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Cancer

Lifestyle affects risk of second breast cancer

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Lifestyle affects risk of second breast cancer

Surviving breast cancer is no guarantee that a new cancer won’t appear in the other breast. However, research now suggests that women can build their own personal armor to at least partially protect themselves from this occurring.

All it takes, says Dr. Christopher I. Li, is to “stay at a normal weight, don’t smoke, and drink in moderation.”

The research, headed up by Li at the Fred Hutchinson Cancer Center in Seattle, Washington, suggests that obesity, smoking and drinking too much are all risk factors for breast cancer in the opposite breast — also called the “contralateral” breast — of women who’ve had an “estrogen receptor-positive invasive breast cancer.”

That’s because estrogen can fuel these tumors’ growth, and both fat tissue and excessive alcohol use directly increase estrogen levels in the body, Li and his team propose. They believe that smoking contributes to the risk because of all the cancer-causing substances one inhales when smoking.

Until now, there haven’t been many studies regarding ways that women could protect themselves from second breast cancers, according to the report in the September 8th online issue of the Journal of Clinical Oncology.

The new study included 365 women with a first estrogen receptor-positive breast cancer and a second contralateral cancer and 726 control subjects. By reviewing medical charts and interviewing the women directly, the researchers determined body mass index (BMI) and alcohol and tobacco use. BMI is an estimate of a person’s relative body fat calculated from her height and weight.

Compared with normal weight women, those who were obese were almost half again – by 40% — as likely to develop a contralateral breast cancer. Consumption of 7 or more alcoholic drinks per week nearly doubled the risk compared with no alcohol use. Findings were similar for current smoking.

Women who both smoke and drink following diagnosis of the first cancer had an even greater risk of a second cancer. The study showed that consuming 7 or more alcoholic drinks per week coupled with current smoking increased the odds of contralateral breast cancer more than 7-fold.

In a related editorial, Dr. Jennifer A. Ligibel, from the Dana-Farber Cancer Institute in Boston, points out that the study by Li and his team took place before use of hormonal therapy for estrogen receptor-positive breast cancer became routine. Therefore, a more modern study examining the effect of modifiable lifestyle factors should involve patients treated according to current guidelines.

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Researchers find prostate cancer stem cell

Researchers find prostate cancer stem cell

Cancer stem cells (CSCs) are cancer cells (found within tumors or hematological cancers) that possess characteristics associated with normal stem cells, specifically the ability to give rise to all cell types found in a particular cancer sample. CSCs are therefore tumorigenic (tumor-forming), perhaps in contrast to other non-tumorigenic cancer cells. CSCs may generate tumors through the stem cell processes of self-renewal and differentiation into multiple cell types. Such cells are proposed to persist in tumors as a distinct population and cause relapse and metastasis by giving rise to new tumors. Therefore, development of specific therapies targeted at CSCs holds hope for improvement of survival and quality of life of cancer patients, especially for sufferers of metastatic disease.

Existing cancer treatments have mostly been developed based on animal models, where therapies able to promote tumor shrinkage were deemed effective. However, animals could not provide a complete model of human disease. In particular, in mice, whose life spans do not exceed two years, tumor relapse is exceptionally difficult to study.

The efficacy of cancer treatments is, in the initial stages of testing, often measured by the ablation fraction of tumor mass (fractional kill). As CSCs would form a very small proportion of the tumor, this may not necessarily select for drugs that act specifically on the stem cells. The theory suggests that conventional chemotherapies kill differentiated or differentiating cells, which form the bulk of the tumor but are unable to generate new cells. A population of CSCs, which gave rise to it, could remain untouched and cause a relapse of the disease.

Researchers have found a stem cell, a kind of master cell, that may cause at least some types of prostate cancer.

Their findings are only experimental — the stem cells were found in mice — but could explain at least some types of prostate cancer and eventually offer new ways to treat it, they reported on Wednesday in the journal Nature.

The findings also show a potential new source for prostate tumors — so-called luminal cells, which secrete various compounds used in the prostate.

“The role of stem cells in the development of prostate cancer has been a focus of speculation for many years,” Dr. Helen Rippon of Britain’s Prostate Cancer Charity said in a statement.

“Importantly, this new stem cell does not rely on androgens — the male sex hormones that control prostate growth — to survive and grow. This may give a clue as to why prostate cancer often becomes resistant to treatments designed to regulate these androgens in the later stages of the disease,” added Rippon, who was not involved in the research.

“This improved knowledge will also be a step forward in learning how we might help to prevent the disease from developing in men in the first place.”

Michael Shen of Columbia University Medical Center and colleagues named the new stem cells CARNs, for castration-resistant Nkx3.1-expressing cells.

They normally regenerate part of the tissue that lines the inside of the gland, which produces semen. But the cells can also form tumors if certain genes meant to stop out-of-control growth get turned off.

Shen said researchers had believed that tumors arise from a different layer of cells in the prostate, called basal cells.

“Previous research suggested that prostate cancer originates from basal stem cells, and that during cancer formation these cells differentiate into luminal cells,” Shen said in a statement. “Instead, CARNs may represent a luminal origin for prostate cancer.”

Prostate cancer is the second most common cancer in men worldwide after lung cancer, killing 254,000 men a year globally.

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Prostate cancer screening: More harm than good?

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Prostate cancer screening: More harm than good?

One meaning of screening is the investigation of a great number of something (for instance, people) looking for those with a particular problem or feature. For example at an airport many bags are screened by x-ray to try to detect any which may contain weapons or explosives, and people are screened by passing through a metal detector. If only part of a population is screened, screening is equivalent to sampling in statistics.

Screening can also mean preventing access of something by some sort of barrier. Particular cases:

Electromagnetic shielding in physics, the exclusion of electric, magnetic, or electromagnetic fields by a metallic screen or shield

In atomic physics and chemistry, the screening effect or atomic shielding is the reduction of effective nuclearcharge by intervening electron shells

Screening (printing), a process that represents lighter shades as tiny dots, rather than solid areas, of ink by passing ink through a perforated screen

The investigation of a large population is related; the members of a population are filtered by a metaphorical, rather than physical, screen

Screening is a process stage when cleaning paper pulp

Routine screening for prostate cancer has resulted in more than 1 million U.S. men being diagnosed with tumors who might otherwise have suffered no ill effects from them, U.S. researchers said on Monday.

They said prostate cancer screening is a double-edged sword, catching serious cancers in a few but causing needless worry and expense for the majority of men, who may be getting treatment for tumors growing too slowly to do any harm.

The team looked to see how many additional men have been diagnosed with prostate cancer since the introduction in 1986 of a widely used blood test for prostate cancer that looked for a prostate-cancer specific antigen, or PSA.

“Our estimate is that number is about 1.3 million people in the United States. That is a huge effect,” said Dr. H. Gilbert Welch of the VA Outcomes Group in White River Junction, Vermont, whose study appears in the Journal of the National Cancer Institute.

More than 1 million of those were treated, they found.

“These are men who could not be helped by treatment because their cancer was not destined to cause them symptoms or death,” Welch said in a telephone interview.

The increased diagnosis rate more than tripled in men aged 50 to 59 and increased more than a sevenfold in men under age 50.

And while prostate cancer deaths have declined since the introduction of PSA testing, Welch said about 20 men had to be diagnosed and treated for every one who benefited.

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