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Posts Tagged ‘gastrointestinal’


Curator: Gail S. Thornton, M.A.

Co-Editor: The VOICES of Patients, Hospital CEOs, HealthCare Providers, Caregivers and Families: Personal Experience with Critical Care and Invasive Medical Procedures

  •  In a national survey, the Fiber Choice® line of chewable prebiotic fiber tablets and gummies, achieved the #1 share of gastroenterologist (GE) recommendations, more than four times greater than that for the nearest branded competitor
  • Fiber Choice contains a well-studied prebiotic fiber that promotes regularity and supports the growth of beneficial microorganisms for general digestive health
  • The convenience, taste and efficacy of Fiber Choice, makes it a GE-endorsed choice toward helping address the “fiber gap” in American diets

 Boca Raton, Fla. – (June 3, 2018) – IM HealthScience® (IMH), innovators of medical foods and dietary supplements, today announced a high-quality and replicated nationwide survey conducted among a representative and projectible sample of U.S. gastroenterologists, which revealed Fiber Choice® as the #1-recommended chewable prebiotic fiber brand.

The results of a ProVoice survey, fielded in May 2018 by IQVIA, showed Fiber Choice as the leader by far. Its share of gastroenterologist endorsements was more than four times greater than that of its nearest branded competitor.

Less than 3 percent of Americans get the recommended minimum amount of fiber, and 97 percent need to increase their fiber intake[1]. Although the recommended daily fiber intake is 25 to 38 grams[2], most Americans only get about half that amount. This “fiber gap” reflects a diet with relatively few high-fiber foods, such as fruits, vegetables, nuts, legumes and whole-grains, and is large enough for the U.S. government to deem it a public health concern for most of the U.S. population.

To help bridge this gap, gastroenterologists recommend fibers including Fiber Choice chewable tablets and gummies. For doctors, it’s a simple, convenient and tasty way to help their patients get the fiber needed for overall good digestive health.

“Dietary fiber is known for keeping our bodies regular,” said Michael Epstein, M.D., FACG, AGAF, a leading gastroenterologist and Chief Medical Advisor of IM HealthScience. “Most importantly, it’s essential that you get enough fiber in your diet. One way to do that is to supplement your daily intake of dietary fiber with natural, prebiotic fiber supplements.”

Inulin, the 100 percent natural prebiotic soluble fiber in Fiber Choice, has been studied extensively and has been shown to support laxation and overall digestive health as well as glycemic control, lowered cholesterol, improved cardiovascular health, weight control and better calcium absorption.

Fiber Choice can be found in the digestive aisle at Walmart, CVS, Target, Rite Aid and many other drug and food retailers.

About ProVoice Survey
ProVoice has the largest sample size of any professional healthcare survey in the U.S., with nearly 60,000 respondents across physicians, nurse practitioners, physician assistants, optometrists, dentists, and hygienists, measuring recommendations across more than 120 over-the-counter categories. Manufacturers use ProVoice for claim substantiation, promotion measurement, and HCP targeting.

IQVIA fielded replicated surveys in April 2018 and May 2018 respectively among U.S. gastroenterologists for IM HealthScience. The ProVoice survey methodology validated the claim at a 95 percent confidence level that “Fiber Choice® is the #1 gastroenterologist-recommended chewable prebiotic fiber supplement.”

About Fiber Choice®

The Fiber Choice® brand of chewables and gummies is made of inulin [pronounced: in-yoo-lin], a natural fiber found in many fruits and vegetables. Inulin works by helping to build healthy, good bacteria in the colon, while keeping food moving through the digestive system. This action has a beneficial and favorable effect in softening stools and improving bowel function.

Research shows that the digestive system does more than digest food; it plays a central role in the immune system. The healthy bacteria that live in the digestive tract promote immune system function, so prebiotic fiber helps nourish the body. Inulin also has secondary benefits, too, of possibly lowering cholesterol, balancing blood chemistry and regulating appetite, which can help reduce calorie intake and play a supporting role in weight management.

The usual adult dosage with Fiber Choice Chewable tablets is two tablets up to three times a day and for Fiber Choice Fiber Gummies is two gummies up to six per day.

About IM HealthScience®

IM HealthScience® (IMH) is the innovator of IBgard and FDgard for the dietary management of Irritable Bowel Syndrome (IBS) and Functional Dyspepsia (FD), respectively. In 2017, IMH added Fiber Choice®, a line of prebiotic fibers, to its product line via an acquisition. The sister subsidiary of IMH, Physician’s Seal®, also provides REMfresh®, a well-known continuous release and absorption melatonin (CRA-melatonin™) supplement for sleep. IMH is a privately held company based in Boca Raton, Florida. It was founded in 2010 by a team of highly experienced pharmaceutical research and development and management executives. The company is dedicated to developing products to address overall health and wellness, including conditions with a high unmet medical need, such as digestive health. The IM HealthScience advantage comes from developing products based on its patented, targeted-delivery technologies called Site Specific Targeting (SST). For more information, visit www.imhealthscience.com to learn about the company, or www.IBgard.com,  www.FDgard.comwww.FiberChoice.com, and www.Remfresh.com.

This information is for educational purposes only and is not meant to be a substitute for the advice of a physician or other health care professional. You should not use this information for diagnosing a health problem or disease. The company will strive to keep information current and consistent but may not be able to do so at any specific time. Generally, the most current information can be found on www.fiberchoice.com. Individual results may vary.

SOURCE/REFERENCES

[1] Greger, Michael, M.D., FACLM. (2015, September 29). Where Do You Get Your Fiber? [Blog post]. Retrieved from https://nutritionfacts.org/2015/09/29/where-do-you-get-your-fiber/

[2] Institute of Medicine. 2005. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. Washington, DC: The National Academies Press. https://doi.org/10.17226/10490.

Other related articles published in this Open Access Online Scientific Journal include the following:

2018

Benefits of fiber in diet

https://pharmaceuticalintelligence.com/2018/03/14/benefits-of-fiber-in-diet/

2016

Nutrition & Aging: Dr. Simin Meydani appointed Vice Provost for Research @Tufts University

https://pharmaceuticalintelligence.com/2016/08/01/nutrition-aging-dr-simin-meydani-appointed-vice-provost-for-research-tufts-university/

2015

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Anti-diabetic Drugs Affect Gut bacteria

Reported by: Irina Robu

Gut bacteria produces several types of substances that affect human physiology and health. However, any change in composition of this gut microbiome can have negative health effects. In a recent study, scientists have tried to understand the signatures of gut microbiota in diabetic patients. 

Using over 700 available human gut metagenomes, the scientists analyzed in detail the effects of the most widely used antidiabetic drug – metformin. Their findings indicated that metformin causes favorable changes in the gut microbiota of type 2 diabetes patients. The drug boosts the capability of the gut bacteria to produce butyric acid and propionic acid. These molecules act to reduce blood glucose levels in diabetics.

Metformin is known for its negative effects on the gastrointestinal tract, such as bloating and flatulence. The patients treated with metformin were found to have more coliform bacteria in their gut and it may be one of the reasons for these adverse effects. When looking at type 2 diabetes patients that were not treated with metformin, the researchers concluded that they had fewer bacteria that produced butyric acid and propionic acid. The study underscores the need to disentangle the gut microbiota signatures of human diseases from medication-induced effects.

Source

http://www.ncbi.nlm.nih.gov/pubmed/26633628

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Natural Drug Target Discovery and Translational Medicine in Human Microbiome

Author and Curator: Demet Sag, PhD

 

Remember Ecology 101, simple description of ecosystem includes both living, biotic, and non-living, abiotic, that response to differentiation based on external and internal factors.  Hence, biodiversity changes since living systems are open systems and always try to reach stability. Both soil and human body are rich in microbial life against ever changing conditions. Previously, discovery of marine microorganisms for treatment of complex diseases especially cancer and drug discovery for pharmaceutical applications was discussed. (https://pharmaceuticalintelligence.com/2014/03/20/without-the-past-no-future-but-learn-and-move-genomics-of-microorganisms-to-translational-medicine/)

Here, the focus will be given to clinical drug discovery based on how lactose intolerance and human microbiome related to treat cancer patients or other diseases. In sum, creating clinical relevance with human microbiome require knowledge of both of the worlds to make best of it to solve complex diseases naturally.

The huge undertake as a roadmap to biomedical research originated by NIH under The Human Microbiome Project (HMP) (http://nihroadmap.nih.gov) with 250 healthy individuals as a starting point.  Recent developments opened the doors to pursue us to understand how human microbiome reflects on metabolism, drug interactions and numerous diseases.  Finally, association between clinical states and microbiome are improving with advanced algorithms, bioinformatics and genomics. In classical reading tests questions finding the simile between two groups of words can well relate how microbiome- human and soil-earth relates.  Both are rich in microbial life with quite changing characters to survive through commensal living.

Thus, it is also good to talk about how we can synthesize existing info on interactions between soil microorganisms and decomposers for human diseases and human microbiome. Epidemiology of living organisms is diverse but they all share common interest. In soil, for example, radioactively contaminated soil can’t support plant growth well so Nitrosomonas may support to bring the life to soil through supplying nitrogen. And others can be added to bring a favorable enriched soil.

In human microbiome nutrition-diseases interacts in such a harmony with genetic make up (the information received at time of birth germline- or acquired later in life due to mutations by various reasons). For example, the simplest example is lactose intolerance and the other is development of diabetes.  Generally, it is described as If person is missing a gene to metabolize lactose (sugar) this person become Lactose intolerant yet this can be gained before birth or after. The fix is easy since avoiding certain food groups i.e. milk products.

Yet, this is not that simple!

In human microbiome, the rich gastrointestinal (GI) tract contains many organisms and one of the most important ones is Enterococci that are often simply described as lactic-acid–producing bacteria—by under- appreciation of their power of microbial physiology and outcomes as well as their ubiquitous nature of enterococci.  Schleifer & Kilpper-Bälz, 1984 also reported that the Group D streptococci, such as Streptococcus faecalis and Streptococcus faecium, were included in the new genus called Enterococcus.

The importance of this genius, consists of 37 species, coming from their spectrum of  habitats that include the gastrointestinal microbiota of nearly every animal phylum and flexibility with ability to widely colonize, intrinsic resistance to many inhabitable conditions even though they don’t have spores but they can survive against desiccation and can persist for months on dried surfaces.  Furthermore, they can tolerate extreme conditions such as pH changes, ionizing radiation, osmotic and oxidative stresses, high heavy metal concentrations, and antibiotics.

There is a double sword application as these organisms used as probiotics to improve immune system of the host.  If it is human to prevent contaminated food related diseases or in animals prevent transmitting them to the consumers. Thus, E. faecium and E. faecalis strains are used as probiotics and are ingested in high numbers, generally in the form of pharmaceutical preparations to treat diarrhea, antibiotic-associated diarrhea or irritable bowel syndrome, to lower cholesterol levels or to improve host immunity.

When it comes to human body within each system specific organs may create distinct values.  For example the pH values of GI tract vary and during diseases since pH levels are not at at correct levels.  As a result, due to mal-absorption of nutrients and elements such as food, vitamins and minerals body can’t heal itself. This changing microbial genomics on the surface of GI reflects on general health.  Entrococcus family among the other GI’s natural flora has the microbial physiology adopt these various pH conditions well. 

 

Our body has its own standards to function, such as  pH, temperature, oxygen etc these are basics so that enzymatic reactions may happen to metabolize,synthesizing (making) or catalyzing (breaking) what we eat.  The pH is the measure of hydrogen-ion concentration  in solution.  For example, human blood has a narrow pH (7.35 – 7.45 ) and below or above this range means symptoms and disease yet if blood pH moves to much below 6.8 or above 7.8, cells stop functioning and the patient dies since the ideal pH for blood is 7.4.  This value is unified.  On the other hand, the pH in the human digestive tract or GI changes tremendously to adopt and carry on its function, the pH of saliva (6.5 – 7.5), upper portion of the stomach (4.0 – 6.5) where “predigestion” occurs, the lower portion of the stomach is secreting hydrochloric acid (HCI) and pepsin until it reaches a pH between 1.5 – 4.0; duodenum, small intestine, (7.0 – 8.5) where 90% of the absorption of nutrients is taken in by the body while the waste products are passed out through the colon (pH 4.0 – 7.0).

 

Why is pH important and how related to anything?

Development and presence of cancer always require an acid pH and lack of oxygen.  Thus, prevention of these two factors may be the key for treatment of cancer as it progress the acidity increases such that the level raises even up to 1000 more than normal levels.

Mainly, due to Warburg effect body opt to get its energy from fermentation of glucose and produce lactic acid that decreases the body pH from 7.3 down to 7 then to 6.5 in advanced stages of cancer.  Furthermore, during metastases this level even reaches to 6.0 and even 5.7 where body can’t fight back with the disease. (Warburg effect is well explained previously by Dr. Larry Berstein (www.linkedin.com/pub/larry-bernstein/38/94b/3aa).

How to bypass the lack of oxygen naturally?

One of the many solution can be a natural solution. The nature made the hemoglobin carrying bacteria, Vitreoscilla hemoglobin (VHb), which is first described by Dale Webster in 1966. The gram negative and obligate aerobic bacterium, Vitreoscilla synthesizes elevated quantities of a homodimeric hemoglobin (VHb) under hypoxic growth conditions.   The main role is likely the binding of oxygen at low concentrations and its direct delivery to the terminal respiratory oxidase(s) such as cytochrome o.  Then, after 1986 with detailed description of the molecule other hemoglobins and flavohemoglobins were identified in a variety of microbes, indicating the widespread occurrence of Hb-like proteins.   Currently, it is the most studied bacterial hemoglobin with application potentials in biotechnology.

It is a plausible solution to integrate Vitroscilla and Enterobacter powers for cancer detection and treatment naturally with body’s own microbiome.

However, there are many microbial organisms and differ person to person based on gender, age, background, genetic make-up, food intake, habits, location etc.  The huge undertake as a roadmap to biomedical research originated by NIH under The Human Microbiome Project (HMP) (http://nihroadmap.nih.gov) with 250 healthy individuals as a starting point.

There were three goals in the agenda of The Human Microbiome Project (HMP) simply:

 1. Utilize advanced high throughput technology,

2. Identify any association between microbiome and disease/health stages,

3. Initiate scientific studies to collect more data.

In sum, creating clinical relevance with human microbiome require knowledge of both of the worlds to make best of it to solve complex diseases naturally.

Previously  Discussed:

AMPK Is a Negative Regulator of the Warburg Effect and Suppresses Tumor Growth In Vivo
Reporter-Curator: Stephen J. Williams, Ph.D.
https://pharmaceuticalintelligence.com/2013/03/12/ampk-is-a-negative-regulator-of-the-warburg-effect-and-suppresses-tumor-growth-in-vivo/

Is the Warburg Effect the Cause or the Effect of Cancer: A 21st Century View?
Author: Larry H. Bernstein, MD, FCAP
https://pharmaceuticalintelligence.com/2012/10/17/is-the-warburg-effect-the-cause-or-the-effect-of-cancer-a-21st-century-view/

Otto Warburg, A Giant of Modern Cellular Biology
Reporter: Larry H Bernstein, MD, FCAP
https://pharmaceuticalintelligence.com/2012/11/02/otto-warburg-a-giant-of-modern-cellular-biology/

Targeting Mitochondrial-bound Hexokinase for Cancer Therapy
Author: Ziv Raviv, PhD
https://pharmaceuticalintelligence.com/2013/04/06/targeting-mito…cancer-therapy

Nitric Oxide has a ubiquitous role in the regulation of glycolysis -with a concomitant influence on mitochondrial function
Curator, Larry H. Bernstein, MD, FCAP
https://pharmaceuticalintelligence.com/2012/09/16/nitric-oxide-has-a-ubiquitous-role-in-the-regulation-of-glycolysis-with-a-concomitant-influence-on-mitochondrial-function/

Potential Drug Target: Glucolysis Regulation – Oxidative stress-responsive microRNA-320
Reporter: Aviva Lev-Ari, PhD, RN
https://pharmaceuticalintelligence.com/2012/07/25/potential-drug-target-glucolysis-regulation-oxidative-stress-responsive-microrna-320/

Differentiation Therapy – Epigenetics Tackles Solid Tumors
Author-Writer: Stephen J. Williams, Ph.D.
https://pharmaceuticalintelligence.com/2013/01/03/differentiation-therapy-epigenetics-tackles-solid-tumors/

Prostate Cancer Cells: Histone Deacetylase Inhibitors Induce Epithelial-to-Mesenchymal Transition
Reporter-Curator: Stephen J. Williams, Ph.D.
https://pharmaceuticalintelligence.com/2012/11/30/histone-deacetylase-inhibitors-induce-epithelial-to-mesenchymal-transition-in-prostate-cancer-cells/

Mitochondrial Damage and Repair under Oxidative Stress
Curator: Larry H Bernstein, MD, FCAP
https://pharmaceuticalintelligence.com/2012/10/28/mitochondrial-damage-and-repair-under-oxidative-stress/

Mitochondria: Origin from oxygen free environment, role in aerobic glycolysis, metabolic adaptation
Curator: Larry H Bernsatein, MD, FCAP
https://pharmaceuticalintelligence.com/2012/09/26/mitochondria-origin-from-oxygen-free-environment-role-in-aerobic-glycolysis-metabolic-adaptation/

Expanding the Genetic Alphabet and Linking the Genome to the Metabolome
Reporter& Curator: Larry Bernstein, MD, FCAP
https://pharmaceuticalintelligence.com/2012/09/24/expanding-the-genetic-alphabet-and-linking-the-genome-to-the-metabolome/

What can we expect of tumor therapeutic response?
Author: Larry H. Bernstein, MD, FCAP
https://pharmaceuticalintelligence.com/2012/12/05/what-can-we-expect-of-tumor-therapeutic-response/

A Second Look at the Transthyretin Nutrition Inflammatory Conundrum
Larry H. Bernstein, MD, FACP
https://pharmaceuticalintelligence.com/2012/12/03/a-second-look-at-the-transthyretin-nutrition-inflammatory-conundrum/

 

Further  Readings and References:

Palmer KL, van Schaik W, Willems RJL, Gilmore MS. “Enterococcal Genomics Enterococci: From Commensals to Leading Causes of Drug Resistant Infection.” 2014-.2014 Feb 8

Franz CM, Holzapfel WH, Stiles ME. Enterococci at the crossroads of food safety?

Int J Food Microbiol.” 1999 Mar 1; 47(1-2):1-24.

Franz CM, Huch M, Abriouel H, Holzapfel W, Gálvez A.Int J Food Microbiol. “Enterococci as probiotics and their implications in food safety.” 2011 Dec 2; 151(2):125-40. Epub 2011 Sep 8.

Kayser FH.”Safety aspects of enterococci from the medical point of view.” Int J Food Microbiol. 2003 Dec 1; 88(2-3):255-62.

Webster DA, Hackett DP (1966). “The purification and properties of cytochrome o fromVitreoscilla“. J Biol Chem 241 (14): 3308–3315

Stark BC, Dikshit KL, Pagilla KR (2011). “Recent advances in understanding the structure, function, and biotechnological usefulness of the hemoglobin from the bacterium Vitreoscilla“. Biotechnol Lett 33 (9): 1705–1714

Stark BC, Dikshit KL, Pagilla KR (2012). “The Biochemistry  of Vitreoscillahemoglobin“. Computational and Structural Biotechnology Journal 3 (4): e201210002.

Brenner K, You L, Arnold F. (2008). “Engineering microbial consortia: A new frontier in synthetic biology.” Trends in Biotechnology 26: 483489.

Dunbar J, White S, Forney L. (1997). “Genetic diversity through the looking glass: Effect of enrichment bias.Applied and Environmental Microbiology 63: 13261331.

Foster J. (2001). “Evolutionary computation Nature Reviews Genetics 2: 428436.

Dinsdale EA, et al. 2008. “Functional metagenomic profiling of nine biomes.” Nature452: 629632.

Gudelj I, Beardmore RE, Arkin SS, MacLean RC. (2007). “Constraints on microbial metabolism drive evolutionary diversification in homogeneous environments.” Journal of Evolutionary Biology 20: 1882–1889.

Haack SK, Garchow H, Klug MJ, Forney L. (1995). “Analysis of factors affecting the accuracy, reproducibility, and interpretation of microbial community carbon source utilization patterns.” Applied and Environmental Microbiology 61: 14581468.

Lozupone C, Knight R. (2007). “Global patterns in bacterial diversity.” Proceedings of the National Academy of Sciences 104: 1143611440.

Thurnheer T, Gmr R, Guggenheim B,  (2004). “Multiplex FISH analysis of a six-species bacterial biofilm. “Journal of Microbiological Methods 56: 3747.

VijayKumar M, Aitken JD, Carvalho FA, Cullender TC, Mwangi S, Srinivasan S,Sitaraman S, Knight R, Ley RE, Gewirtz AT. (2010). “Metabolic syndrome and altered gut microbiota in mice lacking Toll-like receptor 5.” Science 328: 228231

Williams HTP, Lenton TM. (2007). “Artificial selection of simulated microbial ecosystems.” Proceedings of the National Academy of Sciences 104: 89188923.

 

 

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What`s new in pancreatic cancer research and treatment?

Reporter: Aviva Lev-Ari, PhD, RN

What`s new in pancreatic cancer research and treatment?

Research into the causes, diagnosis, and treatment of pancreatic cancer is under way in many medical centers throughout the world.

Genetics and early detection

Scientists are learning more about some of the changes in DNA that cause cells in the pancreas to become cancerous. Inherited changes in genes such as BRCA2p16, and the genes responsible for hereditary non-polyposis colorectal cancer (HNPCC) can increase a person’s risk of developing pancreatic cancer. Researchers are now looking at how these and other genes may be altered in cases of pancreatic cancer that do not seem to be inherited. They have discovered that pancreatic cancer does not form suddenly. It develops over many years in a series of steps known as pancreatic intraepithelial neoplasia or PanIN. In the early steps, such as PanIN 1, there are changes in a small number of genes, and the duct cells of the pancreas do not look very abnormal. In later steps such as PanIN 2 and PanIN 3, there are abnormalities in several genes and the duct cells look more abnormal.

Researchers are using this information to develop tests for detecting acquired (not inherited) genetic changes in pancreatic cancer pre-cancerous conditions. One of the most common DNA changes in these conditions affects theKRAS oncogene and alters regulation of cell growth. New diagnostic tests are often able to recognize this change in samples of pancreatic juice collected during an ERCP (endoscopic retrograde cholangiopancreatography).

For now, imaging tests like endoscopic ultrasound (EUS), ERCP, and genetic tests for changes in certain genes (such as KRAS) are options for people with a strong family history of pancreatic cancer. But these tests are not recommended for widespread testing of people at average risk who do not have any symptoms.

Treatment

The major focus of much research is on finding better treatments for pancreatic cancer. Improving surgery and radiation therapy are major goals, as is determining the best combination of treatments for people with certain stages of cancer.

Chemotherapy

Many clinical trials are testing new combinations of chemotherapy drugs for exocrine pancreatic cancer. Studies have looked to see if combining gemcitabine with other drugs would help patients live longer. Adding cisplatin, docetaxel, or irinotecan doesn’t seem to be helpful, but adding capecitabine (Xeloda) does seem to help some patients. Also, the combination of gemcitabine, irinotecan, and celecoxib (an arthritis drug) shows promise. Other studies are testing the best ways to combine chemotherapy with radiation therapy or newer targeted therapies.

Targeted therapies

As researchers have learned more about what makes pancreatic cancer cells different from normal cells, they have started to develop newer drugs that should be able exploit these differences by attacking only specific targets. These “targeted therapies” may provide another option for treating pancreatic cancer. They may prove to be useful along with, or instead of, current treatment regimens. In general, they seem to have fewer side effects than traditional chemotherapy drugs. Looking for new targets to attack on cancers is an active area of research.

Growth factor inhibitors: Many types of cancer cells, including pancreatic cancer cells, have certain molecules on their surface that help them to grow. These molecules are called growth factor receptors. One example is epidermal growth factor receptor (EGFR). Several drugs that target EGFR are now being studied. One, known as erlotinib (Tarceva), is already approved for use along with gemcitabine.

Anti-angiogenesis factors: All cancers depend on new blood vessels to nourish their growth. To block the growth of these vessels and thereby starve the tumor, scientists have developed anti-angiogenesis drugs. These are being studied in clinical trials and may be used in patients with pancreatic cancer.

Other targeted therapies: Many drugs targeting other aspects of cancer cells are now being studied for use in pancreatic cancer. For example, drugs that target the action of farnesyl transferase, an enzyme that is thought to stimulate the growth of many cancers, are now being tested. Other drugs, such as sunitinib, have several different targets.

Immune therapy

Immune therapies attempt to boost a person’s immune system or give them ready-made components of an immune system to attack cancer cells. Some studies of these treatments have shown promising results.

One form of immune therapy injects man-made monoclonal antibodies into patients. These immune system proteins are made to home in on a specific molecule, such as carcinoembryonic antigen (CEA), which is sometimes found on the surface of pancreatic cancer cells. Toxins or radioactive atoms can be attached to these antibodies, which bring them directly to the tumor cells. The hope is that they will affect cancer cells while leaving normal cells alone. For use in pancreatic cancer, these types of treatments are available only in clinical trials at this time.

Radiation therapy

Some current studies are looking at different ways to give radiation to treat exocrine pancreas cancer. One study is looking at the effect of intraoperative radiation therapy, in which a single large dose of radiation is given to the pancreas at the time of surgery (in the operating room). Another study is looking at using a special type of radiation called proton beam radiation with chemo.

Individualization of therapy

Some drugs seem to work better if certain types of mutations can be found in the patient’s tumor. For example, erlotinib may work better in patients if their tumors have a particular change in the gene for EGFR. This concept is an area of intense study. There might also be some genetic alterations that affect how well gemcitabine will work in a particular patient. Identifying markers that may predict how well a drug will work before it is given is an important area of research in many types of cancer.

New treatments for pancreatic neuroendocrine cancers

Many pancreatic neuroendocrine tumors have receptors for somatastatin on their cells. These tumors can be treated with octreotide and other drugs like it. A new drug has been developed in which the octreotide has been labeled with radiation. This drug shrunk some tumors and kept others from growing in an early trial. It also helped patients live longer.

Last Medical Review: 01/28/2013
Last Revised: 09/06/2013

SOURCE

http://www.cancer.org/cancer/pancreaticcancer/detailedguide/pancreatic-cancer-new-research

 

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Reporter and Curator: Dr. Sudipta Saha, Ph.D.

Conventional tumor markers are unsuitable for detecting carcinoma at an early stage and lack clinical efficacy and utility. Multiple classification analysis revealed that the variations in the levels of malonic acid and L-serine largely contributed to the separation of esophageal cancer; gastric cancer was characterized by changes in the levels of 3-hydroxypropionic acid and pyruvic acid; and L-alanine, glucuronoic lactone and L-glutamine contributed to the separation of colorectal cancer. Some metabolites are more sensitive for detecting gastrointestinal cancer than conventional biomarkers and thus metabolomics has the potential as an early diagnostic tool for cancer. Studies also showed that global metabolic profiling of colon mucosae would define metabolic signatures that not only discriminate malignant from normal mucosae, but also could distinguish the anatomical and clinicopathological characteristics of colorectal cancer. Thus it is suggested that metabolic profiling of colorectal cancer mucosae could provide new phenotypic biomarkers for colorectal cancer management.

A full spectrum of metabolic aberrations that are directly linked to colorectal cancer at early curable stages is critical for developing and deploying molecular diagnostic and therapeutic approaches that will significantly improve patient survival. A number of dysregulated metabolic pathways, such as glycolysis, tricarboxylic acid cycle, urea cycle, pyrimidine metabolism, tryptophan metabolism, polyamine metabolism, as well as gut microbial-host co-metabolism in colorectal cancer subjects are reported. Significantly increased tryptophan metabolism, and disturbed tricarboxylic acid cycle and the gut microflora metabolism were observed in the colorectal cancer patients. The urinary metabolite profile of postoperative colorectal cancer subjects altered significantly from that of the preoperative stage. The significantly down-regulated gut microflora metabolism and tricarboxylic acid cycle were observed in postoperative colorectal cancer subjects, presumably due to the colon flush involved in the surgical procedure and weakened physical conditions of the patients. The expression of 5-hydroxytryptophan significantly decreased in postsurgery cases, suggesting a recovered tryptophan metabolism toward healthy state. Abnormal histamine metabolism and glutamate metabolism were found only in the urine samples of colorectal cancer patients. There are distinct urinary metabolic footprints of colorectal cancer patients characterized by altered levels of metabolites derived from gut microbial-host co-metabolism. A panel of metabolite markers composed of citrate, hippurate, p-cresol, 2-aminobutyrate, myristate, putrescine, and kynurenate was able to discriminate colorectal cancer subjects from their healthy counterparts. These potential metabolite markers provide a novel and promising molecular diagnostic approach for the early detection of colorectal cancer.

Source References:

http://www.ncbi.nlm.nih.gov/pubmed/21773981

http://www.ncbi.nlm.nih.gov/pubmed/22792336

http://www.ncbi.nlm.nih.gov/pubmed/19063642

http://www.ncbi.nlm.nih.gov/pubmed/20121166

http://www.ncbi.nlm.nih.gov/pubmed/22148915

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Reporter: Ritu Saxena, Ph.D.

With the number of cancer cases plummeting every year, there is a dire need for finding a cure to wipe the disease out. A number of therapeutic drugs are currently in use, however, due to heterogeneity of the disease targeted therapy is required. An important criteria that needs to be addressed in this context is the –‘tumor response’ and how it could be predicted, thereby improving the selection of patients for cancer treatment. The issue of tumor response has been addressed in a recent editorial titled “Tumor response criteria: are they appropriate?” published recently in Future Oncology.

The article talks about how the early tumor treatment response methods came into practice and how we need to redefine and reassess the tumor response.

Defining ‘tumor response’ has always been a challenge

WHO defines a response to anticancer therapy as 50% or more reduction in the tumor size measured in two perpendicular diameters. It is based on the results of experiments performed by Moertel and Hanley in 1976 and later published by Miller et al in 1981. Twenty years later, in the year 2000, the US National Cancer Institute, with the European Association for Research and Treatment of Cancer, proposed ‘new response criteria’ for solid tumors; a replacement of 2D measurement with measurement of one dimen­sion was made. Tumor response was defined as a decrease in the largest tumor diameter by 30%, which would translate into a 50% decrease for a spherical lesion. However, response criteria have not been updated after that and there a structured standardization of treatment response is still required especially when several studies have revealed that the response of tumors to a therapy via imaging results from conventional approaches such as endoscopy, CT scan, is not reliable. The reason is that evaluating the size of tumor is just one part of the story and to get the complete picture inves­tigating and evaluating the tissue is essential to differentiate between treatment-related scar, fibrosis or micro­scopic residual tumor.

In clinical practice, treatment response is determined on the basis of well-established parameters obtained from diagnostic imaging, both cross-sectional and functional. In general, the response is classified as:

  • Complete remission: If a tumor disappears after a particular therapy,
  • Partial remission: there is residual tumor after therapy.

For a doctor examining the morphology of the tumor, complete remission might seem like good news, however, mission might not be complete yet! For example, in some cases, with regard to prognosis, patients with 0% residual tumor (complete tumor response) had the same prognosis com­pared with those patients with 1–10% residual tumor (subtotal response).

Another example is that in patients demonstrating complete remission of tumor response as observed with clinical, sonographic, functional (PET) and histopathological analysis experience recur­rence within the first 2 years of resection.

Adding complexity to the situation is the fact that the appropriate, clinically relevant timing of assess­ment of tumor response to treatment remains undefined. An example mentioned in the editorial is – for gastrointestinal (GI) malignancies, the assessment timing varies considerably from 3 to 6 weeks after initia­tion of neoadjuvant external beam radiation. Further, time could vary depending upon the type of radiation administered, i.e., if it is external beam, accelerated hyperfractionation, or brachytherapy.

Abovementioned examples remind us of the intricacy and enigma of tumor biol­ogy and subsequent tumor response.

Conclusion

Owing to the extraordinary het­erogeneity of cancers between patients, and pri­mary and metastatic tumors in the same patients, it is important to consider several factors while determining the response of tumors to different therapie in clinical trials. Authors exclaim, “We must change the tools we use to assess tumor response. The new modality should be based on individualized histopathology as well as tumor molecular, genetic and functional characteristics, and individual patients’ charac­teristics.”

Future perspective

Editorial points out that the oncologists, radiotherapists, and immunologists all might have a different opinion and observation as far as tumor response is considered. For example, surgical oncologists might determine a treatment to be effective if the local tumor control is much better after multimodal treatment, and that patients post-therapeutically also reveal an increase of the rate of microscopic and macroscopic R0-resection. Immunologists, on the other hand, might just declare a response if immune-competent cells have been decreased and, possibly, without clinical signs of decrease of tumor size.

What might be the answer to the complexity to reading tumor response is stated in the editorial – “an interdisciplinary initiative with all key stake­holders and disciplines represented is imperative to make predictive and prognostic individualized tumor response assessment a modern-day reality. The integrated multidisciplinary panel of international experts need to define how to leverage existing data, tissue and testing platforms in order to predict individual patient treatment response and prog­nosis.”

Sources:

Editorial : Björn LDM Brücher et al Tumor response criteria: are they appropriate? Future Oncology August 2012, Vol. 8, No. 8, 903-906.

Miller AB, Hoogstraten B, Staquet M, Winkler A. Reporting results of cancer treatment. Cancer 1981, 47(1),207–214.

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