Do You Know Oolong Tea Could Be A Precautionary Remedy For Most Cancers?

Vorteile der Oolong-Tee werden bereits seit Jahrtausenden von gemeinsamen chinesische Medizin anerkannt. Vorliegenden aktuellen Western holt Medizin auf. Mit Hilfe von Antioxidantien, Vitaminen und Mineralstoffen, Oolong-Tee ist wirklich zuverlassig zur Verhinderung von Tumoren. Untersuchungen behauptet Nationen mit grosere Populationen von Tee-Liebhaber, erhalten Sie eine uber-All viel Wahrscheinlichkeit geringeren, dass Krebs.

Nationale wissenschaftliche Untersuchungen haben ergeben, dass die Frauen, die junger als 50, die tranken Tee, Chance, Brustkrebs um 37 % zuruckgegangen. Forscher in China ergab, dass die Moglichkeit der Prostata Art von Krebs Tee trinken reduziert werden. In China vermindert ein weiteres Forschungsprojekt mit 1000 Freiwillige, mit Tee bestimmt die Moglichkeit der Eierstock Tumor.

Oxidation ist eigentlich ein naturlicher Prozess unseres eigenen Korpers. Altere Zellen sind ausgeloscht, um Raum fur Wachstum und Entwicklung der brandneuen Korperzellen zu liefern. Dennoch, wenn die Mechanismen zur Oxidation unausgewogen sind, erhohen freie Radikale im Korper. Umgebungsvariablen fur Beispiel Luftverschmutzung sowie Zigaretten, produzieren eine Unwucht, Zucht von freien Radikalen. Freie Radikale Gewebe konnen sehr gut ungesund sein, die eine normale Zelle zu helfen, sich selbst zu reparieren beschadigen konnen.

Dieser Trend wird abgerissen Korperzellen mit dem Eimer, gleichzeitig irrefuhrende Hinweise auf unseren Oxydation-Kurs buchen. Es kommt zu dieser Art von gestorter Zellen dieser Kick-Start der Korper in gesunde Zellen einzudringen oder in einem anderen Begriff, Krebs.

Oolong-Tee bietet Ihnen gute naturliche Antioxidantien, die Polyphenol, Tee Gerbstoffe, Catechine und auch Flavonoide enthalt. Diese Art von Antioxidantien neutralisieren uberreizt Oxidation und auch detox Ihren gesamten Korper von freien Radikalen, folglich abnehmender zellulare Probleme durch freie Radikale und geben viel mehr Platz fur das Gewebe gesund und ausgewogen. Oolong-Tee besteht aus Mengen an Vitamin C und E. Diese Vitamin-Erganzungen konnen Formationen der krebsartigen Nitrosamine anhalten.

Nitrosamine sind normalerweise in verarbeiteten Produkten gefunden, die wir konsumieren. Vitamin C ist eine effektive Ascorbinsaure, wahrend Alpha-Tocopherol e Vitamin ein Antioxidans ist. Als Ganzes diese Ernahrung tendenziell gefunden werden, um die Fahigkeit, Form Nitrosamine Einhalt zu Gebieten. Oolong-Tee fordert Ihre Gesundheit, durch Reinigung des gesamten Korpers aus Zelle zerstoren freie Radikale wahrend behindern Nitrosamine mithilfe von Vitamin C und E, daher starke Anti-Krebs-Funktionen geben.

Oolong-Tee ist nicht nur gros, verbrauchen, Sie werden feststellen, dass es wunderbar fur den Korper ist. Wissenschaft hat bewiesen, Tees sind gesund fur Ihr Wohlbefinden, aber Oolong-Tee ist besser als vorsorgliche Heilmittel fur die meisten Krebsarten. Hier finden Sie vier Arten von Krebs-Bekampfung Oolong-Tee, alle bestehend aus dieselben gesundheitlichen Vorteile, nur mit einem abwechslungsreichen Hauch von Geschmack. Eisen Buddha, eines der besten chinesischen Oolong oder Tie Guan Yin, ist eine beliebte Wahl, aufgrund seiner blumiger Duft und susen Geschmack.

In den nachsten paar Artikeln werde ich weiterhin uber andere gesundheitliche Vorteile von Oolong-Tee, einer der beruhmtesten Tee in China gehen. Es ist wirklich diesen Tag immer beliebt. Ich hoffe, Sie konnen bei mir bleiben und diese naturliche Gabe zu erkunden. Fur weitere Informationen besuchen Sie bitte meine Website: OolongTeaCommuntiy.Com

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700 Women with urinary Cancers missing out on prompt diagnosis each year

Main category: Urology / Nephrology
Also included in: Cancer / Oncology;??Women's health / Gynecology
Article Date: June 25, 2013-0:00 PDT current ratings for:
700 Women with urinary Cancers missing out on prompt diagnosis each year

Family physicians can be attributing symptoms of cancer of the bladder and kidneys, causes harmless

About 700 women in England with the symptoms of cancer of the kidney or bladder are missing out on a fast diagnosis and treatment of their condition, each year, research reveals in the journal online only BMJ Open.

It may be because of family physicians tend to give women, rather than men - first symptoms benign causes, such as bacterial infections and some women therefore need to visit their doctor several times before they are referred to a specialist, i.e. researchers.

Currently, the survival rates for cancer of the kidney and bladder in England show that fewer women than men living five years after diagnosis.

The researchers studied the numbers of patients diagnosed as cancer of the kidney and the bladder in England between 2009 and 2010. They used data from the National Audit of the diagnosis of Cancer in Primary Care, covering general practices representing 1170 - equivalent to about 14% of the total national. They studied two interrelated measures of the speed of diagnosis: the number of consultations, the patient is before he transferred. and the time interval between the first visit to the GP with symptoms and specialist referral.

In total, 920 patients have been diagnosed with cancer of the bladder during the study period, 252 (27%) were women; and 398 have been diagnosed with cancer of the kidney, 165 (42%) were women. These proportions are similar to national figures: 28% and 38%, respectively.

Women were nearly twice as likely than men to have consulted their doctor three or more times, before they were referred to a specialist, the analysis showed.

About one in ten (11%) men with bladder cancer had three or more visits before referral, compared to 27% of women. The corresponding figures for the kidney cancer were 18% and 30%.

The interval between the first GP consultation mean and specialist orientation is a not differ greatly between men and women - four against six days for bladder cancer and 10 to 16 days for kidney cancer. But among the 25% of women experiencing more delays, it took two more weeks to get referred that the 25% of men with longer deadlines. When this has been reduced to 10% of those who know longer delays, the figure rose to more than two months for women with bladder cancer and more than three weeks for those who have cancer of the kidney, compared with men.

Two-thirds of all patients with cancer of the bladder and a quarter of people with kidney cancer had blood in their urine (Hematuria), a symptom of the red flag for further investigation.

But the presence or absence of this symptom could not explain the difference between the sexes in the period of reference, the analysis said.

Even when they came to see their doctor with hematuria, women with bladder cancer were more than three times as likely to have three or more visits GP before the switch compared to men with the same symptom.

And women with kidney cancer were almost twice as likely as men to discover three or more consultations, when he had blood in their urine.

As nearly 3,000 women are diagnosed every cancer each year in England, the authors calculate that about 700 women will experience delays in diagnosis.

Reinforce the need to follow the guidelines and view the blood in the suspicious urine could encourage GPs to guide women faster, but it will not help in cases where this symptom is not present, warn the authors, requiring new approaches to address this problem.

"Great potential to improve the speed of diagnosis of cancer of the urinary tract in women, the conclusions of signals", the authors write. "Interventions to prevent the initial allocation of hematuria in women with cancer of the urinary tract to cause benign [GPs] must be quickly developed and evaluated," they urge.

Article adapted by Medical News Today press release original. Click on "references" tab above for the source.
Visit our Urology / Nephrology section for the latest news on this subject. "Gender inequalities in the promptness of the bladder and the kidney after symptomatic presentation: evidence from secondary analysis of a survey of primary care English checking ',
Georgios Lyratzopoulos et al.
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A Wide Variety Of Advanced Cancers Harbor Abnormalities In HER2 Gene

Main Category: Cancer / Oncology
Also Included In: Genetics
Article Date: 04 Jun 2013 - 1:00 PDT Current ratings for:
A Wide Variety Of Advanced Cancers Harbor Abnormalities In HER2 Gene

The HER2 growth-factor gene is known to be over-active in breast and gastro-esophageal cancers. But now, irregularities in the genes 's expression - among them mutations, amplifications, substitutions, and translocations - have been found in 14 different advanced solid tumors.

The results of the study of more than 2,000 tumors, presented at the annual meeting of the American Society of Clinical Oncology (ASCO), both surprised researchers and provided hope that some of these tumors might benefit from the three anti-HER2 therapies now in clinical use.

"No one ever thought that there would be such a variety of genomic alterations in HER2 in this many solid tumors," says Massimo Cristofanilli, MD, FACP, Professor of Medical Oncology and Director of the Jefferson Breast Center at the Kimmel Cancer Center and Thomas Jefferson University Hospital.

"But this may be good news, both clinically and scientifically," he says. "It tells us that these tumors might benefit from treatment that we already have on hand, and, from a research perspective, it builds on the idea that it is the genomic profile of a tumor that is relevant in providing biological information for planning of personalized treatments - not where the cancer is located or where it develops.'

Dr. Cristofanilli presented the results of the study in an oral presentation at the ASCO meeting. He is one of a group of co-authors from many institutions who donated tumor samples to Foundation Medicine, a cancer diagnostics company in Cambridge, Massachusetts. Foundation Medicine led and paid for the study.

Dr. Cristofanilli contributed about 50 metastatic breast tumor samples for the analysis, and found out that one of his patients with advanced triple negative breast cancer had a HER2 mutation. "My patient was treated with Herceptin as well as chemotherapy, and derived clinical benefit," he says. "No one looks for HER2 mutations in this form of breast cancer. To me, this makes the case for the value of genome-driven therapy."

In the study, Foundation Medicine conducted a genetic screen of more than 182 genes and 14 genetic rearrangements known to be linked to cancer in 2,223 tumor specimens. Twenty different advanced solid cancers were represented.

Researchers found HER2 alterations in 14 types of solid tumors, including 29 percent of esophageal, 20 percent of uterine, 14 percent of breast, 12 percent of stomach carcinomas, and 6 percent of all lung cancer samples.

They also found HER2 irregularities varied widely - 4.9 percent of specimens had 116 different HER2 alterations. That included 58 percent with amplifications, 25 percent with substitutions, 14 percent with indels (insertions/deletions of DNA), 2 percent with splice site variants, 2 percent with translocations, 5 percent with multiple alterations, and 2 tumors had both HER2 substitution and amplification.

Anti-HER2 therapies such as Herceptin can also treat HER2 mutations, and may also help block HER2 that is altered in the ways seen in the study, Dr. Cristofanilli says.

"This study highlights the need to study a broad range of genes at a high level of sensitivity and specificity when searching for novel targets of therapy," he says. "Widespread use of this approach could provide more treatment options and enable more rapid accrual to ongoing and planned trials of agents targeting pathways under study."

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. Dr. Cristofanilli declares no conflicts of interest related to this study.
Thomas Jefferson University Please use one of the following formats to cite this article in your essay, paper or report:

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posted by John M. on 4 Jun 2013 at 11:37 am

I often think of cancer as a disease where the body doesn't attack its own tissue and autoimmune diseases as a disease where it attacks it too much. So it occurs to me that like cancer maybe some autoimmune diseases of different organs may be caused by the same underlying genetic mutation and therefore you could determine if drugs that treat one type of autoimmune disease might treat others . . .

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'A Wide Variety Of Advanced Cancers Harbor Abnormalities In HER2 Gene'

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HER2 Abnormalities Found In Many Advanced Cancers

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Main Category: Cancer / Oncology
Also Included In: Genetics
Article Date: 03 Jun 2013 - 3:00 PDT Current ratings for:
HER2 Abnormalities Found In Many Advanced Cancers

We already know that an over-active HER2 growth factor gene features in breast and gastric cancers. Now a new study reports finding mutations and other abnormalities of the gene in 14 different advanced cancers.

Massimo Cristofanilli, Director of the Jefferson Breast Center at the Kimmel Cancer Center and Thomas Jefferson University Hospital, announced the study results at an oral presentation during the annual meeting of the American Society of Clinical Oncology (ASCO), which is taking place in Chicago until Tuesday.

The gene for human epidermal growth factor receptor 2 (HER2) codes for a protein that promotes the growth of cancer cells. In around 1 in 5 breast cancers, a mutation in the gene causes cancer cells to make too much HER2 protein. The same mutation and the higher protein levels that result, occur in many types of cancer.

But Cristofanilli's results suggest there may be several kinds of gene alteration that can have this effect: not just known mutations but also other irregularities such as amplifications, substitutions, and translocations.

Cancer is essentially a disease of failure to regulate tissue growth. It is when the genes that regulate normal cell growth become altered in some way that the cell becomes cancerous.

Every time a cell divides, the enormous amount of data contained in its genetic material is replicated. When this happens, the chances are that some errors (mutations) will occur. Cells have complex mechanisms to prevent and correct such errors. And even if the faulty cell survives, there is another process, cell suicide or apoptosis, that the body uses to deal with rogue cells.

But if all these error controls fail, then the mutations and alterations survive and are passed on to daughter cells, to sow the seeds of a tumor.

Large-scale mutations occur when a large portion of genetic material is deleted or an extra portion is added. Amplification is when a cell gains many copies of genetic material, usually containing genes known to be cancer-causing. Translocation is when two separate regions become fused.

Small-scale mutations such as point substitutions, deletions and insertions are alterations to the building block units of DNA. For instance, a substitution is a mutation that exchanges two letters of the DNA code, like changing the spelling of a word by swapping around two of its letters.

Small-scale mutations usually affect the expression of a gene and alter the function or stability of the protein it codes for.

There are also other ways genes can change to make cells cancerous, such as when viruses insert bits of their DNA into the genetic material of the host cell, causing, for example, switched off cancer genes to switch on.

In this new study, which examined more than 2,000 tumors, Cristofanilli, a professor of Medical Oncology, and colleagues, found HER2 gene irregularities in 14 different advanced solid tumors.

"No one ever thought that there would be such a variety of genomic alterations in HER2 in this many solid tumors," Cristofanilli says in a statement.

But he says the findings could be good news, "both clinically and scientifically".

It could mean Herceptin and other anti-HER2 cancer therapies that are already in clinical use might help patients with some of these tumors.

From a research point of view, the results add weight to the growing idea of "genome-driven therapy", where the genome profile of the tumor, rather than where it develops, is more important when considering how best to treat the individual patient's cancer.

A number of institutions donated tumor samples for analysis, and their researchers are co-authors of the study. Cristofanilli contributed about 50 breast cancer samples. He discovered that one sample showed one of his patients, who had been diagnosed with triple negative breast cancer, had an HER2 mutation.

"My patient was treated with Herceptin as well as chemotherapy, and derived clinical benefit," says Cristofanilli.

"No one looks for HER2 mutations in this form of breast cancer. To me, this makes the case for the value of genome-driven therapy," he explains.

Foundation Medicine, a cancer diagnostics company in Cambridge, Massachusetts led and paid for the study. They screened 2,223 solid tumor specimens from 20 different advanced cancers, for more than 182 genes alterations known to be linked to cancer.

The results showed HER2 alterations in 14 types of solid tumor. Of these, 29% were esophageal cancer samples, 20% were uterine, 14% were breast, 12% were stomach, and 6% were lung.

They also found large variations in HER2 abnormalities. They found nearly 5% of samples had 116 different abnormalities, including 58% with amplifications, 25% with substitutions, 14% with insertions or deletions, 2% with splice site variants, 2% with translocations, and 5% with more than one alteration. Plus, two of the tumors had both HER2 substitution and amplification.

Cristofanilli says the study "highlights the need to study a broad range of genes at a high level of sensitivity and specificity when searching for novel targets of therapy".

"Widespread use of this approach could provide more treatment options and enable more rapid accrual to ongoing and planned trials of agents targeting pathways under study," he adds.

Another study reported earlier this year found that while some gene alterations may actively drive tumor growth, there may also be some "passenger" alterations that do the opposite and slow cancer down, suggesting cancer may not be a sequence of inevitable accumulation of driver events, but a delicate balance between drivers and passengers.

Written by Catharine Paddock PhD

Copyright: Medical News Today
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Gene-Silencing Activity Discovery Could Lead To Treatment For Viral Infections, Cancers And Other Diseases

Main Category: Infectious Diseases / Bacteria / Viruses
Also Included In: Cancer / Oncology;??Genetics
Article Date: 13 May 2013 - 0:00 PDT Current ratings for:
Gene-Silencing Activity Discovery Could Lead To Treatment For Viral Infections, Cancers And Other Diseases

A team led by scientists at The Scripps Research Institute (TSRI) has found how to boost or inhibit a gene-silencing mechanism that normally serves as a major controller of cells' activities. The discovery could lead to a powerful new class of drugs against viral infections, cancers and other diseases.

"Learning to control natural gene silencing processes will allow an entirely new approach to treating human disease," said Ian J. MacRae, assistant professor in TSRI's Department of Integrative Structural and Computational Biology and principal investigator for the study, which appears as the cover story in the May 9, 2013 issue of the journal Molecular Cell.

A Scientific Mystery and Technical Conundrum

The gene-silencer in question is Argonaute 2, a molecular machine in cells that can grab and destroy the RNA transcripts of specific genes, preventing them from being translated into proteins. Argonaute 2 and other Argonaute proteins regulate the influence of about a third of the genes found in humans and other mammals - and thus are among the most important modulators of our cells' day-to-day activities. Argonautes' gene-silencing functions also help cells cope with rogue genetic activity from invading viruses or cancer-promoting DNA mutations.

Yet Argonautes' workings are complex and not yet entirely understood. For example, before it starts a search-and-destroy mission against a specific type of target RNA, an Argonaute 2 protein takes on board a target-recognition device: a short length of "guide RNA," also known as a microRNA (miRNA). The miRNA's sequence is mostly complementary to the target RNA's - a sort of chemical mirror-image - so that it can stick tightly to it.

But how do an Argonaute protein and its miRNA guide, having formed their partnership, manage to part company? It has been a scientific mystery and technical conundrum for researchers, who have found it hard to separate Argonaute proteins from miRNAs in the lab dish.

"That problem led us to look for a way to get Argonautes to unload these miRNAs," said Nabanita De, a postdoctoral fellow in MacRae's laboratory who was first author of the new study.

Matches and Mismatches

In an initial set of experiments, the team demonstrated that when an miRNA hooks up with an Argonaute 2, the pair do remain locked together and functioning for an exceptionally long time: days to weeks, whereas solo miRNA normally is degraded within minutes.

Yet prior studies by other laboratories have hinted at the existence of mechanisms that can hasten the separation of miRNAs from Argonautes. Some viruses, for example, produce decoy target RNAs that virtually nullify the activity of the corresponding miRNAs, seemingly by destabilizing the miRNA-Argonaute pairing. A key feature of these decoy target RNAs is that they make an almost perfect complementary match to the miRNAs - especially at one end of the miRNAs, known as the three-prime or 3' end. In this respect, they match the miRNAs much better than the natural gene transcripts that the miRNAs evolved to target.

De confirmed that decoy RNAs designed to match miRNAs this way can greatly hasten the miRNAs' "unloading" from Argonautes, thus effectively dialing down these miRNAs' normal gene-silencing activities. By contrast, mismatches at the 3' end delayed unloading, enhancing the gene-silencing activity.

Why do these matches and mismatches have such effects on the miRNA-Argonaute pairing? The mechanisms aren't obvious. But De noted that mismatches at the opposite end of miRNAs - the 5' end - have the opposite effect. "Targets with 5'-end mismatches are actually better at unloading miRNAs from Argonaute," she said.

"The next thing we're trying to figure out is how all that works," said MacRae. "We have some guesses but no clear answer."

In a study reported last year, MacRae's laboratory used X-ray crystallography to determine the first high-resolution atomic structure of an Argonaute 2-miRNA complex. Now the team is working on a structural study of the complex as it grabs a target RNA. "When we can see the structural details of that interaction, then I think we'll have a much better handle on this loading and unloading process," said MacRae.

Many Potential Applications

Scientists already have begun developing gene-silencing drugs that work like miRNAs; they are taken up by Argonaute proteins as guide RNAs and lead to the silencing of targeted gene transcripts. Pharmaceutical companies also are developing drugs that bind directly to miRNAs to inhibit their activity. The findings here suggest a new and, in principle, more powerful class of miRNA inhibitors/enhancers, aimed at destabilizing or stabilizing the miRNA-Argonaute complex.

"I can think of many applications for these," said MacRae. "One of the most obvious would be against hepatitis C virus, which requires a certain miRNA in liver cells for efficient replication; an RNA-based drug that speeds up the unloading of this virus-enhancing miRNA would be a powerful approach for shutting down the virus."

A better understanding of the miRNA loading and unloading process also should lead to better miRNA-type drugs, he added.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject. Other contributors to the study, "Highly Complementary Target RNAs Promote Release of Guide RNAs from Human Argonaute 2," were Lisa Young, Nicole-Claudia Meisner and David V. Morrissey of the Novartis Institutes for Biomedical Research, and Pick-Wei Lau of the MacRae laboratory at TSRI.
The study was funded by the National Institutes for Health (grant R01 GM086701).
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Breast-Conserving Therapy May Outperform Mastectomy Alone for Women with Early-Stage Triple-Negative Breast Cancers

For women with early-stage triple-negative breast cancer, treatment with breast-conserving surgery plus radiation therapy may result in fewer cancer recurrences in or near the breast than mastectomy without radiation therapy. These results were published in the Journal of Clinical Oncology.???

Breast cancers that are estrogen receptor-negative, progesterone receptor-negative, and HER2-negative are called triple-negative breast cancers. Triple-negative breast cancers tend to be more aggressive than other breast cancers and have fewer treatment options.???

For women with small breast cancers that have not spread to the lymph nodes, treatment often includes breast-conserving surgery (lumpectomy) plus radiation therapy or mastectomy (removal of the entire breast) without radiation therapy. These two approaches are generally thought to produce similar outcomes, but it’s possible that for certain subtypes of breast cancer one approach may be more effective than the other.?????

To compare breast-conserving therapy (lumpectomy plus radiation therapy) to mastectomy among women with early-stage (T1-2N0) triple-negative breast cancers, researchers evaluated information from 468 patients. The group was fairly evenly split in terms of how many had been treated with breast-conserving therapy and how many had been treated with mastectomy without radiation therapy.???

Study participants were followed for a median of 7 years. One of the outcomes of interest was locoregional recurrence. This refers to a recurrence of the cancer in the breast, chest wall, or nearby lymph nodes.???

Five-year survival without a locoregional recurrence was 96% among women treated with breast-conserving surgery and 90% among women treated with mastectomy without radiation therapy. In other words, women treated with breast-conserving therapy had a lower risk of recurrence in the breast, chest wall, or lymph nodes than women treated with mastectomy without radiation therapy.?At the time of the analysis, overall survival was similar in the two groups.?

Although additional studies are needed, it’s possible that adding radiation therapy may improve outcomes among women who undergo mastectomy for early-stage, triple-negative breast cancer. In the current study, the risk of recurrence within or near the breast was lower among women treated with breast-conserving therapy (lumpectomy plus radiation therapy) than among women treated with mastectomy without radiation therapy.????

Reference: Abdulkarim BS, Cuartero J, Hanson J et al. Increased risk of locoregional recurrence for women with T1-2N0 triple-negative breast cancer treated with modified radical mastectomy without adjuvant radiation therapy compared with breast-conserving therapy. Journal of Clinical Oncology. Early online publication June 13, 2011.?

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