The figures mean that on average, a new cancer patient was being diagnosed in the country every 7 minutes, 10 seconds in 2006, up slightly from the average of 7 minutes, 38 seconds in 2005, when 68,907 new cases were recorded, according to Chao Kun-yu, deputy chief of the DOH’s Bureau of Health Promotion.

The report showed that for the first time, colorectal cancer replaced liver cancer as the most common type among new cases recorded in a single year.

Compared with 2005, the number of new colorectal cancer cases rose by 644 to 10,248 in 2006, and liver cancer or intrahepatic bile duct cancer was found among 10,092 people – a jump of 176 cases.

Chao attributed the increased prevalence of colorectal cancer among Taiwanese to increasingly unhealthy dietary habits, such as high consumption of red meat and fat and low fiber intake.

Although people between ages 50 and 69 are advised to have fecal occult blood tests every two years to help early diagnosis of colorectal cancer, DOH statistics indicate that only 11 percent of that age group received the tests in 2008 or 2007, he said.

The third highest number of new cases in 2006 were cancers of the lung, trachea or bronchus, totalling 8,748, followed by breast cancer among women, 6,895 cases; and cancer of the mouth, oropharynx or hypopharynx, 5,352 cases, according to the report.

Rounding out the list of top 10 most common types of cancer in 2006 were stomach cancer, with 3,794 new cases; prostate cancer, with 3,073 new cases; skin cancer, with 2,457 new cases; cervical cancer, with 1,828 new cases; and uterine cancer, with 1,159 new cases.

In terms of age-adjusted incidence rate, an average 50 per 100,000 women were diagnosed with breast cancer in 2006; 37.44 per 100,000 people were diagnosed with cancer of the liver or intrahepatic bile duct cancer; and 37.35 per 100,000 people were found to have colorectal cancer.

The report revealed that in Taiwan, the risk of cancer among men was 1.4 times higher than among women.

Because of an almost exclusively male habit of chewing betel nuts, the age-adjusted incidence rates of esophageal cancer and oral cancer among men were 15.6 times to 10.4 times higher than among women in 2006, the report stated.

However, women were found to develop cancer at an earlier age than men, with the median age at diagnosis being 59 among women and 65 among men.

Colorectal cancer most common:

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An independent committee monitoring the study recommended halting it after concluding that patients on Sutent stayed free of disease progression for longer than those on placebo plus best supportive care.

The patients in the study had advanced pancreatic islet cell tumors, a rare cancer with limited treatment options, according to Pfizer.

Sutent is currently approved for treating both advanced renal cell carcinoma and gastrointestinal stromal tumors.

Pfizer Cancer Drug Shows Benefits, Shares Rise

The so-called Million Women Study of middle-aged women in the United Kingdom found that low to moderate consumption of alcohol increased the risk of and might be responsible for 13 percent of breast, liver, rectal and certain digestive tract cancers.

Researchers determined that only one glass of wine a night might raise the risk of cancer in women.

While prior studies indicated that moderate alcohol consumption could be good for heart health, it now appears that cancer risks from consumption may outweigh the possible cardiovascular benefits.

Oncologists endorsed the findings saying that they had promoted a healthy lifestyle for some time as primary means of reducing cancer risk.

According to the Million Women Study, for every additional drink regularly consumed per day, the increase in incidence up to age 75 years per 1000 for women in developed countries is estimated to be about 15 excess cancers per 1000 women up to age 75.

Million Woman Study Links Alcohol Use to Cancer in Women

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Far more potent than similar compounds already in clinical trial, the drug short-circuits the normal ability of cells to sense the need to grow and divide — a signal that cancer cells exploit to spread in the body.

The scientists are working with clinicians to test the drug’s effectiveness against a range of cancers that have proven difficult to treat.

The discovery is reported in the Feb. 10, 2009 edition of PLoS Biology, a journal published by the Public Library of Science.

The research was led by scientists at the University of California, San Francisco (UCSF) and the UCSF Helen Diller Family Comprehensive Cancer Center. Senior author of the paper is Kevan Shokat, PhD, Howard Hughes Medical Investigator and professor of cellular and molecular pharmacology at UCSF.

Normally, in response to growth signals, a multi-protein unit in cells called mTOR integrates information about the cell’s nutritional and energy needs, and prompts the cell to manufacture key proteins for cell growth. But cancer exploits this signal for its own growth.

Clinical trials are underway to stymie cancer proliferation by using a drug called rapamycin—marketed as Rapamune–or related compounds to block the growth signal cycle. The new drug greatly improves on rapamycin’s effectiveness, the scientists reported. The name mTOR stands for “mammalian target of rapamycin.”

Of serious concern to clinicians, rapamycin and related drugs can actually promote cancer at the same time they thwart it. This happens, the scientists found, because the drugs only partially block the cells response to a growth signal. When this happens, the drugs end up augmenting the growth signal itself because a feedback process in the cell kicks in to assure adequate nutrition. With the feedback system in play, cancer cells can regain needed nutrients and continue to proliferate.

The new drug totally blocks this feedback loop, said Shokat, who also is a faculty affiliate at the California Institute for Quantitative Biosciences, known as QB3, which is headquartered at UCSF.

“We were trying to synthesize compounds that could help us learn more about how cancer exploits normal growth controls,” he explained. “Once we made it, though, we found it was even better than we thought it would be at blocking mTor signaling. It does everything that rapamycin does and more.”

The new drug succeeds because there are two mTOR signal pathways, and it blocks both, the scientists found. Rapamycin only blocks one, and so allows the growth-signaling system to still function.

The scientists think that the drug’s total blockage of the nutrient-sensitive mTOR and its feedback loop offer a major advance over rapamycin based drugs, which have been approved to treat only renal call carcinoma effectively.

“I hope the new drug can be used to treat a range of cancers,” Shokat said. “We will work with clinicians to test it against a number of types of cancer – colorectal, lung, breast, multiple myeloma and others. We want to first find the cancer that is most sensitive to it.”

The new compound has been dubbed a TORKinib because it inhibits the mTOR signal. UCSF has applied for a patent and licensed the patent to a startup biotech company, co-founded by Shokat and colleagues, to advance its use in clinical trials to treat cancer.

mTOR is known as a kinase, a ubiquitous type of signaling molecule – there are more than 500 different kinases in the body – that essentially switches proteins on or off. The switch is one of the most common interactions in the body. The kinase adds a small molecule known as a phosphate group to the protein, and that single action either turns on the protein or dampens its activity.

Like all signaling systems in the body, the one involving mTOR goes through many steps to accomplish its duties. The different steps form a cascade that can ramp the signal up or down, depending on the conditions of the cells or tissues. These kinase cascades are embedded within complicated feedback loops, such as the one activated by rapamycin.

Research on the mTOR pathway is of increasing interest to drug companies, Shokat said.

Since mTOR acts “upstream” and “downstream” of other key kinases that are found to cause cancer– such as the much-studied kinases PI3K and Akt– he thinks blocking it will short-circuit the many feedback loops cancer cells use to generate and maintain a growth signal.

“We are extremely excited about the potential of targeting mTOR in this way to treat a number of cancers, although we are aware that there are many hurdles to reaching the finish line,” Shokat said.

Lead author on the paper is Morris E. Feldman, a graduate student in Shokat’s lab.

Shokat’s colleague, Davide Ruggero, PhD, who studies cancer’s effect on protein synthesis, is also a coauthor. Ruggero is assistant professor of urology in the UCSF Helen Family Comprehensive Cancer Center. Other coauthors are Beth Apsel, PhD, a graduate student in chemistry and chemical biology; and Zachary Knight, PhD, a postdoctoral scientist in Shokat’s lab during the research project. Also: Aino Uotila and Robbie Loewith in the department of molecular biology, University of Geneva.

The research was funded by the Howard Hughes Medical Institute.

The private company co-founded by Shokat is called Intellikine. He is the chairman of its scientific advisory board and holds stock options in the company.

Drug Discovery Short-circuits Cancer Growth

If a man has smoked marijuana on a weekly basis or has been exposed to hashish for an extended period of time, the chances of testicular cancer double compared to someone who has never smoked marijuana.

The study found that marijuana could also decrease sperm quality, decrease testosterone levels and cause impotency, since these are similar side effects of testicular cancer.

Men already produce a “cannabinoid-like chemical,” which protects the reproductive system from cancer, but marijuana use could reverse that protective chemical and instead work against the body. The marijuana link is somehow associated with “nonseminoma,” malignant germ cell tumors, and is increasing the risk.

The study has prompted more research as it has open up a bevy of questions, said Stephen Schwartz, a member of the Public Health Sciences Division at the Hutchinson Center.

Testicular cancer linked to marijuana use

In typical breast cancers, the tumor forms a lump that a person can feel or see on a mammogram. In the inflammatory kind, which makes up 1 to 2 percent of the roughly 180,000 new breast cancer cases per year, the cancer “is often not a mass,” says Dr. Eric Winer, chief of the Division of Women’s Cancers at Dana-Farber Cancer Institute. “Instead, the breast is often warm, red, swollen and tender.” The cancer is often misdiagnosed as an infection treatable by antibiotics.

The cancer moves so quickly “that the breast can become noticeably larger in just a few weeks,” says Dr. Barbara Smith, director of the breast program at Massachusetts General Hospital. What makes the cancer so dangerous, she says, is that it grows in the lymphatic vessels, “the highways out of the breast to the rest of the body.” Immediate treatment is essential.

Women with inflammatory cancer get chemotherapy first to get rid of cancer cells that have spread to the rest of the body, then surgery and radiation.

A potent drug called Herceptin can also be used.

Two years ago, the M.D. Anderson Cancer Center in Texas became the first clinic in the world to open a specialized program for inflammatory breast cancer. Other centers, including Dana-Farber, are developing such programs.

Because care is specialized, doctors advise women to seek treatment at major medical centers.

What is inflammatory breast cancer and is it worse than regular breast cancer?

Testicular cancer is relatively rare — a man’s lifetime chance of developing the disease is about 1 in 300 (and dying of it is about 1 in 5,000). Frequent or long-term marijuana smokers could have about double the risk of nonusers, according to the report in the February 9 issue of the journal Cancer.

In the study, a team led by Dr. Janet R. Daling of the Fred Hutchinson Cancer Research Center in Seattle, Washington, interviewed 369 men between the ages of 18 and 44 from the Seattle-Puget Sound area whose testicular cancer had been diagnosed. They compared those men with 979 men who lived in the same area, but did not have cancer.

Overall, 26 percent of the testicular cancer patients were pot smokers (15 percent who used daily or weekly) at the time of diagnosis, compared with 20 percent of men without cancer (10 percent who used daily or weekly). Health.com: Is there a link between drugs, alcohol, and ADHD?

Marijuana users had 2.3 times the risk of a type of testicular cancer known as a nonseminoma as those who were not. Testicular cancer is divided into two types, pure seminomas (60 percent of cases) and nonseminomas (40 percent of cases.) The link was much weaker in men with seminomas.

These types of studies have one important caveat — cancer patients may be more likely to remember – or may be more honest about – past drug use than men in the general population.

Because marijuana use was more closely associated with one type of tumor, rather than testicular cancer in general, it reduces the chances that the study participants were less than honest, Daling said. “That certainly makes us feel better that the associations are true associations,” she said.

Still, the results are considered preliminary and need to be confirmed with more research. “There have been studies done on testicular cancer, but ours is the first to look at marijuana,” said Daling. Health.com: Dogs sniff out clues in the fight against cancer

Scientists believe that most cases of testicular cancer actually get their start in early fetal life. Having an undescended testicle – a relatively common birth defect – a key risk factor for the disease.

There has been an increase in testicular cancers in the last half of the 20th century, however, which spurred the team to examine other factors that might explain the rise. Marijuana use increased over the same period, and chronic use has been shown to affect sperm formation and fertility, they note. Health.com: Boost your mood naturally

Some experts say the association is a tenuous one, particularly because seminomas have increased 64 percent from 1973 to 1998, while nonseminoma rates rose only 24 percent.

“These researchers have an association that they’ve picked up on, but it’s a weak association,” said Steve Shoptaw, a professor in the department of family medicine and psychiatry at UCLA. “Marijuana tends to be one of those firebrand issues were people can make statements to get airtime, so I’d like to see these findings replicated.”

The authors note that nonseminoma rates did go up in a couple of places in the world in recent decades. One is Norway and the other is the Netherlands, a country where cannabis use is tolerated. The next step, said Daling, is to collect tumor tissue, evaluate it for marijuana receptors, and study how those relate to tumor development. Visit CNNhealth.com: Your connection for better living

“Certainly we’re going to continue forward with this,” she added.

Without stronger proof, critics say the study should be taken with a grain of salt. “There’s always been the thought that cannabinoids had some interaction with the reproductive systems, so maybe they’re onto something. Who knows?” said Shoptaw. “But now we need to isolate the actual physiological responses.”

For patients using cannabis for medicinal purposes, the improvement in quality of life may outweigh any potential risk of testicular cancer, said Shoptaw.

“The bottom line is that I would not start warning my marijuana smokers that they are going to get testicular cancer,” he said. “I don’t think there’s enough here to go forward with that message, at least not yet.”

Could smoking pot raise testicular cancer risk? – CNN.com

Yes — but only the 20% to 30% of breast cancers that express the HER2 molecules, suggest studies by Javier A. Menendez, PhD, at the Catalan Institute of Oncology in Girona, Spain, and colleagues.

The Spanish researchers wondered why some studies show that the olive-oil-rich Mediterranean diet cuts breast cancer risk while other studies do not. They theorized that the active compounds in olive oil only affect certain cancers.

The breast cancer drug Herceptin targets the HER2 molecule on tumor cells. Could olive oil compounds have the same target?

Menendez’s team first isolated various compounds from EVOO — which, because it is made without heat, keeps most of the olive compounds that are lost in more processed, lower quality olive oils.

They found that two types of these compounds, secoiridoids and lignans, killed off HER2-positive human breast cancer cells but had little effect on HER2-negative cells.

They also found that when they fed large amounts of EVOO to rats with carcinogen-induced breast cancers, the animals’ tumors became less malignant.

But this does not mean that eating a lot of EVOO will prevent or treat breast cancer.

“Extreme caution must be applied” in interpreting their findings, Menendez and colleagues warn.

One class of EVOO anticancer compounds, the secoiridoids, “rapidly split into inactive compounds” when eaten. These compounds likely won’t help if eaten, but could be a starting point for development of new breast cancer drugs.

On the other hand, the lignan compounds “may represent a different molecular scenario,” Menendez and colleagues suggest. In mouse-feeding studies, tumor tissues accumulate lignans, “thus suggesting that the anti-cancer activity of lignans may be due to their direct local effects on the breast cancer tissues.”

A recent study suggested that eating flaxseed is beneficial to women with newly diagnosed breast cancer. Flaxseed has high lignan concentrations.

Even so, Menendez and colleagues note that much more study will be needed before doctors can recommend EVOO for breast cancer prevention or treatment.

Extra Virgin Olive Oil vs. Breast Cancer

“Most young women at risk of breast cancer following chest radiation for a pediatric cancer, including women at highest risk (Hodgkin lymphoma survivors), are not being appropriately screened,” Kevin C. Oeffinger, MD, of Memorial Sloan-Kettering Cancer Center in New York, and colleagues write.

About 20,000 to 25,000 women 25 and older in the U.S. have received chest radiation for a childhood cancer, according to background information in the journal report. For the past decade, experts have recommended yearly screening mammograms for women who received moderate- to high-dose chest radiation beginning either at age 25 or eight years after the treatment, whichever occurs last.

In 2008, the Children’s Oncology Group (COG) updated the guidelines to include breast magnetic resonance imaging (MRI) along with yearly mammograms. The American Cancer Society recommends the same.

But some women in the new study had never even had a mammogram.

About 12% to 20% of women who receive moderate- to high-dose chest radiation for a childhood cancer will be diagnosed with breast cancer by age 45, but some develop the disease much earlier. “The risk of breast cancer begins to increase as early as 8 years after radiation and the [midpoint] age of breast cancer diagnosis ranges from 32 to 35 years,” Oeffinger’s team writes.

Oeffinger and colleagues based their findings on a 114-item questionnaire filled out by 625 female participants, aged 25 to 50, of the Childhood Cancer Survivors Study (CCSS). All the women had survived childhood cancer and had been treated with chest radiation.

The researchers compared the women’s responses to similarly aged childhood cancer survivors who did not receive chest radiation, and siblings with no history of childhood cancer.

Among women 25 to 39 who had received chest radiation for childhood cancer:

* Most (47.3%) never had a mammogram.
* 63.5% had not received a screening mammogram within the past two years, despite guidelines that recommend annual exams.
* Less than a fourth (23.3%) had a screening or diagnostic mammogram in the previous year.
* They were three times more likely to have had a mammogram if their doctor recommended one.

Among women 40 to 50 who had received chest radiation for childhood cancer:

* They were more likely to have had mammograms than those aged 25 to 39.
* About two-thirds (76.5%) had a screening mammogram in the past two years (compared with 70% for women who did not receive chest radiation during childhood and 67% for siblings without history of childhood cancer).
* Slightly more than half (52%) had regular breast cancer screenings. (This finding was not significantly higher than those who never had chest radiation.)

Many Childhood Cancer Survivors Skip Breast Cancer Screenings

“Our research findings reveal that Baxß protein levels are normally kept at essentially undetectable levels in healthy cells by the protein degradation machine in cells known as proteasomes,” said Dr Victor Yu, who led the Institute of Molecular and Cell Biology (IMCB) research team.

In a researcher article in the journal Molecular Cell, the researchers describe proteasomes as “protein-digesting machines” that regulate cellular levels of various proteins, including that of the lethal Baxß, by breaking them into smaller components within the cell.

“Thus, the proteasomes are there to keep the lethal Baxß in check. This is exciting — if the proteasome-mediated degradation of Baxß could be inhibited specifically in cancer cells, it could cause the harmful cancer cells to go through apoptosis,” Dr Victor Yu said.

In apoptosis, unwanted, damaged and infected cells are eliminated. Before the discovery of Baxß, only one single protein called Bax-alpha (Baxa) had been extensively studied in cells.

The researchers have now found that Baxß is able to associate with, and promote, Baxa activation, and that Baxß, in its native form, is 100 times more potent than its sibling Baxa in triggering a key step in apoptosis.

They believe that the development of such compounds as can elevate levels of Baxß, or stimulate its interaction with Baxa, may pave the way for new drug approaches to cancer treatment, as these compounds are likely to enhance the apoptotic signals triggered by many conventional cancer drugs, which frequently cause toxic side effects in patients when higher doses of drugs are needed.

Dr David Andrews, Professor of Biochemistry and Biomedical Sciences at McMaster University, Canada said: “The beta-isoform4 of Bax has been enigmatic for several years. Although earlier research had hinted at its existence, the protein has proven extremely difficult to detect or examine functionally. Even attempts to produce the protein in the laboratory have been largely unsuccessful.

In this study the Yu group resolves these issues by demonstrating that in cells Baxß is normally rapidly degraded and kept at low levels, and when it is not degraded, it is profoundly apoptotic on its own and works in concert with Baxa. These studies provide information necessary for the elucidation of the importance of Baxß in cell physiology.”

Protein for cancer cell death discovered-Science-Health & Science-The Times of India