Archive for the ‘Colon Cancer’ Category

Has an achilles’ heel for cancer been found?

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Posted 03 Jan 2012 — by James Street
Category Colon Cancer, DNMT1, genetic research, MBD2

RESEARCH into a gene called MBD2 could lead to new treatments for colon cancer, after experts discovered that switching it off prevents tumours from forming.

The breakthrough has been described as a “potential Achilles’ heel” by lead research Professor Alan Clarke.

It comes from the work at the Cancer Research UK Centre in Cardiff into how genes and proteins are involved in the formation of cancer.

Prof Clarke said: “The interesting thing about cancer is that one of its primary features is to turn off a number of defensive mechanisms. As the cancer develops, these defensive mechanisms are got around, usually because the genes are switched off or deactivated.”

 The first breakthrough came with the discovery of the DNMT1 gene, which, when switched off meant that cancers couldn’t develop.

But deactivating DNMT1 also had a significant effect on other bodily functions, meaning it would not make a good target for cancer therapies.

MBD2 belongs to a family of proteins which turn off other genes and research carried out in Cardiff has found that deactivating it prevents colon tumours from developing.

“It’s fantastic and does it with virtually 100% efficiency,” Prof Clarke said. “And, taking out MBD2 isn’t that damaging to other tissues and systems – it appears to be tolerated reasonably well.

“Therefore, if we were to have a therapy targeting MBD2, any off-target effects would be limited.”

The research team has been examining the impact of MBD2 by creating mice which lack the gene. But many questions remain unanswered.

Prof Clarke said: “We have to show that if you don’t have MBD2 then the likelihood of getting a tumour is much reduced. And we don’t know if you take out MBD2 from a tumour whether it will disappear.

“We’ve been trying to develop a drug that specifically targets MBD2 but, unfortunately, attempts have not been successful because it’s a very difficult protein.

“We think that MBD2 deficiency suppresses tumorigenesis by failing to turn off a number of genes – some these will be important. We’re trying to delve down and find out which of the genes it regulates are important.

“We have a potential Achilles’ heel here to stop tumours forming and we’re also trying to find a drug target.

“We can imagine that this will be useful for patients who have had a tumour and have had therapy but who have a chance of relapsing. But we’re also testing the notion that regulating MBD2 will cause tumours to regress.”

Prof Clarke added: “The remarkable thing about the way we treat cancer is that we’re stuck with pretty much ancient technology.

“We mostly use poisons but although we have made progress with virtually all forms of cancer in terms of improving treatment, if we are going to make a huge step change it will have to come from a better understanding of the mechanisms that lead to cancer.

“That will come from a molecular understanding of cancer – if we really understand the molecular basis we can create drugs that make a big difference rather than small, incremental differences.”

New analytical method enhances the possibility of selecting optimal cancer treatment

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Posted 12 Nov 2011 — by James Street
Category Colon Cancer, genetic research, Individualized treatment, Personalized, Tumor biomarkers

For a cancer treatment to be adapted to each individual patient, a large number of tumor samples need to be examined carefully.

Collaboration between a company and Uppsala University has now led to a method that makes this process ten times more efficient than in the past.

New cancer treatments that target specific molecules in the tumor are under development. But for this to be effective, it’s necessary to know first what mutations caused the tumor. By analyzing the sequence of genes that are often mutated in certain tumor forms, it is possible to increase the possibility of selecting optimal treatment for each patient.

Researchers at the Department of Immunology, Genetics, and Pathology at Uppsala University are collaborating with the company Halo Genomics in a project designed to identify mutations that cause cancer of the large intestine. The scientists selected 560 genes in 192 tumor samples, and Halo Genomics produced a so-called HaloPlex™ PCR-analysis that covered all the genes.

– With this analytical method it took a week for one person to prepare the 192 samples for sequencing, without any need for special equipment. This increases productivity by a factor of up to ten compared with conventional methods, says Professor Mats Nilsson, who has directed the project.

The samples are now being sequenced at SciLifeLab in Uppsala. The researchers expect to be able to identify exactly what molecules are affected in tumor cells from individual patients.

– This will be of significance when it comes to selecting the right kind of targeted treatment for patients in the future, says Mats Nilsson. The method is promising for use in diagnostics because of its low cost and high efficiency.

Read more about SciLifeLab.

Ginger Root Extract’s Potential in Colorectal Cancer Prevention

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Posted 28 Oct 2011 — by James Street
Category Colon Cancer, gengerol, Inflamation, Prevention
By Anna Azvolinsky, PhD | October 25, 2011
 A small phase II clinical trial published in the Journal of Clinical Oncology has shown that consuming ginger root decreased harmful inflammatory prostaglandins in the colon and was tolerable and non-toxic (DOI:10.1158/1940-6207.CAPR-11-0224). The trial participants taking ginger root extract had lower levels of colon inflammation markers compared to those taking placebo. The research team, which includes Suzanne Zick, assistant research professor at the University of Michigan Department of Family Medicine and others at the University of Pittsburgh and the Baylor College of Medicine believe the result warrants further trials in individuals that are at high risk for development of colorectal cancer.

The randomized, blinded study compared colon inflammation levels in 16 individuals taking daily ginger root extract with 17 individuals taking placebo. All study participants had normal risk for developing colon cancer with no evidence of disease or family history of the cancer. The experimental arm consumed 2 grams of ginger root supplement for 28 days. The dose—two grams of ginger extract—was chosen based on the highest tolerated dose in a phase I trial and because two grams of the extract is approximately 20 grams of raw ginger root, “a large, but not unreasonable amount to consume” in one’s diet according to the researchers. The composition of the ginger root extract was tested biochemically to measure the amount of active gingerols and shogaols that are responsible for the therapeutic properties of ginger.

Gingerols and shogaols are two components of ginger that are known to have both both antioxidant and anti-inflammatory actions. While the way that ginger exerts its anti-carcinogenic function is still being teased out, it is known from animal models that ginger inhibits several different lipoxygenases (LOX) and cyclooxygenases (COX) enzymes. These enzymes have a role in the formation of eicosanoids, including prostaglandins, which have a pro-inflammatory function. Mouse models have shown that ginger can be preventive of colon carcinogenesis but not in the treatment of early stage colonic tumors. What makes ginger an attractive colorectal carcinogenesis preventive agent is that it not only impacts the metabolism of the COX enzymes, but also other eicosanoid enzymes, potentially shifting these pathways towards an anti-inflammatory state in the gut.

Ginger root has had a long tradition of easing gastrointestinal distress. Its effects on the digestive tract have recently been supported by scientific research that shows ginger has important therapeutic properties that include antioxidant effects, direct anti-inflammatory effects and the inhibition of the formation of certain inflammatory compounds. Ginger’s anti-inflammatory effects have also been demonstrated for those with osteoarthritis or rheumatoid arthritis that consume ginger on a daily basis.

Not surprisingly, ginger root is one of the most consumed dietary agents worldwide and is one of the most-bought herbal supplements in the United States.

The participants of the study underwent signmoidoscopies prior to the study and following the 28-day regimen. Biopsies were analyzed for colon inflammation levels including the levels of eicosanoid enzymes such as prostaglandins. Prostaglandin E2 (PGE2), an inflammatory eicosanoid produced during early colorectal cancer development, was decreased by 28.0% on average, and by 7% when normalized to protein from baseline colon mucosal levels. Interpretation of this result will have to await more research, however, as the amount PGE2 needs to be decreased in colonic mucosa in order to prevent cancer-onset is not yet known.

The authors suggest that a larger trial in individuals at high-risk for colorectal cancer is warranted based on the results of this phase II trial to test whether ginger also has an anti-inflammatory effect in these individuals. Additionally, the mechanisms of anti-inflammation and antioxidant function of ginger components need to be studied and their effects of the COX and LOX pathways of inflammation and anti-inflammatory eicosanoids.

Harvard Scientists Discover How Cancer Outwits Erbitux Drug

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Posted 08 Sep 2011 — by James Street
Category Breast Cancer, Colon Cancer, Erbitux, genetic research, HER2/neu
By Robert Langreth – Sep 7, 2011

Harvard University scientists have discovered how colon cancer resists effects of the cancer drug Erbitux, a mechanism that may be overcome by adding certain treatments used to combat breast tumors.

Researchers from Harvard Medical School found that tumors in which Eli Lilly & Co.’s and Bristol-Myers Squibb Co. (BMY)’s Erbitux didn’t work well or stopped working had excess activity in a growth-promoting protein known for its role in breast tumors. The finding suggests that breast cancer medicines including Herceptin from Roche Holding AG (ROG) might be combined with Erbitux to surmount resistance.

Recent studies are showing how tumors sidestep targeted cancer drugs by activating other growth-promoting molecules. The findings may help doctors develop new drug combinations that squelch the resistance, said Pasi Janne, senior author of the study and a medical oncologist at Dana-Farber Cancer Institute and Harvard Medical School in Boston.

“Until now we didn’t know what caused acquired resistance to Erbitux,” Janne said in a telephone interview. “Our hope is that this will very rapidly translate into clinical trials” of new drug combinations. The study, done in collaboration with researchers at Kinki University School of Medicine in Osaka, Japan and other universities, is published today in Science Translational Medicine.

Scientists studied colon tumor samples from patients who were treated with Erbitux, as well as tumor cells in the test tube that resisted Erbitux’s effects.

Cancer-Growth Genes

The research began when Janne and his colleagues generated lung cancer cells in the test tube that were able to evade the effects of Erbitux by making additional copies of a growth- boosting gene called ERBB2, or HER2. The protein made by the gene is overabundant in some breast cancers and is targeted by Herceptin and GlaxoSmithKline Plc (GSK)’s Tykerb breast cancer drug.

The researchers decided to investigate whether human colon tumors also could evade Erbitux by activating HER2. When they looked at tumor samples from 233 colon cancer patients who received Erbitux, they found that the 13 patients with excess HER2 died sooner than other patients who didn’t have excess HER2. They also obtained tumor or blood samples from 11 patients whose tumors had progressed after initially responding to Erbitux. In four of the patients, HER2 levels were higher at the time of disease progression compared with before treatment.

When the researchers treated animals whose tumors were resistant to Erbitux alone with a combination of both Erbitux and a HER2 blocking drug, the tumor growth was held in check again.

HER2 Overactivation

The findings indicate that overactivation of the HER2 protein may be a way that some colon tumors become resistant to Erbitux, Janne said. He said he hoped that clinical trials combining Erbitux with HER2 blocking drugs in advanced colon cancer patients could begin within six months.

“Maybe we can extend the benefits of Erbitux much further” by developing drug combinations that attack the resistance mechanisms, he said. “This has real implications” for patients.

Bristol-Myers Squibb, based in New York, reported $662 million in Erbitux sales in 2010.

“The companies will review these data, but cannot provide further comment about the findings at this time,” Sarah Koenig, a Bristol-Myers spokeswoman, said in an e-mail.

Krysta Pellegrino, a spokeswoman for Roche, said that while the company wasn’t familiar with the research, it thinks that “the hypothesis is scientifically sound.”

To contact the reporter on this story: Robert Langreth in New York at rlangreth@bloomberg.net;

To contact the editor responsible for this story: Reg Gale at rgale5@bloomberg.net

Blood test to detect colon cancer gains traction, radiologists remain unconcerned

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Posted 04 Aug 2011 — by James Street
Category Colon Cancer, CT Colonoscopy, Diagnostic
By Rebekah Moan | December 9, 2010

 

Despite the increasing popularity of blood testing for colorectal cancer, radiologists don’t have to worry CT colonography will be replaced just yet, according to experts.

A new test from Epigenomics and Warnex Medical Laboratories is infiltrating the ranks of the colon cancer screening world. On Dec. 6 the companies announced the Canadian launch of their diagnostic blood testing service. The test is derived from a blood sample and detects cell-free methylated DNA of the Septin9 gene shed into the bloodstream by colorectal tumors.

Diagnostic Imaging first reported on the Septin9 test in October. But researchers remain unconvinced Septin9 will edge out CT colonography.

“The Septin9 blood test is meant to identify colorectal cancer after it has developed and potentially already spread outside of the bowel wall,” said Dr. Judy Yee, a professor and vice chair of radiology and biomedical imaging at the University of California, San Francisco and a CT colonography expert. “It is not meant to prevent colorectal cancer.”

The purpose of CT colonography, on the other hand, is to identify precursor polyps before cancer develops, she said.

“The goals of the two tests are very different,” she said.

The Septin9 blood test may not be mature enough yet for use, according to Dr. Perry Pickhardt, a professor of radiology at the University of Wisconsin, Madison and also a CT colonography expert.

In the PRESEPT study, Septin9 detected two-thirds of colorectal cancers with a specificity of only 88%.

That means one in every three cancers would be missed, Pickhardt said.

“If this were applied to a screening population, where cancer is present in about one in every 500 adults, there would be more than 60 false-positive tests for every cancer detected,” Pickhardt said. “I don’t believe these are acceptable results, especially when you compare other noninvasive options, such as CT colonography, where the sensitivity and specificity for cancer detection is >95%.”

An attractive option might be following the Septin9 blood test with CT colonography because the risk of cancer is too low to justify colonoscopy in all cases, he said.

In any case, CT colonography remains viable in the radiology world for the detection of colon cancer.

STAT3 Found to be Associated with Adverse Clinical Outcomes in Colorectal Cancers

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Posted 29 Jun 2011 — by James Street
Category Colon Cancer, STAT3
By Anna Azvolinsky, PhD | March 11, 2011

 

A model example of personalized cancer therapy that has demonstrated improved patient outcomes is the use of anti-HER2 treatment. Breast cancer patients screened via molecular diagnostics and identified as having amplification of the HER2 gene generally have a poorer prognosis, but show better responses to anti-HER2 treatment.


Structure of the STAT3 protein. Source: Wikimedia Commons user Emw

Identification of biomarkers that are both predictive of outcome and are good candidates for the development of targeted treatments is a major goal of oncology research. Recent studies in colorectal cancer patients have found that as many as 99% of patients harboring a KRAS mutation do not respond to EGFR antibody treatment. This type of tumor classification has a very high value in predicting outcomes and selecting appropriate treatment, but unfortunately, the development of predictive markers for most cancers is still in its infancy.

STAT3 shown potential as prognostic factor in colorectal cancer
In a paper published on February 10, 2011 in the online version of Clinical Cancer Research (doi:10.1158/1078-0432.CCR-10-2694), researchers from the Dana-Farber Cancer Institute and Harvard Medical Schools have identified the activated signal transducer and activator of transcription (STAT3) protein as a potential predictive marker in colorectal cancer. The large-scale, 724-patient study found that higher levels of the activated version of the STAT3 protein was associated with adverse clinical outcomes among colorectal cancer patients. This work supports further study of this molecular target as both a prognostic marker and a therapeutic target.

STAT3 is a transcription factor that is constitutively activated in some cancers and appears to play a role in many important cellular processes including cell division, survival, angiogenesis, and tumor-related inflammation. STAT3 has also been shown to thwart anti-tumor immune response. Whether STAT3 has utility as a prognostic factor in colorectal cancer has not been well studied with one previous small sample size study showing no association, two showing poor prognosis and one study showing better prognosis associated with activated STAT3.

The authors used a database of 724 colorectal cancer patients from two prospective studies that had clinical, pathological, and molecular data, including KRAS, BRAF, and PIK3CA mutation status to evaluate the relationship of these variables to activated STAT3 status to eliminate potential cofounding variables

The Results
18% of patients had high levels activated STAT3 expression. High levels of activated STAT3 were significantly associated with shorter cancer-specific survival and significantly higher colorectal cancer-specific mortality as compared to STAT3-negative cases. The study researchers did not find an significant modifying effects of other variables, including age, sex, BMI, family history of colorectal cancer, tumor location, stage, grade, and molecular mutations, on STAT3 expression status.

Activated STAT3 expression appears to be an independent prognostic factor for colorectal cancer and may serve as a prognostic marker for colorectal cancer patients in the future and for patient selection in future clinical trials when the results of this study are well validated.

Growth-inhibitory effects of the astaxanthin-rich alga Haematococcus pluvialis in human colon cancer cells

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Posted 16 Jun 2011 — by James Street
Category Apoptosis, Colon Cancer, Drug Testing, General Cancer Research
Paola PalozzaaCorresponding Author Informationemail address, Cristiana Torellia, Alma Boninsegnaa, Rossella Simonea, Assunta Catalanoa, Maria Cristina Meleb, Nevio Piccic

Received 19 December 2008; received in revised form 17 March 2009; accepted 18 March 2009. published online 08 May 2009.

Abstract

The growth-inhibitory effects of the astaxanthin-rich Haematococcus pluvialis were studied in HCT-116 colon cancer cells. H. pluvialis extract (5–25μg/ml) inhibited cell growth in a dose- and time-dependent manner, by arresting cell cycle progression and by promoting apoptosis. At 25μg/ml of H. pluvialis extract, an increase of p53, p21WAF-1/CIP-1 and p27 expression (220%, 160%, 250%, respectively) was observed, concomitantly with a decrease of cyclin D1 expression (58%) and AKT phosphorylation (21%). Moreover, the extract, at the same concentration, strongly up-regulated apoptosis by modifying the ratio of Bax/Bcl-2 and Bcl-XL, and increased the phosphorylation of p38, JNK, and ERK1/2 by 160%, 242%, 280%, respectively. Growth-inhibitory effects by H. pluvialis were also observed in HT-29, LS-174, WiDr, SW-480 cells. This study suggests that H. pluvialis may protect from colon cancer.

CT Colonography Equal to Ocular Colonoscopy, says Study

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Posted 13 May 2011 — by James Street
Category Colon Cancer, Cost, CT Colonoscopy, Diagnostic, Ethics of Science, Finance and Politics of cancer research and treatment
By Deborah Abrams Kaplan | May 5, 2011

 

CT colonography is a better screening test than optical colonoscopy (OC), according to a new study published in the MayRadiology print issue. Using meta-analysis of studies done over a 15 year period, authors found that the sensitivity of CT colonography for colorectal cancer detection was 96.1 percent, compared with 94.7 percent for OC.

Authors noted that their study supported the clinical equivalence of CTC and OC for screening invasive cancers. They felt the CTC was mature enough to be seen as a universal procedure.

Aside from the sensitivity rates being roughly equal, there are other reasons that the CTC can be better for screening, including cost and the minimal invasiveness. One potential downside, however, is that CTC exposes the patient to radiation, though lead author Perry J. Pickhardt, MD, a professor of radiology at the University of Wisconsin School of Medicine doesn’t think the amount is concerning. “CTC is a low-dose exam applied to adult patients,” he said. “There are no meaningful implications related to the radiation exposure.”

The meta-analysis ultimately included 49 studies covering 11,551 patients, done from January 1994 (the year that CT colonography was first mentioned), through 2009. All the CTC studies were for screening, to diagnose colorectal polyps and cancer, and all positive results were proven histologically. Six studies, encompassing 42 percent of the participants, focused on asymptomatic patients typical in a screening setting. The remaining 43 studies included symptomatic patients and/or a disease-enriched population.

Authors note the low prevalence of invasive colon cancer in screenings, citing a cumulative 3.6 percent rate from the meta-analysis. A total of 414 colorectal cancers were found in the studies, including 20 in the screening group (less than a 0.5 percent prevalence rate) and 394 in the disease-enriched group (almost a 6 percent prevalence rate).

As for the cost, Pickhardt says that using CTC is less expensive. “Our work has shown that CTC is considerably more cost-effective as a primary screening test compared with colonoscopy.”

One reported reason that patients are less likely to get a colonscopy is because the evacuatory and uncomfortable nature of the bowel preparation. Plus, OC requires the use of some anesthesia or medication for patient comfort. With CTC, those issues are diminished, according to Pickhardt. “CTC is much less invasive, requires no IV for sedation or pain medication, and requires no recovery time,” said Pickhardt, adding that patients don’t need a driver to take them home. “In addition, our low-volume bowel prep is much better tolerated than the typical colonoscopy preps in use.”

Research breakthroughs may lead to colonoscopy alternative: NetWellness

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Posted 30 Apr 2011 — by James Street
Category Colon Cancer, genetic research
Published: Friday, April 29, 2011, 1:37 PM     Updated: Friday, April 29, 2011, 1:42 PM

From the Cleveland Plain Dealer

For men and women combined, colon cancer stands as the leading cause of cancer-related deaths in the United States. Given this reality, researchers across the globe work to make advancements in the detection, diagnosis and treatment of this disease.

A leading example of this work can be found in the Markowitz laboratory at the Case Western Reserve University School of Medicine. The laboratory research can be separated into three broad categories: inheritance and colon cancer, the effect of mutations on colon cancer defense, and advancements in colon cancer screenings.

Inheritance and colon cancer

The research focus of the Markowitz laboratory concerns cancer inheritance; the genetic risk for developing colon cancer. By identifying inherited risk, tests can be created to recognize individuals at high risk for colon cancer who can benefit from screening to detect colon cancer and precancers in early stages when there is a better chance of the disease being cured. A growth is considered to be precancerous when cells are undergoing abnormal changes that, left untreated, could lead to cancer. As the process continues, these cells may develop changes that are definitive for cancer.

Sanford Markowitz.pngThis week’s NetWellness column is authored by Dr. Sanford Markowitz, professor, Department of Molecular and Microbiology, School of Medicine, Case Western Reserve University . 

For more information, visit the NetWellness Colorectal diseases health topic.

Along with other CWRU faculty members, the lab led a study to determine if there was an genetic (inherited) marker in families for colon cancer. A genetic marker is an alteration in DNA that may indicate an increased risk of developing a specific disease. By finding these markers, researchers are able to trace a certain trait (like colon cancer) from person to person within families.

This particular study involved families in which two or more siblings who at age 65 (or younger) developed colon cancer or large precancerous polyps. This “colon cancer sibling study” gained exposure with the help of CBS Evening News anchor Katie Couric and recruited families from across the country.

In 2003, researchers discovered that many of the people who had developed colon tumors inherited the same abnormal region on a specific chromosome, chromosome 9. (A chromosome is a single piece of coiled DNA that contains many genes, which determine a person’s inherited characteristics.)

By 2009, the team was able to identify that certain people who developed colon cancer inherited a nonworking form of a specific gene in this region named the GALNT12 gene. Research to date suggests that this defective gene may result in defective colonic mucins and in inflammation of the inner wall of the colon, giving rise in turn to colon cancer. Many genes other than GALNT12 have been shown to affect the creation of mucins in the intestines. Therefore, this discovery is only the tip of the iceberg and more research is under way.

How mutations limit cancer defense

Like brakes on a car, the role of tumor suppressor genes is to slow and even stop abnormal cells from dividing. When left unchecked, the fast division of these defective cells leads to cancer. Mutations (abnormal DNA) in special genes that prevent tumors from developing (tumor suppressor genes) remove one tool of the body’s defense to cancer. Finding the culprit attacking the tumor suppressor genes is an important way to identify how cancer is brought on and how it can be treated.

Since 1995, one of the initiatives of the laboratory has been the discovery of mutations that wipe out the body’s normal ability to keep colon cancer from forming. Research conveyed that more than one-third of human colorectal cancers showed mutations in a particular gene, called TGF-beta Receptor 2 (RII). One role of RII is to turn on another gene, named 15-PGDH, which in turn keeps tumors in the colon from forming. Similar to a domino effect, when RII does not work properly, 15-PGDH is not present. This is now believed to be one key cause of colon cancer.

By knowing how a cancer starts, more specific and targeted therapies can be discovered. Research shows that the levels of 15-PGDH in the colon determine how effective existing drugs will be in people with colon cancer. In some cases drug therapies may be the best option, but the lab is now working on developing gene therapies for those who lack 15-PGDH in their colon. Medications are being investigating by the Markowitz Lab to increased or reactivate the effective functioning of this gene as a new treatment for colon cancer.

From lab bench to bedside

Currently, colonoscopies remain the physician’s best tool for the early detection of colon cancer in patients. However, many patients remain fearful of the test, due to its uncomfortable, laxative-based preparation and its cost (when not covered by insurance). In an effort to give patients another colon cancer screening option, researchers at CWRU have developed an alternative, marketed as Colosure. In 2009, the American Cancer Society added DNA testing to its colon cancer screening guidelines.

Through research, it was discovered that abnormal DNA is produced by colon cancer, and could be identified from the stool of colorectal cancer patients. Regardless of the location of the cancer in the colon, the test was able to detect 77 percent of stage I and stage II colorectal cancers.

Using a stool sample that is taken at home, this noninvasive test identifies DNA markers for colon cancer. Though not covered by some insurances, the $250 cost of this test is much less than that of a colonoscopy, which can cost more than $3,000 when not covered by insurance or when insurance is unavailable. Colosure is now available for order by doctors and more testing is under way to improve the sensitivity of the test. This stool DNA test should be considered in cases where colonoscopies are not feasible, for reasons such as financial and medical concerns.

Also in 2009, collaboration between researchers at CWRU and Johns Hopkins University showed that a colon cancer blood test proved promising. By detecting genetic cancer markers in colon cancer patient’s blood, nearly half of early-stage colon cancer cases were able to be detected in studies. Further studies are planned to improve the sensitivity of the test. Its use as a detection tool for early recurrences of colon cancer following initial surgery is also being investigated.

© 2011 cleveland.com. All rights reserved.

Colorectal Cancer No Match for Tumor-Sniffing Dog?

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Posted 04 Feb 2011 — by James Street
Category Colon Cancer, Diagnostic, Dog Osteosarcoma, Osteosarcoma
Posted by David W Freeman
labrador retriever, stock, 4x3Scientists in Japan say they’ve trained a Labrador retriever to detect colon cancer. (istockphoto)

(CBS) Some dogs have trouble with basic commands like “Sit” and “Fetch.” Marine’s moved on something a bit more complicated:

“Detect colon cancer.”

It’s no joke. Researchers in Japan say the specially trained Labrador retriever can literally sniff out colorectal cancer with 98 percent accuracy.

Marine’s initial training was for water rescue, and she had already demonstrated an ability to detect 12 different kinds of cancer simply by taking a whiff of patients’ breath, HealthDay reported.

To find out if Marine could also detect colon cancer, researchers led by Dr. Hideto Sonoda, a professor of surgery at Kyushu University in Fukuoda, Japan, let her sniff samples of stool and exhaled breath from 30 people with colorectal cancer and 320 healthy people.

Marine was able to tell cancerous samples in 33 or 36 breath tests and in 37 of 38 stool tests, according to HealthDay. Just as impressive, she was good at detecting early-stage cancers – something that isn’t always possible with fecal occult blood screening, a noninvasive test in which blood in the stool reveals the presence of cancer.

What’s Marine’s secret?

“Scientists suspect that the dog recognizes the scent of volatile chemicals present in colon cancer,” the American Cancer Society’s Dr. Ted Gansler told Aol. “These chemicals are apparently released from the cancer cells into the feces and also absorbed into the bloodstream and then released into air as blood flows through the lungs.”

Will a cancer-detecting mutt be on hand for your next doctor’s visit? Don’t bet on it. Given the cost and time required to train dogs like Marine, doctors are hoping to develop a new sensor capable of detecting the same cancer-specific compounds Marine detected, the Daily Mail reported.

Marine’s cancer-screening prowess was described in a report published in the Jan. 31 online edition of the journal “Gut.”

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