lifetime risk of developing breast and ovarian cancer.

To evaluate the relationship between BRCA1 or BRCA2 mutations and risk of a subsequent contralateral breast cancer, researchers conducted a study among more than 2,000 breast cancer patients, some of whom had been diagnosed with a contralateral breast cancer and some of whom had not. Women were only included in the contralateral breast cancer group if their contralateral cancer was diagnosed at least one year after their initial cancer. All of the women had been diagnosed with their first breast cancer before the age of 55.

All of the study participants were tested for BRCA1 and BRCA2 mutations.

Compared with women without a BRCA1 or BRCA2 mutation, risk of a subsequent contralateral breast cancer was 4.5 times higher among women with a BRCA1 mutation and 3.4 times higher among women with a BRCA2 mutation.

Among women with a BRCA1 mutation, a younger age at the time of initial breast cancer diagnosis increased the likelihood of a subsequent contralateral breast cancer.

Information about risk of a subsequent contralateral breast cancer may help guide breast cancer management among women with BRCA1 or BRCA2 mutations.

Reference: Malone KE, Begg CB, Haile RW et al. Population-based study of the risk of second primary contralateral breast cancer associated with carrying a mutation in BRCA1 or BRCA2. Journal of Clinical Oncology. [early online publication]. April 5, 2010.

View the original article here

Study Findings May Offer New Way To Kill Cancer Cells By Forcing Them Into An Alternative Programmed Death Pathway

Main Category: Cancer / Oncology
Also Included In: Genetics
Article Date: 16 May 2013 - 1:00 PDT Current ratings for:
Study Findings May Offer New Way To Kill Cancer Cells By Forcing Them Into An Alternative Programmed Death Pathway

When cells suffer too much DNA damage, they are usually forced to undergo programmed cell death, or apoptosis. However, cancer cells often ignore these signals, flourishing even after chemotherapy drugs have ravaged their DNA.

A new finding from MIT researchers may offer a way to overcome that resistance: The team has identified a key protein involved in an alternative death pathway known as programmed necrosis. Drugs that mimic the effects of this protein could push cancer cells that are resistant to apoptosis into necrosis instead.

While apoptosis is a tightly controlled procedure that breaks down and disposes of the dying cell in a very orderly way, necrosis is a messier process in which the cell's membrane ruptures and its contents spill out.

"People really used to think of necrosis as cells just falling apart, that it wasn't programmed and didn't require gene products to make it happen," says Leona Samson, a member of MIT's Center for Environmental Health Sciences and Koch Institute for Integrative Cancer Research. "In the last few years it has become more clear that this is an active process that requires proteins to take place."

In the online edition of the journal Genes and Development, Samson and colleagues report that a protein known as ALKBH7 plays a key role in controlling the programmed necrosis pathway. Dragony Fu, a former postdoc in Samson's lab, is the paper's lead author, and postdoc Jennifer Jordan is also an author.

Unexpected findings

ALKBH7 belongs to a family of proteins first discovered in E. coli about a dozen years ago as part of a DNA-repair mechanism. In humans, there are nine different ALKBH proteins, which Samson's lab has been studying for several years.

Most of the mammalian ALKBH proteins appear to be involved in DNA repair, similar to the original E. coli version. In particular, they respond to DNA damage caused by alkylating agents. These agents can be found in pollutants such as fuel exhaust and tobacco smoke, and are also used to treat cancer.

In the new paper, Samson, a professor of biology and biological engineering, and her colleagues found that ALKBH7 has an unexpected effect. When the researchers lowered ALKBH7 levels in human cells grown in the lab, those cells were much more likely to survive DNA damage than cells with normal ALKBH7 levels. This suggests that ALKBH7 actually promotes cell death.

"That was a surprising finding, because previously all of these ALKBH proteins were shown to be helping the cell survive when exposed to damage," says Fu, who is now a visiting research fellow at the University of Zurich.

Upon further investigation, the researchers found that when healthy cells suffer massive DNA damage from alkylating agents, they enter the programmed necrosis pathway. Necrosis, which can also be initiated by bacterial or viral infection, is believed to help the body's immune system detect threats.

"When dying cells release their contents during necrosis, it serves as a warning signal for your body that there is a virus there and recruits macrophages and other immune cells to the area," Fu says.

Potential drug targets

The findings suggest that when DNA is so badly harmed that cells can't repair it, the programmed necrosis pathway kicks in to prevent cells with major genetic damage from potentially become cancerous.

Other researchers have shown that some types of cancer cells have much lower ALKBH7 levels than normal cells. This suggests that the cancer cells have gained the ability to evade programmed necrosis, helping them to survive, Fu says.

The necrosis pathway appears to be initiated by an enzyme called PARP, which becomes hyperactive following DNA damage and shuts down the cell's production of two molecules that carry energy, ATP and NAD. The MIT team found that ALKBH7 prevents ATP and NAD levels from returning to normal by disrupting the function of mitochondria - the cell structures that generate energy for a cell.

Without an adequate supply of those critical energy-carrying molecules, the cell cannot survive and undergoes necrosis. In cells that lack ALKBH7, ATP and NAD levels rebound, and the cells survive, carrying a heavy burden of DNA damage.

The researchers are now investigating the molecular details of the programmed necrosis pathway in hopes of identifying ways to activate it in cancer cells.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. Written by: Anne Trafton, MIT News Office
The research was funded by the National Institutes of Health and the American Cancer Society.
Massachusetts Institute of Technology Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Massachusetts Institute of Technology. "Study Findings May Offer New Way To Kill Cancer Cells By Forcing Them Into An Alternative Programmed Death Pathway." Medical News Today. MediLexicon, Intl., 16 May. 2013. Web.
20 May. 2013. APA
Massachusetts Institute of Technology. (2013, May 16). "Study Findings May Offer New Way To Kill Cancer Cells By Forcing Them Into An Alternative Programmed Death Pathway." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/260555.php.

Please note: If no author information is provided, the source is cited instead.

'Study Findings May Offer New Way To Kill Cancer Cells By Forcing Them Into An Alternative Programmed Death Pathway'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Acupuncture Reduces Hot Flashes in Breast Cancer Patients

Among women treated with hormonal therapy for breast cancer, acupuncture and EffexorR (venlafaxine) were similarly effective at reducing the frequency of hot flashes. These results were published in the Journal of Clinical Oncology.

The majority of breast cancers are hormone receptor-positive. These cancers are stimulated to grow by the circulating female hormones estrogen and/or progesterone. Treatment of hormone receptor-positive breast cancer often involves hormonal therapies that suppress or block the action of estrogen. These therapies include tamoxifen (NolvadexR) as well as agents known as aromatase inhibitors. Tamoxifen acts by blocking estrogen receptors, whereas aromatase inhibitors suppress the production of estrogen in postmenopausal women.

Common side effects of hormonal therapy include hot flashes and night sweats. Antidepressants such as Effexor have shown some effectiveness in managing these symptoms but can produce side effects and may not be acceptable to all women.

Acupuncture is a form of traditional Chinese medicine that aims to improve health by stimulating specific points of the body. [1] Because acupuncture has shown some promise in reducing hot flashes in breast cancer patients, researchers conducted a study to compare it to Effexor. [2] The study involved 50 women with Stage 0-III breast cancer who were experiencing hot flashes during hormonal therapy. Half the women received acupuncture for 12 weeks, and half the women were treated with Effexor for 12 weeks.

Both groups (acupuncture and Effexor) experienced significant decreases in hot flash frequency. Acupuncture appeared to be as effective at reducing hot flashes as Effexor.By two weeks after completing treatment with acupuncture or Effexor, hot flash frequency increased in the Effexor group but remained at low levels in the acupuncture group.Side effects among women treated with Effexor included nausea, dry mouth, dizziness, and anxiety. Acupuncture did not produce any negative side effects.

These results suggest that acupuncture may be as effective as Effexor at reducing the frequency of hot flashes in breast cancer patients treated with hormonal therapy.

References:

[1] National Center for Complementary and Alternative Medicine. Acupuncture: An Introduction. Available at: http://nccam.nih.gov/health/acupuncture/introduction.htm. Accessed January 4, 2010.

[2] Walker EM, Rodriguez AI, Kohn B et al. Acupuncture versus venlafaxine for the management of vasomotor symptoms in patients with hormone receptor-positive breast cancer: a randomized controlled trial. Journal of Clinical Oncology [early online publication]. December 28, 2009.

View the original article here

How Nerve Wiring Self-Destructs Has Relevance To Diseases Of Peripheral And Central Nervous Systems

Main Category: Neurology / Neuroscience
Also Included In: Lymphoma / Leukemia / Myeloma;??Cancer / Oncology
Article Date: 13 May 2013 - 0:00 PDT Current ratings for:
How Nerve Wiring Self-Destructs Has Relevance To Diseases Of Peripheral And Central Nervous Systems

Many medical issues affect nerves, from injuries in car accidents and side effects of chemotherapy to glaucoma and multiple sclerosis. The common theme in these scenarios is destruction of nerve axons, the long wires that transmit signals to other parts of the body, allowing movement, sight and sense of touch, among other vital functions.

Now, researchers at Washington University School of Medicine in St. Louis have found a way the body can remove injured axons, identifying a potential target for new drugs that could prevent the inappropriate loss of axons and maintain nerve function.

"Treating axonal degeneration could potentially help a lot of patients because there are so many diseases and conditions where axons are inappropriately lost," says Aaron DiAntonio, MD, PhD, professor of developmental biology. "While this would not be a cure for any of them, the hope is that we could slow the progression of a whole range of diseases by keeping axons healthy."

DiAntonio is senior author of the study that appears online in the journal Cell Reports.

While axonal degeneration appears to be a major culprit in diseases like multiple sclerosis, it also paradoxically plays an important role in properly wiring the nervous systems of developing embryos.

"When an embryo is building its nervous system, there can be inappropriate or excessive axonal sprouts, or axons that are only needed at one time in development and not later," DiAntonio says. "These axons degenerate, and that's very important for wiring the nervous system. And in adult organisms, it might be useful to have a clean and quick way to remove a damaged axon from a healthy nerve, instead of letting it decay and potentially damage its neighboring axons."

DiAntonio compares the process to programmed cell death, or apoptosis, which is also important in embryonic development. Apoptosis culls unnecessary or damaged cells from the body. If cell death programs become overactive, they can kill healthy cells that should remain. And if apoptosis fails to destroy damaged cells in adults, it can lead to cancer.

The new discovery also underscores the relatively recent understanding that loss of axons is not a passive decay process resulting from injury. Just as apoptosis actively destroys cells, axonal degeneration results from a cellular program that actively removes the damaged axon. In certain diseases, the program may be inappropriately triggered.

"We want to understand axonal degeneration at the same level that we understand programmed cell death, in the hopes of developing drugs to block the process when it becomes overactive," DiAntonio says.

DiAntonio's major collaborators in this project include Jeffrey D. Milbrandt, MD, PhD, the James S. McDonnell Professor and head of the Department of Genetics, and first author Elisabetta Babetto, PhD, postdoctoral research scholar.

Studying mice, the researchers found that a gene called Phr1 plays a major role in governing the self-destruction of injured axons. When they removed Phr1 from adult mice, the severed portion of the axons remained intact for much longer than in genetically normal mice.

In the normal mice, a severed axon degenerated entirely after two days. In mice without Phr1, they found that about 75 percent of the severed axons remained at five days, with a quarter persisting at least 10 days after being cut. The mice showed no side effects and suffered no obvious problems due to the missing Phr1.

The findings raise the possibility that blocking the Phr1 protein with a drug could keep damaged axons alive and functional when the body would normally cause the axons to self-destruct.

DiAntonio emphasizes that he is not trying to save axons that have no connection to the rest of the nerve. The paradigm is simply a good way to model nerve injury. In many instances, such as a crush injury or disease processes in which the axon is not severed, blocking the Phr1 protein could potentially preserve an attached axon that would otherwise self-destruct.

Importantly, the research team also looked at optic nerves of the central nervous system, which are damaged in glaucoma, and found similar protective effects from the loss of Phr1.

"This is not the first gene identified whose loss protects mammalian axons from degeneration," DiAntonio says. "But it is the first one that shows evidence of working in the central nervous system. So it could be important in conditions like glaucoma, multiple sclerosis and other neurodegenerative diseases where the central nervous system is the primary problem."

DiAntonio also points out possible ways to help cancer patients. Many chemotherapy drugs cause damage to peripheral axons, which may limit the doses a patient can tolerate.

As part of the new study, the researchers showed that intact axons without Phr1 were protected from the damage caused by vincristine, a chemotherapy drug used to treat leukemia, neuroblastoma, Hodgkin's disease and non-Hodgkin's lymphoma, among other cancers.

"In this case, the loss of axons is not caused by disease," DiAntonio says. "It's caused by the drug doctors are giving. You know the date it will start. You know the date it will stop. This is probably where I am most optimistic that we could make an impact."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our neurology / neuroscience section for the latest news on this subject. This work was supported by the American-Italian Cancer Foundation, the European Molecular Biology Organization, the Muscular Dystrophy Association and the National Institutes of Health (NIH) grant numbers DA020812, NS065053 and NS078007.
Babetto E, Beirowski B, Russler EV, Milbrandt J, DiAntonio A. The Phr1 ubiquitin ligase promotes injury-induced axon self-destruction. Cell Reports. May 9, 2013.
Washington University School of Medicine Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Washington University School of Medicine. "How Nerve Wiring Self-Destructs Has Relevance To Diseases Of Peripheral And Central Nervous Systems." Medical News Today. MediLexicon, Intl., 13 May. 2013. Web.
13 May. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'How Nerve Wiring Self-Destructs Has Relevance To Diseases Of Peripheral And Central Nervous Systems'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Cancer-Suppressing Protein Found To 'Multitask'

Categorie principale : Cancer / oncologie
Egalement inclus dans : genetique
Date de l'article : 13 mai 2013 - 1:00 PDT courants nominaux pour :
Proteine suppresseur du cancer avere ? Multitache ?

La comprehension de la facon dont une puissante proteine appelee p53 protege contre le developpement du cancer a ete bouleversee par une decouverte par des chercheurs de l'Institut Walter et Eliza Hall.

Plus de la moitie des cancers humains portent des defauts dans le gene p53, et presque tous les autres cancers, avec un gene p53 normal, transporter d'autres defauts qui en quelque sorte portent atteinte a la fonction de la proteine p53. Herite de mutations du gene p53, mettre les gens a un tres haut risque de developper une gamme de cancers.

Fonctions de la proteine p53 sont normalement stimulees par potentiellement cancerigenes des evenements, tels que les dommages a l'ADN de rayonnement ultraviolet (une cause de cancer de la peau), ou la sur-activite des cancerigenes genes.

Mme Liz Valente, Dr Ana Janic et professeur Andreas Strasser de la division de genetique moleculaire du Cancer a l'Institut Walter et Eliza Hall ont ete disseque les processus controles par p53, pour decouvrir comment cette proteine peut supprimer le developpement du cancer. Leurs resultats surprenants sont publies en ligne dans la revue Cell Reports.

Dr Janic a dit que beaucoup de scientifiques croyait que les plus importants processus actives par p53 afin d'empecher la formation de cancer etaient arret cellules avec alteration de l'ADN de se diviser jusqu'a ce que l'ADN pouvait etre repare et rendant les cellules meurent s'ils avaient subi des dommages genetiques irreparable.

? Changements qui rendent les cellules endommagees deviennent longue duree de vie et de diviser de maniere incontrolee sont caracteristiques principales de la formation de cancer ?, a declare le Dr Janic. "Parce que p53 peut controler la survie cellulaire et la division cellulaire, on a suppose que ces deux processus constituaient les fonctions essentielles que p53 utilise pour prevenir le cancer. Le but de notre recherche etait d'examiner si cette hypothese etait correcte".

Mme Valente dit les cellules contre l'equipe qui n'avait pas de p53 avec cellules dans lequel p53 ne pouvait pas regler la survie cellulaire et la division cellulaire. "Dans les 20 dernieres annees qu'il est devenu clair quelles les proteines sont activees par p53 de bloquer la division cellulaire et de promouvoir la mort cellulaire,", a declare Mme Valente. "Nous avons pu supprimer tous ces proteines (appelees p21, Puma et Noxa) de cellules, de desactiver completement la possibilite de la p53 d'arreter la division cellulaire et declencher la mort des cellules. A notre grande surprise, p53 pourrait encore empecher la formation de cancer, meme sans etre en mesure de fabriquer des cellules meurent ou arreter divisant apres des dommages a l'ADN."

Professeur Strasser dit decouverte de l'equipe avait bouleverse la comprehension de la facon dont les fonctions p53. ? Lorsque le p53 suppresseur du cancer fonction a ete decouvert, qu'il etait important de comprendre le fonctionne de cette proteine, ? dit-il. ? Beaucoup de scientifiques avait conclu ce reglement de la division et la mort cellulaire ont ete les roles cles de p53, ? dit-il.

"Nos resultats ont rouvert la question de savoir comment les fonctions de p53. Mon soupcon est que ce n'est pas une proteine mais plusieurs avec de tres nombreuses fonctions critiques qui travaillent ensemble pour prevenir la formation de cancer par coordonner la bonne reparation de l'ADN endommage, plutot que de s'arreter de diviser ou de tuer les cellules. Autres recherches a dechiffrer comment ces processus sont integres sera une etape importante dans la comprehension de la fonction de suppresseur de tumeur p53 fonction. Ces connaissances, a son tour, puis peuvent etre exploitees pour developper des traitements ameliores,"a declare le professeur Strasser.

Article adapte par Medical News Today de communique de presse original. Cliquez sur ? references ? onglet ci-dessus pour la source.
Visitez notre cancer / oncologie section pour les dernieres nouvelles sur ce sujet. La recherche a ete financee par l'Australian National Health et Medical Research Council, la leucemie et Lymphoma Society (Etats-Unis), Cancer Council Victoria, The Lady Tata Memorial Trust, la bourse de Beatriu de Pinos (Union europeenne/Espagne) et le gouvernement de Victoria.
Walter et Eliza Hall Institute s'il vous plait utilisent un des formats suivants pour citer cet article dans votre essai, le papier ou le rapport :

MLA

Institut Walter et Eliza Hall. ? Proteine suppresseur du Cancer avere ? Multitache ?. ? Nouvelles medicales aujourd'hui. MediLexicon, aeroport international, 13 mai. 2013. Web.
13 Mai. 2013. APA

Veuillez noter : si aucune information de l'auteur est indiquee, la source est citee a la place.

? Proteine suppresseur du Cancer avere ' multitache ''

Veuillez prendre note que nous publions votre nom, mais nous ne publions pas votre adresse email. Il est seulement utilise pour vous avertir lorsque votre message est publie. Nous ne l'employons pas a d'autres fins. S'il vous plait voir notre politique de confidentialite pour plus d'informations.

Si vous ecrivez sur des medicaments specifiques ou les operations, s'il vous plait ne sont pas professionnels de la sante du nom par nom.

Tous les avis sont moderes avant d'etre inclus (pour arreter le spam)

Contactez nos redacteurs de News

Pour toutes les corrections d'informations factuelles, ou pour communiquer avec les editeurs, veuillez utiliser notre formulaire de commentaires.

Veuillez envoyer toute nouvelles medicales ou communiques de sante de presse a :

Note: des renseignements medicaux publies sur ce site ne sont pas concus comme un substitut a un avis medical eclaire et vous devriez prendre pas toute action avant de consulter des soins de sante professionnels. Pour plus d'informations, veuillez lire nos termes et conditions.

View the original article here