Green tea may have a therapeutic and positive effect in reducing risk and treatment of esophageal cancer, some scientists suggested.
Esophageal cancer is a medical condition characterized by irregular cell growth in the tissues of the esophagus. At the later stage, the cancerous cells may travel a distance away to invade other healthy tissues and organs.
According to statistic, in 1028 over 17,000 adults in the United States will be diagnosed with esophageal cancer.
The disease accounts for 1% of all cancers diagnosed in the United States.
The means of the 5-year survival rate of esophageal cancer is 19%. It is very low compared to other types of cancer. Sadly, early diagnosed with 5 years survival rate of esophageal cancer is only 43%.
Researchers as of today, do not know why people with the same health condition and family history, some are susceptible to the early onset of the disease while others do not.
However, researchers do know that smoking, age, family history, unhealthy diet and occupation that requires frequent contact with irritants are associated to increase the risk of esophageal cancer.
Other researchers suggested that certain medical condition such as obesity, GERD, achalasia and genetic mutation inherited from the parents are also the prevalent risk factors in the onset of the disease.
If you are experiencing symptoms of difficult or painful swallowing, a persistent sensation of having food lodged in the chest, and pain in the throat or back, behind the breastbone or between the shoulder blades, unintentional weight loss, coughing up blood, and heartburn that cannot go away, you may have esophageal cancer, please check with your doctor to rule out the possibility.
Green tea a precious drink processes numbers of health benefit known to almost everyone in Asia and the Western world.
In esophageal cancer cell lines Eca109 and Ec9706, injection of green tea EGCG plus chemo drug adriamycin (ADM) after 24 hours displayed a significantly increased cellular apoptosis.
According to flow cytometry assay, the combined application induced the elevation of ROS and ADM concentration in the production of cytotoxicity to the tumor cells by reducing the expression of mitochondrial membrane potential and ABCG2 protein that protect cancer cells apoptosis. without harming healthy cells.
ABCG2 protein expression plays a major role in multi-drug resistance, produced by tumor cells to accounter reaction to chemo-medicine.
Mitochondrial membrane potential is a central intermediate in oxidative energy metabolism, the deceased levels caused by toxicity ROS may result in energy deletion and subsequently, causing cells death.
Further observation also indicated that EGCG inhibited the growth of Eca109 and Ec9706 cells through ameliorating anti-apoptotic bcl-2 protein expression and promoted Bax and caspase-3 protein expressions with functions of promoting apoptosis in a dose- and time-dependent manner.
BCL2 family members form hetero- or homodimers and play an important anti-apoptotic protein.
Caspase-3 prote plays a central role in the execution-phase of cell apoptosis.
BAX gene. BAX is a member of the Bcl-2 gene family. plays an important role in the mediation of cell death by apoptosis.
Compared to ADM treatment alone, the Eca109/ABCG2 multi-drug resistance cancer cells, the rate of apoptosis and ADM concentration were significantly higher and levels of mitochondrial membrane potential and ABCG2 expression were lower.
In other words, injection of green tea plus ADM was more effective in inducing cells death in Eca109/ABCG2 multi-drug resistance cancer cells through expression ROS and ADM in enhancing elevation of cytotoxic activity compared to ADM treatment alone.
After taking into account others co and confounders, Dr, Liu L the lead author said, " EGCG inhibited cell growth and induced esophageal cancer cell apoptosis. It reduced the bcl-2 protein expression and increased the bax and caspase-3 protein expression. EGCG reversed multi-drug resistance by reducing ABCG2 expression and increasing the anticancer drug concentration in cancer cells".
In esophageal squamous cell carcinoma, application of Epigallocatechin-3-gallate (EGCG) without ADM measured by flow cytometry assay, after 24 hours also inhibited cancer site proliferation by increasing the expression of ROS to attenuate mitochondrial membrane potential function in energy metabolism and increase caspase-3 protein function in the induction of malignant cellular apoptosis, in a dose-and time-dependent manner.
Furthermore, in the examine the PCR-TRAP argentation analysis during the experiment, EGCG also inhibited the viability of Eca109 and Ec9706 cells by suppressing cancer cell in alternating DNA transcript through telomerase activity.
More interestingly, the continuation of the study of epigallocatechin-3-gallate (EGCG) on the human esophageal cancer cell line ECa109 also discovered, EGCG decreased cancer cell viability and increased cancer apoptosis through expression of p16 gene demethylation in cancer cell cycle arrest.
P16 gene demethylation plays an important role in cell cycle arrest and apoptosis. gene alternation was found in several types of cancer.
Low level of p16 mRNA expression is associated to the progression of cancer with malignant and aggressive behavior.
Abnormalities of p16 gene and loss of p16 protein expression may be related to the pathogenesis and development of some cancers.
Taken together, green tea with an abundance of phytochemical Epigallocatechin-3-gallate (EGCG) may be considered an adjunct therapy or in combination with standard chemo-medicine for treatment of esophageal cancer.
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Back to Kyle J. Norton Homepage http://kylejnorton.blogspot.ca
Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bioscience, ISSN 0975-6299.
Sources
(1) Epigallocatechin-3-gallate promotes apoptosis and reversal of multidrug resistance in esophageal cancer cells by Liu L1, Ju Y2, Wang J3, Zhou R3. (PubMed)
(2) Epigallocatechin-3-gallate suppresses cell proliferation and promotes apoptosis in Ec9706 and Eca109 esophageal carcinoma cells by Liu L1, Zuo J1, Wang G1. (PubMed)
(3) Epigallocatechin-3-gallate inhibits growth and induces apoptosis in esophageal cancer cells through the demethylation and reactivation of the p16 gene by Meng J1, Tong Q2, Liu X2, Yu Z3, Zhang J3, Gao B3. (PubMed)
In esophageal cancer cell lines Eca109 and Ec9706, injection of green tea EGCG plus chemo drug adriamycin (ADM) after 24 hours displayed a significantly increased cellular apoptosis.
According to flow cytometry assay, the combined application induced the elevation of ROS and ADM concentration in the production of cytotoxicity to the tumor cells by reducing the expression of mitochondrial membrane potential and ABCG2 protein that protect cancer cells apoptosis. without harming healthy cells.
ABCG2 protein expression plays a major role in multi-drug resistance, produced by tumor cells to accounter reaction to chemo-medicine.
Mitochondrial membrane potential is a central intermediate in oxidative energy metabolism, the deceased levels caused by toxicity ROS may result in energy deletion and subsequently, causing cells death.
Further observation also indicated that EGCG inhibited the growth of Eca109 and Ec9706 cells through ameliorating anti-apoptotic bcl-2 protein expression and promoted Bax and caspase-3 protein expressions with functions of promoting apoptosis in a dose- and time-dependent manner.
BCL2 family members form hetero- or homodimers and play an important anti-apoptotic protein.
Caspase-3 prote plays a central role in the execution-phase of cell apoptosis.
BAX gene. BAX is a member of the Bcl-2 gene family. plays an important role in the mediation of cell death by apoptosis.
Compared to ADM treatment alone, the Eca109/ABCG2 multi-drug resistance cancer cells, the rate of apoptosis and ADM concentration were significantly higher and levels of mitochondrial membrane potential and ABCG2 expression were lower.
In other words, injection of green tea plus ADM was more effective in inducing cells death in Eca109/ABCG2 multi-drug resistance cancer cells through expression ROS and ADM in enhancing elevation of cytotoxic activity compared to ADM treatment alone.
After taking into account others co and confounders, Dr, Liu L the lead author said, " EGCG inhibited cell growth and induced esophageal cancer cell apoptosis. It reduced the bcl-2 protein expression and increased the bax and caspase-3 protein expression. EGCG reversed multi-drug resistance by reducing ABCG2 expression and increasing the anticancer drug concentration in cancer cells".
In esophageal squamous cell carcinoma, application of Epigallocatechin-3-gallate (EGCG) without ADM measured by flow cytometry assay, after 24 hours also inhibited cancer site proliferation by increasing the expression of ROS to attenuate mitochondrial membrane potential function in energy metabolism and increase caspase-3 protein function in the induction of malignant cellular apoptosis, in a dose-and time-dependent manner.
Furthermore, in the examine the PCR-TRAP argentation analysis during the experiment, EGCG also inhibited the viability of Eca109 and Ec9706 cells by suppressing cancer cell in alternating DNA transcript through telomerase activity.
More interestingly, the continuation of the study of epigallocatechin-3-gallate (EGCG) on the human esophageal cancer cell line ECa109 also discovered, EGCG decreased cancer cell viability and increased cancer apoptosis through expression of p16 gene demethylation in cancer cell cycle arrest.
P16 gene demethylation plays an important role in cell cycle arrest and apoptosis. gene alternation was found in several types of cancer.
Low level of p16 mRNA expression is associated to the progression of cancer with malignant and aggressive behavior.
Abnormalities of p16 gene and loss of p16 protein expression may be related to the pathogenesis and development of some cancers.
Taken together, green tea with an abundance of phytochemical Epigallocatechin-3-gallate (EGCG) may be considered an adjunct therapy or in combination with standard chemo-medicine for treatment of esophageal cancer.
Natural Medicine for Fatty Liver And Obesity Reversal - The Revolutionary Findings To Achieve Optimal Health And Lose Weight
How To Get Rid Of Eye Floaters
Contrary To Professionals Prediction, Floaters Can Be Cured Naturally
Ovarian Cysts And PCOS Elimination
Holistic System In Existence That Will Show You How To
Permanently Eliminate All Types of Ovarian Cysts Within 2 Months
Back to Kyle J. Norton Homepage http://kylejnorton.blogspot.ca
Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bioscience, ISSN 0975-6299.
Sources
(1) Epigallocatechin-3-gallate promotes apoptosis and reversal of multidrug resistance in esophageal cancer cells by Liu L1, Ju Y2, Wang J3, Zhou R3. (PubMed)
(2) Epigallocatechin-3-gallate suppresses cell proliferation and promotes apoptosis in Ec9706 and Eca109 esophageal carcinoma cells by Liu L1, Zuo J1, Wang G1. (PubMed)
(3) Epigallocatechin-3-gallate inhibits growth and induces apoptosis in esophageal cancer cells through the demethylation and reactivation of the p16 gene by Meng J1, Tong Q2, Liu X2, Yu Z3, Zhang J3, Gao B3. (PubMed)
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