Matrix Genomics

Bitter Melon Extract Decreased Breast Cancer Cell Growth

Larry Corder, PhD — Wed, 24 Feb 2010 16:52:39 +0000

"Our findings suggest that bitter melon extract modulates several signal transduction pathways, which induces breast cancer cell death," said lead researcher Ratna B. Ray, Ph.D., professor in the Department of Pathology at Saint Louis University. "This extract can be utilized as a dietary supplement for the prevention of breast cancer."

Results of this study are published in Cancer Research, a journal of the American Association for Cancer Research.

Previous research has shown Momordica charantia, also known as bitter melon, to have hypoglycemic and hypolipidemic effects, according to Ray. Because of these effects, the extract is commonly used in folk medicines as a remedy for diabetes in locales such as India, China and Central America, according to the researchers.

Using human breast cancer cells and primary human mammary epithelial cells in vitro, Ray and colleagues found the mechanism of bitter melon extract significantly decreased proliferation, that is, cell growth and division, and induced death in breast cancer cells. These early results offer an encouraging path for research into breast cancer.

"Breast cancer is a major killer among women around the world, and in that perspective, results from this study are quite significant," said Rajesh Agarwal, Ph.D., professor in the Department of Pharmaceutical Sciences at the University of Colorado, Denver School of Pharmacy. "This study may provide us with one more agent as an extract that could be used against breast cancer if additional studies hold true."

According to Agarwal, the Cancer Research associate editor for this study, the simple study design, clear-cut results and the overall importance of these findings in breast cancer prevention makes this research different from previous research.

However, he stressed that "this study is only a step towards establishing the cancer preventive efficacy of bitter melon against breast cancer." Additional studies are needed to further understand the molecular targets of bitter melon extract in cancer cells, as well as for establishing its in vivo efficacy. Agarwal gave a note of caution, stating that while these results do provide hope as an anti-cancer agent, it is important to establish the validity of these results in animal models before adding them to one’s diet to inhibit breast cancer cell growth.

Ray and colleagues are currently conducting follow-up studies using a number of cancer cell lines to examine the anti-proliferative effect of the extract. They are also planning a preclinical trial to evaluate its chemopreventive efficacy by oral administration.

Bitter melon extract is cultivated in Asia, Africa and South America. Extract of this vegetable is being popularized as a dietary supplement in Western Countries, since it is known to contain additional glycosides such as mormordin, vitamin C, carotenoids, flavanoids and polyphenols.

Abstracted from Science Daily February 23, 2010

Bitter melon extract, a common dietary supplement, exerts a significant effect against breast cancer cell growth and may eventually become a chemopreventive agent against this form of cancer, according to results of a recent study.

Prevention: An ibuprofen a day could keep Parkinson’s away

Elizabeth Corder, PhD — Fri, 19 Feb 2010 17:35:57 +0000

New research shows people who regularly take ibuprofen may reduce their risk of developing Parkinson’s disease, according to a study released February 17 that will be presented at the American Academy of Neurology’s 62nd Annual Meeting in Toronto April 10 to April 17, 2010.

The research involved 136,474 people who did not have Parkinson’s disease at the beginning of the research. Participants were asked about their use of non-steroid anti-inflammatory drugs (NSAIDs), including aspirin, ibuprofen and acetaminophen. After six years, 293 participants had developed Parkinson’s disease.

The study found regular users of ibuprofen were 40 percent less likely to develop Parkinson’s disease than people who didn’t take ibuprofen. Also, people who took higher amounts of ibuprofen were less likely to develop Parkinson’s disease than people who took smaller amounts of the drug. The results were the same regardless of age, smoking and caffeine intake.

"Ibuprofen was the only NSAID linked to a lower risk of Parkinson’s," said Xiang Gao, MD, with Harvard School of Public Health in Boston. "Other NSAIDs and analgesics, including aspirin and acetaminophen, did not appear to have any effect on lowering a person’s risk of developing Parkinson’s. More research is needed as to how and why ibuprofen appears to reduce the risk of Parkinson’s disease, which affects up to one million people in the United States."

Abstracted from Science Daily, Febuary 18, 2010

Family history and Chronic Disease Risk Assessment

Elizabeth Corder, PhD — Tue, 16 Jun 2009 20:08:20 +0000

Coronary Artery Disease as an Example

Approximately 13 million Americans have coronary artery disease (CAD) and it is the leading cause of death both in the US and across the world. While modification of many known risk factors (such as sedentary lifestyle, smoking, obesity, and high-fat diet) is effective at reducing death and complications related to CAD¹, family history remains one of the strongest independent risk factors for development of this disease.^2,3

Having a sibling or parent with CAD at least doubles your risk for developing the disease. A family history of CAD in second-degree relatives (aunts, uncles and grandparents) can also significantly impact risk.³ Further, personal, modifiable risk factors and family history act in a multiplicative fashion.² Extended 3- to 4-generation family histories are considered by some, e.g. Helix Health of Connecticut, to be the best “genetic test” for many of these conditions.⁴

We do not support this point of view. Each person is genetically unique, deriving risk and protective factors from both parents. Matrix Genomics is able to estimate the level of inherited risk for acute myocardial infarction, a major consequence of CAD, by making a number of genetic determinations in relevant genes. The results are compared to the published high risk pattern for acute myocardial infarction.⁵ This defines a wide range of risk from very low to very high – that might be modified by changes in lifestyle or relevant pharmaceutical interventions. We propose this approach as a he first step in creating a personalized management plan.

http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_Summary.html accessed August 28, 2007
Scheuner MT, Whitworth WC, et al. Familial risk assessment for early-onset coronary heart disease. Genet Med 2006:8(8):525–531
Scheuner MT, Whitworth WC, et al. Expanding the definition of a positive family history for early-onset coronary heart disease. Genet Med 2006;8(8):491-501
Robin NH, Tabereaux PB, et al. Genetic Testing in Cardiovascular Disease. J Am Coll Cardiol 2007; 50(8):727-37
Licastro F, Chiapelli M, Caldarera CM, Caruso C, Lio D, Corder EH. Acute myocardial infarction and proinflammatory gene variants. Ann NY Acad Sci 2007; 1119:227-242

Genetic Testing Pitfalls

Larry Corder, PhD — Thu, 11 Jun 2009 21:17:17 +0000

There are any number of genetic testing services on the world wide web. I am sure their numbers are growing as you read this post. Each of them offers their own array of tests and services which are packaged together in myriad forms. In situations where regulation is limited, it is up to the buyer to evaluate the products that are for sale. A few questions, in my opiinion, should be asked about these products before they are purchased.

First, what is the range of risk covered fby the genetic test? For example, does a test for breast cancer risk cover a 2 fold or a thirty fold range of risk? Based on the number if genes tested and their interactions, what range of risk is available for you to interpret your test score within for a reasonable appraisal of how likely you could be to get the disease? Second, does the price of the genetic test include a report that places the observed level of risk in the context of the population at risk? Ask yourself; if not then why not? Third, if a genetic counselor’s services are available.as part of a package that you are thinking about buying; the customer should verify the background and training of the genetic counselor as well as their availablity. In the United States, genetic counselors are accredited after a course of study that usually ends in a Master’s Degree. Find out about a genetic counselor’s credentials before you sign up.

A genetic signature for a third of Parkinson’s disease (LRRK2 gene)

Elizabeth Corder, PhD — Mon, 08 Jun 2009 20:57:54 +0000

Matrix Genomics, Inc. is offering a new test for Parkinson’s disease. It is based on now-published research. This research identified a concise genetic signature found among a third of Parkinson’s disease (PD) patients—but at very low frequency in the general population. The signature is found in the LRRK2 gene located on chromosome 12. The work was led by Elizabeth H. Corder, PhD, Scientific Director at Matrix Genomics.

We were interested in Parkinson’s disease becasue it is the second most common neurodegenerative disorder in the Western world, and a major cause of disability and distress among older Americans. Family studies have long indicated that Parkinson’s is a genetic disorder when certain mutations are inherited. However, specific genetic factors relevant to the general population have been elusive.

The PD gene that we investigated is called leucine risk repeat kinase 2 (LRRK2) which encodes a protein called dardarin, derived from the Basque word dardara, meaning tremor. Mutations in LRRK2 are a common cause of familial Parkinson’s disease. This study published in the Annals of Human Genetics describes a combination of four gene variants found in a third of Parkinson’s cases, but infrequent in the population. Thus the presence or absence of this signature can be used as a genetic test for Parkinson’s disease. [Patent pending]

Earlier work had identified each of the four variants as being associated with PD risk, but did not combine the information to make a specific risk signature.

Genetic testing using this approach is expected to identify a third of persons at very high risk. It will not identify other genetic factors or level of risk due to environmental exposures, such as pesticides, and lifestyle. Thus the absence of this risk signature does not guarantee low risk. This finding helps us understand what causes PD and could lead to new and more effective avenues for prevention and treatment. The advance is expected to identify individuals at greatest risk for PD before symptoms arise, when therapies and lifestyle changes might be most effective in slowing disease progression.

In 1993, I was the lead author on the Science article that described how risk for Alzheimer’s disease multiplied according to the number of copies of the apolipoprotein E allele 4 inherited from parents. This finding has been replicated in hundreds of studies and remains the one established genetic risk factor for Alzheimer’s disease, and the prototype for investigating common gene variants for common disorders. We continue to investigate the genetic underpinnings of PD.

The World of DNA Testing

Larry Corder, PhD — Mon, 20 Apr 2009 18:29:12 +0000

This is the first post at our blog www.matrixgenomics.com. Matrix Genomics, Inc. is a new company. It specializes in DNA tests for common health conditions that run in families. Not eveyone will be interested, e.g. some people don’t want to know their specific disease risks, for financial reasons, or because they do not view the diseases we test risk for to be particularly relevant to their own circumstances. However, people who have a family history of Parkinson’s disease, Alzheimer’s disease, heart attack, or female breast cancer may wonder about their own risk of getting these diseases and wish to find out more about where they stand. If you have these concerns, we can help you find out a great deal more about you acutual level of risk based on the genes that you inherited from your parents.

We do so by by using many genes known to be associated with a specific disease’s pattern of onset from case control studies to determine the range of risk for the disese in the population and often determines an individual’s risk on that continuum directly based on their genetic endowment. This approach is no small thing and distinguishes our company from many other genetic testing companies which look to provide information on diseases that occur primarily later in life. As a test, try to find out the range of risk used by a company when they tell you about your risk for Alzheirmer’s disease, for example. Do they multipy together results or odds ratios from very different studies to produce a result for you? Do they look a smaller or larger number of genes to give you an idea of your genetic risk for a particular disease ? Is their range of risk specified?

At Matrix Genomics we rank each individual along a range of risk that is at least 30 fold from very low to high risk and may be 50 fold or more for some diseases. In other words, we try to capture all the variation that is currently available about genes and a particular disease to give our custormers highly informed infoprmation about their risk on a detailed disease by disease basis. This approach has sound scientific backing and it is not the cheapest possible way to measure the genetic risk of contracting disease but it does provide very good information to those who are concerned about their future and disease for any reason at all.

When I was a graduate student at the University of Chicago, I was walking across a quiet residential street in the Kenwood neighborhood when Muhamed Ali nearly hit me with his car. Neither he nor I had been focused on safety at the time. I jumped out of the way as he brought his car to a halt. We both apologized and went on our way. Genes are certainly not completely responsible for our length of life or its quality. Accidents and environmental effects can and do have great effects on our lives. Measuring the risk of a particular disease in a meticulous manner can and should give us choices that walk hand in hand with the development of a personalized medical plan which you and your doctor can develop.

Larry Corder, Ph.D.