While previous studies have linked smoking to increased breast cancer risk, they have not been accompanied by molecular biology studies to determine why. In this present study, scientists reveal a link between nicotine itself and breast cancer risk – not just the other non-nicotine components of smoking.

You can read about this study in The Journal of the National Cancer Institute, August 23^rd (2010) issue.

Yuan-Soon Ho, Ph.D., Taipei Medical University, and team examined 276 breast tumor samples from anonymous donors to Taipei Medical University Hospital. They wanted to determine whether subunits of the nicotinic acetylcholine receptor were overexpressed in breast cancer cells compared with other normal cells.

They found that the alpha 9 subunit nAChR (α9-nAchR) was overexpressed in human breast cancer cells. Expression was significantly higher in advanced stage breast cancer than in its early stages.

The investigators reveal that when α9-nAchRs were reduced, tumor growth in the laboratory was inhibited. The opposite promoted cancer growth – if α9-nAchRs was increased, or when treating more normal breast cells with nicotine, the development of cancer characteristics grew.

The researchers wrote:

These results imply that receptor-mediated carcinogenic signals play a decisive role in biological functions related to human breast cancer development.

The authors stress that theirs was a small study with only Asian patients involved. Breast cancer incidence in Taiwan is low.

Ilona Linnoila, M.D., of the Center for Cancer Research at the National Cancer Institute, in an accompanying editorial, writes that the study:

..suggests not only that smoking could be causally related to breast carcinogenesis but also that nicotine could directly contribute to the molecular mechanism of carcinogenesis in addition to indirectly contributing by promoting addiction to smoking.

Better understanding of the molecular mechanisms of the cholinergic pathways will lead to more opportunities for intervention and prevention of tobacco toxicity

“Overexpression and Activation of the {alpha}9-Nicotinic Receptor During Tumorigenesis in Human Breast Epithelial Cells”
Chia-Hwa Lee, Ching-Shui Huang, Ching-Shyang Chen, Shih-Hsin Tu, Ying-Jan Wang, Yu-Jia Chang, Ka-Wai Tam, Po-Li Wei, Tzu-Chun Cheng, Jan-Show Chu, Li-Ching Chen, Chih-Hsiung Wu, Yuan-Soon Ho
JNCI (Journal of the National Cancer Institute), doi:10.1093/jnci/djq300

Written by Christian Nordqvist
Copyright: Medical News Today

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Hitchens is well known to be a heavy cigarette smoker. Although he appeared to have quit in 2008, various sources report that he fell off the nicotine-wagon. Fox News writes that in 2003 he admitted that his alcohol intake was enough to kill or stun the average mule.
Hitchen said:

I have been advised by my physician that I must undergo a course of chemotherapy on my esophagus. This advice seems persuasive to me. I regret having had to cancel so many engagements at such short notice.

Hitchens, an atheist, has been identified as being an exponent of the new atheism movement. He describes himself as a believer in the philosophical values of the Age of Enlightenment. He claims that the concept of God as a supreme being is a totalitarian belief that undermines individual freedom, and that scientific discovery, and free expression should replace religion, which is an obstacle for these things, as a means of teaching ethics and defining human civilization. In his 2007 book God is Not Great, he wrote at length on atheism and the nature of religion. He is an admirer of George Orwell, Thomas Paine, and Thomas Jefferson.

He has both US and British citizenships.

What is cancer of the esophagus (Esophageal cancer)?

Esophageal cancer occurs in the esophagus which is a long hollow tube that runs from the throat to the stomach. The esophagus carries the food that is swallowed all the way to the stomach to be digested.

Esophageal cancer usually begins in the cells that line the inside of the esophagus. Cancer happens when some of the cells multiply in an abnormal way, causing a growth called a tumor to form. Tumors can be benign (not cancerous) or malignant (cancerous). They can occur in any part of the body where the cells multiply abnormally.

Esophageal cancer is not common. In areas of the world, such as Asia and parts of Africa, esophageal cancer is much more common.

Men and people over the age of 55 are most commonly affected esophageal cancer.

Types of cancer of the esophagus:

• Squamous cell carcinoma forms in the upper part of the esophagus when cells on the inside lining of the esophagus multiply abnormally.
• Adenocarcinoma of the esophagus forms in the lower part of the esophagus when cells inside the mucous glands that line the esophagus multiply abnormally. Mucous glands produce a slimy substance to help food slide down the esophagus more easily.
• Other rare types. Rare forms of esophageal cancer include choriocarcinoma, lymphoma, melanoma, sarcoma and small cell cancer.

For more information on cancer of the esophagus, click here.

Written by Christian Nordqvist
Copyright: Medical News Today

The study confirms previous research in which study author Stephen G. Grant, Ph.D., associate professor of environmental and occupational health at Pitt’s Graduate School of Public Health, discovered evidence of abnormalities in the HPRT gene located on the X chromosome in cord blood from newborns of non-smokers exposed to environmental tobacco smoke.

In the current study, Dr. Grant confirmed smoke-induced mutation in another gene called glycophorin A, or GPA, that is representative of oncogenes – genes that transform normal cells into cancer cells and cause solid tumors. The GPA mutation was the same level and type in newborns of mothers who were active smokers and of non-smoking mothers exposed to tobacco smoke. Likewise, the mutations were discernable in newborns of women who had stopped smoking during their pregnancies, but who did not actively avoid secondhand smoke.

“These findings back up our previous conclusion that passive, or secondary, smoke causes permanent genetic damage in newborns that is very similar to the damage caused by active smoking,” said Dr. Grant. “By using a different assay, we were able to pick up a completely distinct yet equally important type of genetic mutation that is likely to persist throughout a child’s lifetime. Pregnant women should not only stop smoking, but be aware of their exposure to tobacco smoke from other family members, work and social situations.”

The research was funded by grants from the National Institute of Child Health and Human Development and the University of Pittsburgh Competitive Medical Research Fund.

Source:
Clare Collins
University of Pittsburgh Schools of the Health Sciences

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You can read the consensus report by experts representing the American Diabetes Association and the American Cancer Society, in the 16 June online before print issue of CA: A Cancer Journal for Clinicians; the print version will appear in the July/August paper edition.

Some evidence suggests that people with diabetes are at a higher risk of developing many types of cancer, and type 2 diabetes and cancer share some risk factors as well as treatments; however, the underlying biology of this overlap is somewhat elusive.

This gap in understanding spurred the American Diabetes Association and the American Cancer Society to bring together experts to address some key questions, for instance, what risk factors are common to both cancer and diabetes, is there a meaningful link between their incidence and prognosis, what might the underlying biological mechanisms be, and do treatments for diabetes affect cancer risk and prognosis?

The experts were asked to investigate each question, identify current gaps in evidence and suggest future strategies so researchers and epidemiologists can work toward closing the gaps.

Here are some points they reached consensus on, and some recommendations they made:

• People with diabetes (mostly type 2), are likely to be at increased risk of developing cancer of the liver, pancreas, endometrium (lining of the uterus), colon, rectum, breast and bladder.
• The evidence, some of which is inconclusive, does not point to a link between diabetes and increased risk of cancer in other parts of the body, and for prostate cancer, having diabetes appears to lower the risk.
• Shared risk factors such as age, obesity, diet and lack of physical activity may explain the link between diabetes and some cancers.
• Biological mechanisms that directly link diabetes and cancer include hyperinsulinemia (too much insulin in the blood), hyperglycemia (too much sugar in the blood), and inflammation.
• Being physically active, managing weight, and keeping to a healthy diet, things that we should all do for sake of our health anyway, reduce the risk and improve outcomes of type 2 diabetes and some cancers.
• Doctors and healthcare professionals should encourage all patients with diabetes to have the recommended cancer screening for their age and sex.
• On the whole, cancer risk should not be a major factor affecting choice of diabetes therapy for most patients. However, some specific cases, such as patients at higher risk of cancer, or at higher risk of recurrence of certain cancers, may need more careful consideration.
• There is limited evidence that specific drugs influence cancer risk. Suggestions that they do could be a result of certain side effects such as impact on body weight and hyperinsulinemia, as well as the complex and progressive way that hyperglycemia and drugs interact in type 2 diabetes.
• The evidence on metformin (an oral anti-diabetic drug) is still patchy, but what there is suggests it is linked to a lower risk of cancer.
• Similarly, early evidence would suggest that exogenous insulin (that is introduced into the body) is linked to a higher risk of cancer.
• More research is needed to confirm or clarify this early evidence, and to evaluate the possible links between insulin and other diabetes medications and cancer risk.

In many respects the report points to a multitude of uncertain issues, and possibly furnishes more questions than answers, for reasons that Dr Edward Giovannucci, co-chair of the consensus report group, attempted to explain:

“Traditionally there hasn’t been much overlap between research in cancer and in diabetes.”

“But recently it’s become clearer that there are fascinating links between the two. Our summary may raise more questions than provide answers, but we hope that it will spur additional studies,” he added.

His colleague and co-chair Dr David M. Harlan said that for the vast majority of diabetes patients, worrying about which diabetes treatment is better or worse as far as cancer is concerned will not be an issue.

“Only patients with a very high risk for cancer occurrence, or re-occurrence, may wish to carefully consider their options. Even then, the association appears to exist for some cancer types, and not for others,” said Harlan, concluding that “we have much to learn”.

“Diabetes and Cancer: A Consensus Report.”
Edward Giovannucci, David M. Harlan, Michael C. Archer, Richard M. Bergenstal, Susan M. Gapstur, Laurel A. Habel, Michael Pollak, Judith G. Regensteiner, and Douglas Yee.
CA Cancer J Clin, published online before print 16 June 2010.
DOI:10.3322/caac.20078

Source: American Cancer Society.

Written by: Catharine Paddock, PhD
Copyright: Medical News Today

Part of the body’s defence system is controlled by a gene called Tumour Necrosis Factor (TNF) that can stop cancers from developing by killing them. But this same response has also been shown to help promote the growth of cancers.

For the first time, scientists at the Cancer Research UK Beatson Institute in Glasgow have shown how TNF turns to the ‘dark side’, helping some cancers to grow and move to new parts of the body. They found that the TNF response is hijacked by two genes linked to cancer.

The two genes are a tumour suppressor gene, that promotes tumour growth when deleted, and a tumour promoter gene that can turn cells cancerous when activated.

In their study, using fruit flies (Drosophila melanogaster), they found that cells which lack a tumour suppressor gene and turn cancerous are targeted and killed by the TNF controlled response. But, if the tumour promoter is also activated, cancer cells are not only able to escape the TNF’s death signal but also produce a signal to help them spread and grow.

The researchers also showed that all three genes need to be involved for the cancer to fully escape control by the body’s defences. If the response is not co-ordinated by TNF, a tumour will develop, but it is a so called benign tumour – unable to spread to other parts of the body.

Dr Marcos Vidal, lead author from Cancer Research UK’s Beatson Institute, said: “This is the first time that the mechanism behind this hijacking of the TNF controlled response to tumours has been demonstrated. The next step is to test if these same interactions are taking place in humans. If it is, we could determine which patients will benefit from drugs that stimulate an inflammatory response and those who would benefit from drugs that dull these signals down, preventing the cancer from using the TNF to spread and grow.”

Dr Lesley Walker, director of cancer information at Cancer Research UK, said: “Cancers are a complex interplay and competition between the body’s defences and the cancer’s attempts to grow and spread. This research reveals more about these interactions and could one day open up new approaches for treating cancer.”

Reference

1. Cordero et al, TNF is a tumour promoter in Drosophila (2010) Developmental Cell

Source
Cancer Research UK