Patients With Rare Cancers Want More Shared-decision Making About Their Cancer Treatment

Cancer patients under 55 and those with some rarer types of cancer want more of a say in the decisions made about their treatment, according to new research being published in the British Journal of Cancer today (Wednesday). Recently, several US states have introduced legislation or other policies supporting share-decision making.

The research also shows that ethnic minorities and patients with rectal, ovarian, multiple myeloma and bladder cancers are more likely to feel they aren't being given a big enough say in how they are treated.

Scientists funded by the National Institute for Health Research at the University of Cambridge looked at more than 40,000 responses to the 2010 English National Cancer Patient Experience Survey. More than 70 per cent said they felt suitably involved in decisions about their treatment. But younger patients in particular responded to the survey saying that decisions are made without enough of their personal input.

Dr Anas El Turabi, study author based at the University of Cambridge, said: "Although the overall results are very positive and most patients do feel suitably involved in their treatment decisions, there are distinct groups where this isn't the case and we need to address this. There appears to be a generation gap, possibly because younger patients expect to have more of a say in their treatment than older patients.

"This study should help us to focus on those groups of patients who feel the least involved. This means doctors, nurses and the patients themselves need to work together and build strong relationships that allow them to discuss treatment options in every case. Some patient groups may also need extra support to make sure they're properly involved in making these decisions, such as having a longer consultation with doctors or specialist nurses."

Dr Georgios Lyratzopoulos, study author, said: "Although there are differences between the US and UK healthcare systems, we would expect to find similar variation between American patients with different cancers.

"Additionally, this evidence highlights the importance of studying the experience of cancer patients using large national patient surveys such as in the UK, and we feel similar US-wide surveys of this kind would be very useful in identifying those patients who feel side-lined during decisions around their own treatment for cancer."

Martin Ledwick, head information nurse at Cancer Research UK, said: "All patients should feel entitled to discuss the options available with their doctors and nurses and be given the chance to do so. It's important that they're made to feel more like the co-pilots, rather than the passengers, on their own cancer journeys.

"Doctors want the best possible outcome for you when they're considering the most appropriate treatment but that doesn't mean the treatment will always suit every patient. Being able to talk freely about different options will help patients feel more involved."

Source-Eurekalert

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Digestive tract can contain clues to cure Cancer

Jian-Guo Geng, an associate professor at the Faculty of dentistry University of Michigan, said that if the digestive tract remains healthy and functioning, the chances of survival increase exponentially.

Recently, the laboratory of Geng discovered a biological mechanism that preserves the gastrointestinal tract in mice which have been delivered to lethal doses of chemotherapy.

The results could revolutionize the treatment of cancer, said Geng.

He stressed that this had not yet been tested in humans and right now there is no way of knowing if people will react in the same way.

"All tumours of different tissues and organs can be killed by high doses of chemotherapy and radiation, but the current challenge for treating cancer metastasis in stages later, it is that you actually kill the host before you kill the tumor,", said Geng.

"It is our belief that this could potentially cure cancer metastasis in steps later. People die of cancer, if our forecast is true.

"We cannot know this yet, but in mice, it has shown promise. Years on the road, we have a way to make humans to tolerate lethal doses of chemotherapy and radiotherapy. In this way, cancer metastasis, put in scene later can be eradicated by added increased doses of chemotherapy and radiation therapy, "Geng.

Geng laboratory found that when certain proteins bind to a specific molecule on intestinal stem cells, it revs into overdrive for intestinal regeneration intestinal stem cells and repair in mice.

Stem cells naturally heal tissues and damaged organs, but 'normal' amounts so-called stem cells in the intestine can not simply follow with the rubble left by the lethal doses of chemotherapy and radiation necessary to successfully treat advanced stage tumours.

However, the phalanx of additional stem cells protect the intestines and gastrointestinal tract, which allows the ingestion of nutrients so that the body can perform other critical functions and bacterial toxins in the intestine are prevented from entering the bloodstream, said Geng.

In the future, if the findings are tested in humans and promising, these factors could give just human cancer patients enough an additional advantage to survive the higher doses of chemotherapy and radiation therapy to the tumor or tumors are eradicated.

Geng said that even if the results seem promising in humans, it could take a decade or longer before an application becomes available for use on people.

In the study, 50-75% of mice treated with the molecule has survived to the otherwise chemotherapy lethal doses. All mice who did not receive the molecule died, said Geng.

The results are published in the journal Nature.

Source-ANI

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Scientists: Sleeping Stem Cells Could Hold Key to Treatment of Aggressive Blood Cancer

by Rukmani Krishna on? August 02, 2013 at 12:02 AM Cancer News Rather than displacing healthy stem cells in the bone marrow as previously believed, the cancer is putting them to sleep to prevent them forming new blood cells, discovers scientists studying an aggressive form of leukaemia.
The finding offers the potential that these stem cells could somehow be turned back on, offering a new form of treatment for the condition, called Acute Myeloid Leukaemia (AML). The work was led by scientists at Queen Mary, University of London with the support of Cancer Research UK's London Research Institute.

Around 2,500* people are diagnosed with AML in the UK each year, both young and old. Although AML is curable in some the majority die from this disease.

Normally, the bone marrow produces haematopoietic stem cells which mature into "adult" blood cells. In people with AML the bone marrow is invaded by leukaemic myeloid cells which aren't able to develop into normal functioning blood cells.

The result is that the body does not have enough red blood cells or platelet cells, which can cause symptoms of anaemia, such as tiredness, and increase the risk of excessive bleeding. Patients are also more vulnerable to infection as the white blood cells, which fight bacteria and viruses, are not properly formed.

Dr David Taussig, from the Barts Cancer Institute at Queen Mary, University of London, who led the research, said: "The widely accepted explanation has held that AML causes bone marrow failure by depleting the bone marrow of normal haematopoietic stem cells by killing or displacing them.

"However, we have found that samples of bone marrow in both mice models and patients with AML contain the same, or more, of these normal stem cells than usual. So the cancer isn't getting rid of them, instead it appears to be turning them off so they aren't going on to form healthy blood cells.

"If we can find out how the cancer cells are doing this, we can look at exploiting it to find ways to wake these stem cells up. This is very important as, while the cure rate for younger patients can be around 40 per cent, in older patients it is much lower. The treatments we have, such as chemotherapy and bone marrow transplants, just aren't very successful in this older patient group."

The scientists studied the levels of haematopoietic stem cells (HSC) in the bone marrow of mice transplanted with human AML. They found the numbers of normal mouse HSCs stayed the same, however what did change was that the HSCs were no longer going through the stages of development which finally results in the formation of new blood cells.

The findings were confirmed by the analysis of bone marrow from 16 patients with AML.

Professor Peter Johnson, Cancer Research UK's chief clinician, said: "Although major progress has been made in treating AML over the years, there's still an urgent need for more effective treatments to improve long-term survival. This study takes us an important step forwards in our understanding of what's going on in the bone marrow of people with AML, an area that we have not known enough about previously, and the challenge now is to turn this understanding into new treatments for patients."

Dr Taussig added: "Usually when the body is stressed, the stem cells become very active. For example, if you have a haemorrhage, they will jump into action to produce more new blood cells. The cancer cells are somehow over-riding this and our next phase of work will concentrate on how they are doing this."

Source-Eurekalert

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Scientists Urge Major Changes for Cancer Screening and Treatment

The "Viewpoint" article will be published online Monday, July 29, in the Journal of the American Medical Association.

When cancer screening programs were widely initiated three decades ago, medical knowledge of the disease was more simplistic. The intent was to detect cancer at its earliest stages to reduce illness and mortality, but in fact early diagnosis has not led to a proportional decline in serious disease and death, the scientists write in the JAMA commentary.

Instead, screening programs are identifying not only malignant cancers, but also slow-growing, low-risk lesions, and sweeping them into the same treatment process. As a result, patients are being diagnosed and treated for forms of cancer that might never actually harm them - a phenomenon that''s been termed overdiagnosis, which translates to "too much medicine."

Now, with the advancement of scientific understanding of the biology of cancer, the authors say it is time for significant changes in practice and policy.

"By recognizing that cancer is not one disease, but a number of different diseases, we can individualize our treatment based on biology and avoid overtreatment," said panel chair Laura J. Esserman, MD, MBA, director of the Carol Franc Buck Breast Care Center at the UCSF Helen Diller Family Comprehensive Cancer Center. "The goal going forward is to personalize screening strategies, and focus screening policies on the conditions that are most likely to result in aggressive illness and death."

The authors recommend creation of a new classification for tumors that are indolent (unlikely to cause patients harm). For example, ductal carcinoma of the breast -- currently considered the earliest form of breast cancer -- would no longer be called cancer. The authors also call for the formation of registries for lesions with low potential for malignancy, and for a multidisciplinary approach across pathology, imaging, surgery and other medical specialties "to revise the taxonomy of lesions now called cancer."

The key, they say, is to improve screening strategies to avoid overtreating tumors that would not be lethal, or that would not even have come to medical attention.

"Although our understanding of the biology of cancer has changed dramatically, perceptions on the part of the public, and among many physicians, have not yet changed," Esserman said. "Cancer is still widely perceived as a diagnosis with lethal consequences if left untreated."

The JAMA article is comprised of recommendations from a working group formed last year during a meeting convened by the National Cancer Institute. The group was charged with developing a strategy to improve current approaches to cancer screening and prevention.?

The commentary was co-written by Ian M. Thompson, MD, professor at the University of Texas Health Science Center at San Antonio; and Brian Reid, MD, PhD, director of the Seattle Barrett''s Esophagus Program and member of the Human Biology Division at the Fred Hutchison Cancer Research Center in Seattle.

The three authors served as chairs of the NCI working group.

Overdiagnosis is occurring across many medical conditions, but is particularly common in breast cancer, lung cancer, prostate, thyroid cancer and melanoma, said the authors.

They cite DCIS, or ductal carcinoma of the breast, and Barrett''s esophagus as illustrations of how the detection and surgical removal of what have been called precancerous lesions have failed to lead to lower rates of invasive cancer.

By contrast, the authors said, colon and cervical cancer serve as examples of "effective screening programs in which early detection and removal of precancerous lesions have reduced incidence as well as late-stage disease."?

Cancer screening should have three important missions, the authors write: To detect disease that would ultimately harm the patient; to uncover tumors that benefit from intervention; and to detect disease that is more likely to be cured or better treated when spotted early.

Optimal screening frequency depends on a cancer''s growth rate. If a cancer is fast growing, screening is less likely to be effective. "If a cancer is slow growing but progressive, with a long latency and a precancerous lesion, screening is ideal and less frequent screening (eg.10 years for colonoscopy) may be effective," the authors said.

Source-Newswise

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Scientists: Sleeping Stem Cells Could Hold Key to Treatment of Aggressive Blood Cancer

by Rukmani Krishna on? August 02, 2013 at 12:02 AM Cancer News Rather than displacing healthy stem cells in the bone marrow as previously believed, the cancer is putting them to sleep to prevent them forming new blood cells, discovers scientists studying an aggressive form of leukaemia.
The finding offers the potential that these stem cells could somehow be turned back on, offering a new form of treatment for the condition, called Acute Myeloid Leukaemia (AML). The work was led by scientists at Queen Mary, University of London with the support of Cancer Research UK's London Research Institute.

Around 2,500* people are diagnosed with AML in the UK each year, both young and old. Although AML is curable in some the majority die from this disease.

Normally, the bone marrow produces haematopoietic stem cells which mature into "adult" blood cells. In people with AML the bone marrow is invaded by leukaemic myeloid cells which aren't able to develop into normal functioning blood cells.

The result is that the body does not have enough red blood cells or platelet cells, which can cause symptoms of anaemia, such as tiredness, and increase the risk of excessive bleeding. Patients are also more vulnerable to infection as the white blood cells, which fight bacteria and viruses, are not properly formed.

Dr David Taussig, from the Barts Cancer Institute at Queen Mary, University of London, who led the research, said: "The widely accepted explanation has held that AML causes bone marrow failure by depleting the bone marrow of normal haematopoietic stem cells by killing or displacing them.

"However, we have found that samples of bone marrow in both mice models and patients with AML contain the same, or more, of these normal stem cells than usual. So the cancer isn't getting rid of them, instead it appears to be turning them off so they aren't going on to form healthy blood cells.

"If we can find out how the cancer cells are doing this, we can look at exploiting it to find ways to wake these stem cells up. This is very important as, while the cure rate for younger patients can be around 40 per cent, in older patients it is much lower. The treatments we have, such as chemotherapy and bone marrow transplants, just aren't very successful in this older patient group."

The scientists studied the levels of haematopoietic stem cells (HSC) in the bone marrow of mice transplanted with human AML. They found the numbers of normal mouse HSCs stayed the same, however what did change was that the HSCs were no longer going through the stages of development which finally results in the formation of new blood cells.

The findings were confirmed by the analysis of bone marrow from 16 patients with AML.

Professor Peter Johnson, Cancer Research UK's chief clinician, said: "Although major progress has been made in treating AML over the years, there's still an urgent need for more effective treatments to improve long-term survival. This study takes us an important step forwards in our understanding of what's going on in the bone marrow of people with AML, an area that we have not known enough about previously, and the challenge now is to turn this understanding into new treatments for patients."

Dr Taussig added: "Usually when the body is stressed, the stem cells become very active. For example, if you have a haemorrhage, they will jump into action to produce more new blood cells. The cancer cells are somehow over-riding this and our next phase of work will concentrate on how they are doing this."

Source-Eurekalert

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Majority of Women Do Not Adopt Lifestyle Choices That Reduce Cancer Risks

by Kathy Jones on? June 15, 2013 at 1:28 PM Women Health News Underlining the challenges facing anti-cancer associations, a new study revealed that a majority of women do not follow the lifestyle choices recommended by the American Cancer Society that can reduce the risk of cancer.
The new survey determined how women view diet and exercise in relationship to cancer and whether they believed that they were engaging in healthy behaviours, and if their diet and exercise choices really met the minimum recommendations.

Jennifer Irvine Vidrine, PhD and colleagues from The University of Texas MD Anderson Cancer Center (Houston) and Prevention Magazine (Emmaus, PA) found that less than 10 percent of women who admitted eating a healthy diet actually met the American Cancer Society's minimum fruit and vegetable intake recommendations, which is 2 servings of fruit and 3 servings of vegetables per day.

Less than 40 percent of women who confessed to doing regular physical activity met the American Cancer Society minimum recommendations of 30 minutes of moderate physical activity five days per week.

The study found that overall, more than half of the women who were surveyed failed to meet the minimum recommendations for physical activity and/or for daily consumption of fruits and vegetables.

The study has been published in the Journal of Women's Health.

Source-ANI

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Working Women at Higher Risk of Breast Cancer

by Dr. Nithin Jayan on? June 15, 2013 at 1:43 PM Health In Focus Professional women are at 70 percent higher risk of developing breast cancer than other women, finds a new study. Increased stress at work, prejudice, discrimination, and resistance may be the reasons that put successful women at risk of cancer.
Breast cancer accounts for 22.9 percent of all cancers in women worldwide. American experts estimate that about one out of every eight women born today will be diagnosed with breast cancer at some time during her life. A woman's risk of developing the cancer increases as she gets older; age is the strongest risk factor for breast cancer. A recent study suggests that increased stress at work and a number of other factors elevate the risk of acquiring breast cancer in successful professional women.

The link between job stress and cancer was revealed by the 55-year study of women who were in their thirties in the 1970's. Nearly 4000 women were included in the study; the longer a woman held her job, the greater was the risk of breast cancer. "Women who entered managerial occupations in the 1970's experienced prejudice and discrimination due to prevailing cultural attitudes that men made better leaders than women," says Dr. Tetyana Pudrovska, who led the study.

"Neither men or women preferred to work for a woman because women were seen as 'temperamentally unfit' for management, which was consistent with the cultural stereotype of the woman boss."

"Exercising job authority was particularly stressful for women in the context of gender inequality embedded in the occupational structure of the time, when women in managerial positions often faced prejudice, tokenism, discrimination, social isolation, and resistance from subordinates, colleagues, and superiors. We believe that women are still facing the same kind of stresses, and therefore the increased risk is likely to be there? today," concludes the researcher.

Source-Medindia

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Breast Cancer Risk In Women Could Be Doubled By Long Term Night Shifts

by Rukmani Krishna on? July 04, 2013 at 1:11 PM Women Health News Women who had worked in nights shifts for 30 or more years are twice as likely to suffer from breast cancer, claim researchers.
In the study, they assessed whether night shifts were linked to an increased risk of breast cancer among 1134 women with breast cancer and 1179 women without the disease, but of the same age, in Vancouver, British Columbia, and Kingston, Ontario.

The women, who had done various different jobs, were asked about their shift work patterns over their entire work history; hospital records were used to determine tumour type.

Around one in three women in both groups had worked night shifts. There was no evidence that those who had worked nights for up to 14 years or between 15 and 29 years had any increased risk of developing breast cancer.

But those who had worked nights for 30 or more years were twice as likely to have developed the disease, after taking account of potentially influential factors, however, the numbers in this group were comparatively small.

The authors said that the suggested link between breast cancer and shift work has been put down to melatonin, but sleep disturbances, upset body rhythms, vitamin D or lifestyle differences could also play their part.

Source-ANI

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Gene That Controls Aggressiveness in Breast Cancer Cells Discovered

The researchers, whose findings are published this week in the journal Cell, report that the ZEB1 gene is held in a poised state in basal non-CSCs, such that it can readily respond to environmental cues that consequently drive those non-CSCs into the dangerous CSC state. Basal-type breast carcinoma is a highly aggressive form of breast cancer. According to a 2011 epidemiological study, the 5-year survival rate for patients with basal breast cancer is 76%, compared with a roughly 90% 5-year survival rate among patients with other forms of breast cancer.

"We may have found a root source, maybe the root source, of what ultimately determines the destiny of breast cancer cells-their future benign or aggressive clinical behavior," says Whitehead Founding Member Robert Weinberg, who is also a professor of biology at MIT and Director of the MIT/Ludwig Center for Molecular Oncology.

Transcription factors are genes that control the expression of other genes, and therefore have a significant impact on cell activities. In the case of ZEB1, it has an important role in the so-called epithelial-to-mesenchymal transition (EMT), during which epithelial cells acquire the traits of mesenchymal cells. Unlike the tightly-packed epithelial cells that stick to one another, mesenchymal cells are loose and free to move around a tissue. Previous work in the Weinberg lab showed that adult cancer cells passing through an EMT are able to self-renew and to seed new tumors with high efficiency, hallmark traits of CSCs.

Other earlier work led by Christine Chaffer, a postdoctoral researcher in the Weinberg lab, demonstrated that cancer cells are able to spontaneously become CSCs. Now Chaffer and Nemanja Marjanovic have pinpointed ZEB1, a key player in the EMT, as a gene critical for this conversion in breast cancer cells.

Breast cancers are categorized into at least five different subgroups based on their molecular profiles. More broadly these groups can be subdivided into the less aggressive ‘luminal'' subgroup or more aggressive ‘basal'' subgroup. The aggressive basal-type breast cancers often metastasize, seeding new tumors in distant parts of the body. Patients with basal breast cancer generally have a poorer prognosis than those with the less aggressive luminal-type breast cancer.

Chaffer and Marjanovic, a former research assistant in the Weinberg lab, studied non-CSCs from luminal- and basal-type cancers and determined that cells from basal cancers are able to switch relatively easily into CSC state, unlike luminal breast cancer cells, which tend to remain in the non-CSC state.

The scientists determined that the difference in ZEB1''s effects is due to the way the gene is marked in the two types of cancers. In luminal breast cancer cells, the ZEB1 gene is occupied with modifications that shut it down. But in basal breast cancer cells, ZEB1''s state is more tenuous, with repressing and activating markers coexisting on the gene. When these cells are exposed to certain signals, including those from TGFs, the repressive marks are removed and ZEB1 is expressed, thereby converting the basal non-CSCs into CSCs.

So what does this new insight mean for treating basal breast cancer?

"Well, we know that these basal breast cancer cells are very plastic and we need to incorporate that kind of thinking into treatment regimes," says Chaffer. "As well as targeting cancer stem cells, we also need to think about how we can prevent the non-cancer stem cells from continually replenishing the pool of cancer stem cells. For example, adjuvant therapies that inhibit this type of cell plasticity may be a very effective way to keep metastasis at bay."

Marjnaovic agrees but cautions that the model may not be applicable for every cancer.

"This is an example of how adaptable cancer cells can be,," says Marjanovic, who is currently a research assistant at the Broad Institute. "We have yet to determine if ZEB1 plays a similar role in all cancer types, but the idea that cancer cells reside in a poised state that enables them to adapt to changing environments may be a mechanism used by many cancers to increase their aggressiveness."

This work is supported Vertex Scholars Program, the National Science Foundation (NSF), Jerome and Florence Brill Fellowship, Croucher and Ludwig Research Fellowship, the National Institutes of Health (NIH) (1 F32 GM099153-01A1, HD 045022 and R37CA084198).

Source-Newswise

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Default Cellular 'Safe Mode' Held Responsible for Cancer

by Dr.Enozia Vakil on? July 06, 2013 at 10:35 AM Cancer News A physicist is trying to shed light on the origin of cancer by tracing the disease back to the dawn of multicellularity, more than a billion years ago.
Paul Davies is researching on this topic, taking into account that the death rates from cancer have remained largely unchanged over the past 60 years.

His new theory, drawn together with Charles Lineweaver of the Australian National University, suggests that cancer is a throwback to an ancient genetic 'sub-routine' where the mechanisms that usually instruct cells when to multiply and die malfunctions, thus forcing the cells to revert back to a default option that was programmed into their ancestors long ago.

"To use a computer analogy, cancer is like Windows defaulting to 'safe mode' after suffering an insult of some sort," Davies writes.

The result of this malfunction is the start of a cascade of events that we identify as cancer - a runaway proliferation of cells that form a tumour, which eventually becomes mobile itself, spreading to other parts of the body and invading and colonizing.

Orthodox explanations suppose that cancer results from an accumulation of random genetic mutations, with the cancer starting from scratch each time it manifests; however, Davies and Lineweaver believe it is caused by a set of genes that have been passed on from our very early ancestors and are "switched on" in the very early stages of an organism's life as cells differentiate into specialist forms.

The pair suggests that the genes that are involved in the early development of the embryo - and that are silenced, or switched off, thereafter - become inappropriately reactivated in the adult as a result of some sort of trigger or damage, such as chemicals, radiation or inflammation.

"Very roughly, the earlier the embryonic stage, the more basic and ancient will be the genes guiding development, and the more carefully conserved and widely distributed they will be among species," Davies writes.

Several research teams around the world are currently providing experimental evidence that shows the similarities between the expression of genes in a tumour and an embryo, adding weight to Davies and Lineweaver's theory.

Davies makes it clear that radical new thinking is needed; however, just like ageing, he states that cancer cannot generally be cured but can be mitigated, which we can only do when we better understand the disease, and its place in the "great sweep of evolutionary history".

Source-ANI

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Mutation in FAM190A Gene Linked With Chromosomal Instability in Cancer

by Kathy Jones on? July 05, 2013 at 11:11 PM Cancer News A gene known as FAM190A plays an important role in the regulation of the normal cell division process, known as mitosis, and mutations in the gene could be responsible for the commonly found chromosomal instability in cancer, a new study by Johns Hopkins researchers reveals.
In laboratory studies of cells, investigators found that knocking down expression of FAM190A disrupts mitosis. In three pancreatic cancer-cell lines and a standard human-cell line engineered to be deficient in FAM190A, researchers observed that cells often had difficulty separating at the end of mitosis, creating cells with two or more nuclei. The American Journal of Pathology published a description of the work online May 17, which comes nearly a century after German scientist Theodor Boveri linked abnormal mitosis to cancer. Until now, there had been no common gene alteration identified as the culprit for cancer-linked mitosis.

"These cells try to divide, and it looks like they succeed, except they wind up with a strand that connects them," explains Scott Kern, M.D., professor of oncology and pathology at Johns Hopkins University School of Medicine and its Kimmel Cancer Center. "The next time they try to divide, all the nuclei come together, and they try to make four cells instead of two. Subsequently, they try to make eight cells, and so on." Movies of the process taken by Kern's laboratory are available on the journal Web site.

Kern's group previously reported that deletions in the FAM190A gene could be found in nearly 40 percent of human cancers. That report, published in 2011 in the journal Oncotarget, and the current one are believed to be the only published papers focused solely on FAM190A, which is frequently altered in human cancers but whose function has been unknown. Alterations in FAM190A messages may be the third most common in human cancers after those for the more well-known genes p53 and p16, Kern says.

"We don't think that a species can exist without FAM190, but we don't think severe defects in FAM190A readily survive among cancers," Kern says. "The mutations seen here are very special - they don't take out the whole gene but instead remove an internal portion and leave what we call the reading frame. We think we're finding a more subtle defect in human cancers, in which mitosis defects can occur episodically, and we propose it may happen in about 40 percent of human cancers."

Abnormalities in FAM190A may cause chromosomal imbalances seen so commonly in cancers, Kern says. Multipolar mitosis is one of the most common functional defects reported in human cancers, and more than 90 percent of human cancers have abnormal numbers of chromosomes.

Kern says he plans to study FAM190A further by creating lab models of the subtle defects akin to what actually is tolerated by human cancer cells.

Source-Eurekalert

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Fusion of Cancer Cell and White Blood Cell Gives Rise to Metastatic Tumor

by Kathy Jones on? July 05, 2013 at 10:30 PM Cancer News The fusion of a leukocyte, or white blood cell, and a cancer cell that leads to the formation of a genetic hybrid, was found to increase the risk of human metastatic tumor, a joint study conducted by researchers at Yale Cancer Center, Denver Police Crime Lab and the University of Colorado reveals.
Their study, published in the journal PLOS ONE, may answer the question of how cancer cells travel from the primary tumor's site of origin to distant organs and tissues of the body ? the deadly process of metastasis.

Such a theory was first proposed as an explanation for metastasis more than a century ago. But until now, the theory was unproven in human cancer because genomic differences between cells from the same patient cannot be distinguished. To get around this problem, the researchers analyzed genomic DNA in the secondary malignancies of a patient who had a melanoma brain metastasis and had received a bone marrow transplant from his brother.

They found signature genes from both the patient and donor together in the tumor cells, providing the first evidence that leukocytes (in this case from the donor) can fuse with cancer cells and initiate a tumor.

"Our results provide the first proof in humans of a theory, proposed in 1911 by a German pathologist, that metastasis can occur when a leukocyte and cancer cell fuse and form a genetic hybrid," said corresponding author John Pawelek, research faculty in the dermatology department of the Yale School of Medicine. "This could open the way to new therapy targets, but much work needs to be done to determine how fusion occurs, the frequency of such hybrids in human cancers, and the potential role of hybrids in metastasis," he added.

Source-Eurekalert

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Cancer Drug Responsiveness in Human Tumors Predicted By UNC Murine Study

UNC scientists used GEMMs to develop biomarkers for challenging molecular subtypes of human breast cancer, those for which there are fewer targets and therapies. Their work helps to further establish genetically engineered mouse models as predictors of human response to therapy.

The molecular subtypes of breast cancer that the UNC group focused on - basal-like, luminal B, and claudin-low - are the most challenging types of breast cancer because these are tumors that don't typically respond to drugs such as Herceptin or aromatase inhibitors. UNC was among the first to characterize these tumor subtypes, and this new report extends the understanding of them.

The UNC team found that GEMMs were able to accurately predict human response to a standard chemotherapy drug combination commonly used in the clinic.

Charles Perou, PhD, study senior author, says, "This is a wonderful example of how well chosen mouse models can inform a human disease state. In this case we used years of research to match the models to specific human subtypes, and then treated the animals with therapies identical to what human cancer patients are receiving. We were ultimately able to develop a biomarker of treatment response from the mouse that works in humans."

Dr. Perou is the May Goldman Shaw Professor of Molecular Oncology Research and a member of UNC Lineberger Comprehensive Cancer Center.

Their findings were published in the June 19, 2013 online issue of the journal Clinical Cancer Research.

The team developed murine-derived gene signatures that corresponded to a distinct treatment response and then tested their predictive potential using human patient data. Their research tested single agents carboplatin, paclitaxel, erlotinib and lapatinib. Although one single agent exhibited exceptional efficacy, other single agents offered more modest results.

The team identified a pair of gene expression signatures that predicted pathological complete response to neoadjuvant anthracycline (doxorubicin)/taxane (paclitaxel) therapy in human patients with breast cancer, even among the difficult to treat triple negative patient subset.

Traditional mouse model research was conducted using mice without immune systems into which human tumors or cell lines were grafted. In contrast, by manipulating genes in GEMMs scientists are able to observe how cancer develops as it does in humans, in the presence of an immune system, thus making the results more similar to human cancers.

Source-Eurekalert

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Chicken Consumption Cuts Colon Cancer Risk

by Sheela Philomena on? June 25, 2013 at 1:17 PM Cancer News Chicken consumption during teenage years may reduce the risk of developing colon cancer, finds new study.
The study of about 20,000 women, found women who consumed more chicken when they were teens had lower risks of suffering from colorectal adenomas - benign tumours, which may progress into colon cancer, Fox News reported.

The researchers found that substituting one serving per day of red meat with a serving of chicken or fish could reduce rectal and advanced adenomas' risk by about 40 percent.

Researchers wrote in their study that Colorectal carcinogenesis is a long process which may take several decades, and the initial steps of carcinogenesis could occur at young ages.

19,771 women in the age group of 34 - 51 gave answered questions about their diet when they were teenagers and over 10 years, 1,494 of women were found to be suffering from colorectal adenomas of which 305 were in an advanced stage.

The study has been published in the American Journal of Epidemiology.

Source-ANI

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New Technique can Detect Breast Cancer by Analyzing Urine Samples

The technique has been developed by Dr Yinfa Ma who made use of a device known as P-scan which can detect the presence of pteredines (metabolites) in the urine samples. While pteredines are present in the urine samples of all humans, high concentrations can be an indicator of cancer.

Dr Ma revealed that the levels of pteredines in the urine samples continue to rise as the cancer advances. The technique has been tested in a group of 400 people, 300 of whom suffered from breast cancer.

While the technique may not be useful for those who already suffer from breast cancer, it could be helpful in early detection of the cancer with the researchers hopeful of concluding their testing by the end of this year.

Source-Medindia

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Risk of Cancer Posed by CT Scans Should be Weighed Against Benefits in Diagnosing Diseases

The study findings are reported in the British Medical Journal today and involved researchers at eight other centres in Australia, Oxford University, and the International Agency for Research on Cancer in Lyon, France.

Professor Mathews said: "CT scans were very useful in providing detailed three dimensional pictures to diagnose or exclude disease in internal organs and in most cases, the benefits of having a scan clearly outweigh the risk of a later cancer. Nevertheless, our new findings will remind doctors to order CT scans only when there is a definite medical reason, and to insist that CT scans use the lowest possible X-ray dose'. he said.

"As an individual patient, your risk of cancer from a CT scan is very low. Nevertheless, it is clear from our study that if we reduce the number of scans performed in a large population, and continue to reduce the doses from individual scans, there will be a small but corresponding reduction in the number of cancers in later years."

It is well known that large doses of radiation can damage DNA and increase the risk of a later cancer. However, the radiation doses from CT scans are very small, and there has been uncertainty about whether such small doses would cause cancer, and whether any small increase in risk could be measured reliably.

This study answered questions by linking de-identified Medicare records of CT exposures for the entire population of young Australians, aged 0-19 years between 1985 and 2005, to cancers diagnosed up to the end of 2007.

The risk of cancer increased with the number of CT scans, and the proportional increase in risk was greater for those exposed at younger ages. Nevertheless, as CT usage increased with age, the majority of cancers in this study followed exposures in the teenage years. Although this study did not directly assess the effects of CT exposures after the age of 19, the results suggest that cancer risk will increase following CT scans in adult life.

With improvements in CT technology, the average radiation dose per scan is expected to fall, although CT scan numbers have continued to increase in many countries.

Source-Eurekalert

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Non-Surgical Breast Cancer Therapy Trial Underway in Japan

by Kathy Jones on? May 25, 2013 at 8:24 PM Cancer News The first clinical trial to test the effectiveness of a powerful, non-surgical, short-term radiation therapy for breast cancer has been started by a cancer specialist in Japan.
The National Institute of Radiological Sciences has begun the trial using "heavy ion radiotherapy" which emits a pinpoint beam that can be accurately directed at malignant cells, said Kumiko Karasawa, radiation oncologist and breast cancer specialist.

The study was launched amid renewed global interest in breast cancer and its treatment after Oscar-winning actress Angelina Jolie revealed she had undergone a preventative double mastectomy.

Heavy ion radiotherapy has proved effective in combating other forms of cancer that have not spread, Karasawa said.

"We are able to conduct this trial because we have greater understanding of what types of breast cancer can benefit from this pinpoint treatment," Karasawa told AFP.

Development of medical apparatus that keeps soft breast tissue immobile for this treatment has also helped, she added.

Japan is a leader in the technology used in the treatment, and is home to three of the world's six medical centres that have the gigantic 10-billion-yen ($97.2 million) facilities, Karasawa said.

The therapy has proved its worth on other forms of cancer, including prostate and lung, Kyodo News said, but has never before been used on breast cancer.

Conventional radiotherapy uses X-rays and gamma rays that are most potent at the surface of the body, but weaken as they travel deeper into the tissue.

Heavy ion particle beams maintain their strength to a much greater depth.

In the trial, Karasawa will treat a total of 20 patients aged at least 60 and with small tumours that have not spread.

The patients will go through an hour of therapy per day for four days, much shorter than conventional radiation therapy that may last for months, Karasawa said.

The trial will follow the patients for five years to assess the outcome, she said.

"Ultimately, this could provide an option for patients who do not want surgery and who cannot go through (common radiation therapy) requiring regular visits to clinics for months," she said.

Japan, which has a high-quality medical system, has a good track record with breast cancer, giving patients a 90 percent five-year survival rate.

Localised and less invasive medical treatments are increasingly important as ageing Japan tries to reduce the physical burden for patients, the national institute said in a statement.

Source-AFP

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New Analysis to Predict Efficacy of Breast Cancer Treatment

by Dr.Enozia Vakil on? May 04, 2013 at 11:35 AM Cancer News A new analysis may help better determine which women with oestrogen-receptor positive breast cancer are at a risk of recurrence, and which ones benefit from endocrine treatment.
The promising new findings will likely benefit the many women with oestrogen-receptor positive breast cancer whose cancer recurs more than five years after diagnosis, researchers told the 5th IMPAKT Breast Cancer Conference in Brussels, Belgium.

The IMPAKT meeting presents cutting edge, 'translational' breast cancer research that is beginning to have an impact for patients.

In oestrogen-receptor positive women, half of all recurrences of breast cancer will occur after the women finish the standard 5 years of hormonal treatment, explains lead author Dr Ivana Sestak from the Wolfson Institute of Preventive Medicine in London, UK.

"There is great interest in establishing which women are at adequate high risk of late recurrence after the initial hormonal treatment period, which is currently 5 years," Dr Sestak says.

At the meeting, researchers reported the findings of a comparison of five different scores designed to predict which women may be at increased risk of developing a late recurrence of their cancer. This is the first time that all five scores have been compared within one dataset.

Knowing which women may be at increased risk of developing a late recurrence would enable doctors to identify those women who may be good candidates for extended hormonal therapy, she says.

The ATAC trial included nearly 10,000 women who were treated with surgery followed by five years of treatment with the drugs anastrozole, tamoxifen or a combination of both. Of these 1,125 from the monotherapy arms (tamoxifen, anastrozole) were included in the transATAC study.

The five scores being compared were the: Clinical Treatment Score, which includes information on the patient's disease and treatments so far; IHC4 score, which characterises the presence of cell surface markers on cancer cells; Three different gene expression scores -- the Oncotype Dx Recurrence Score; the PAM50 Risk of Recurrence Score; and the Breast Cancer Index score. The results showed that the clinical treatment score alone was the best for predicting late recurrence, the researchers report. The components of this score include some that are already widely used by doctors, such as whether the cancer has spread to sentinel lymph nodes, the tumour size and grade.

Among the other tests, the PAM50 risk of recurrence score and the Breast Cancer Index score added the most significant prognostic value between years 5 and 10 after diagnosis.

"The most promising new scores from this study are the PAM50 Risk of Recurrence score and the Breast Cancer Index score, both containing different genetic information that are not included in the clinical treatment score and at the moment not routinely measured in clinics," Dr Sestak says.

"Our further interest now lies in the investigation of which individual components of these scores attribute specifically to the prediction of late recurrence, since the Risk of Recurrence and Breast Cancer Index scores consist of several genes and other components. We are now undertaking these analyses and the results will hopefully tell us which genes specifically predict late recurrence. However, at this stage it is not possible to predict response to treatment."

Commenting on the results, Dr Peter Dubsky from the Medical University of Vienna, Austria, noted that oestrogen-receptor positive and Her2 negative breast cancers are prone to late recurrences.

"About half of all recurrences observed within 15 years of follow-up occur five years after diagnosis. Although there is a sustained benefit of adjuvant endocrine therapy beyond five years, we still see two-thirds of breast cancer deaths occurring after this time. Clearly, the identification of women that are at risk for these late types of recurrences is an important clinical research goal," said Dr Dubsky, who was not involved in the study.

"Sestak and colleagues provide highly relevant new data to meet this end: they have compared five different prognostic scores in order to predict outcome beyond the first five years of follow-up. Of note, none of these scores were primarily trained to specifically predict late recurrence. They show that a Clinical Treatment score (CTS) contained most of the prognostic information relevant to late distant metastases. Interestingly, only the Risk of Recurrence (ROR) score (PAM50) and the Breast Cancer Index (BCI) score provided additional information to the CTS. This data will need further validation before actually being incorporated into clinical decision-making concerning adjuvant endocrine therapy beyond five years."

These findings are similar to those proposed by the Austrian Breast and Colorectal Cancer Study Group recently, Dr Dubsky said. "The Endopredict Score was able to add additional prognostic information to clinical variables concerning distant metastases occurring later than five years after diagnosis. Future research should further address which are the biologic motifs behind late recurrences. Furthermore, molecular tools specifically designed to predict late metastasis should be developed."

Source-Eurekalert

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Study Confirms the Efficacy of Everolimus in Overcoming Resistant Breast Cancer

by Dr.Enozia Vakil on? May 04, 2013 at 11:53 AM Cancer News A new study to determine the efficacy of cancer drug everolimus in overcoming resistance breast cancer has left researchers contemplating a puzzle. The study showed a statistically non-significant benefit in clinical response rates for some patients with early breast cancer when everolimus was added to treatment with trastuzumab.
Yet the results suggest this benefit is achieved independently of the molecular pathways researchers expected would be involved.Prof Mario Campone, Principal Investigator at Institut Cancerologie de l'Ouest in Nantes, France, presented the findings at the 5th IMPAKT Breast Cancer Conference in Brussels, Belgium. The IMPAKT meeting presents cutting edge, 'translational' breast cancer research that is beginning to have an impact for patients. "As more targeted cancer drugs are developed, the challenge is to identify which patients will benefit from individual agents," Prof Campone said.

"One of the objectives of this study was to determine molecular biomarkers that predict whether a patient's cancer is sensitive to the combination of everolimus and trastuzumab compared to trastuzumab alone."Trastuzumab is a monoclonal antibody targeted against the HER2 tyrosine kinase receptor. Many patients who initially respond to trastuzumab develop resistance.

In preclinical studies, everolimus, an oral inhibitor of an important molecule called mammalian target of rapamycin (mTOR), has demonstrated an ability to reverse trastuzumab resistance. However, the mechanisms of action involved in the reversion of trastuzumab resistance are not completely understood."Resistance to trastuzumab may result from several molecular alterations occurring at different levels of the downstream effectors in the PI3K/AKT pathway, all of them resulting in maintenance of signal transduction," Prof Campone explains. "Therefore, using everolimus to inhibit mTOR, a major downstream effector of this pathway, can restore sensitivity to trastuzumab.

In a pre-clinical model, everolimus also reverses trastuzumab resistance caused by upregulation of IGF-1R expression, an alternative signaling pathway, allowing IGF-1 to drive cell growth and proliferation."At the IMPAKT meeting, Prof Campone's group report the first results of a clinical study and analysis of seven biomarkers in patients with early HER2-overexpressing cancers who were receiving treatment with trastuzumab alone, or everolimus plus trastuzumab.Among the 80 patients (40 per arm), the clinical response rate was 35% in the trastuzumab arm and 45% in the patients who received both drugs.

On the other hand, the pathological response rate was 43.5% among patients in the monotherapy arm, and 47.5% in the combination arm of the study."The conclusion of this paper in clinical practice is that the addition of everolimus to trastuzumab seems to improve the clinical response rate but not the pathologic response," Prof Campone said. The researchers also studied a group of seven molecular markers to explore whether they could be used to predict which patients would respond to the combination of everolimus and trastuzumab.

The biomarkers were p4EBP1, pS6, eIF4E, Ki67, pAKT, LKB1, and caspase 3, all of which are involved in pathways that lead to the activation of mTOR."None of these biomarkers was able to predict which patients would see the benefit of the two drugs," Prof Campone said. "It appears the combination of everolimus and trastuzumab is effective independently of the activation of the PI3K/AKT/mTOR pathway and without any anti-proliferative and pro-apoptotic effect."The study provides important confirmation of the benefit of adding everolimus in this clinical setting, comments Prof Christoph Zielinski, Chairman of the Department of Medicine I at Medical University Vienna, Austria."This is a rather small trial with a limited number of patients, although it quite unequivocally shows that the addition of everolimus to trastuzumab leads to an increase in clinical responses in Her-2/neu overexpressing breast cancer, as compared to trastuzumab alone," he said.

"Thus, it not only adds to clinical possibilities which can be offered to patients, but also further explains the modalities of molecularly directed therapeutic manipulation in breast cancer," said Prof Zielinski. However, the limited pathologic response constitutes a clear drawback from clinical observations."Nevertheless this study contributes to our assumptions on the application of molecularly targeted therapies in breast cancer in particular and in malignancies in general. It also helps to move to an era where the targeting of multiple molecular structures (like here with trastuzumab and everolimus) leads to ameliorated results by 'hitting' multiple growth-regulating mechanisms, but also avoiding treatment resistance which continues to be a major challenge in cancer treatment."

Source-Eurekalert

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