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"HOUSTON - A diet that incorporates a daily dose of pistachios may help reduce the risk of lung and other cancers, according to data presented at the American Association for Cancer Research Frontiers in Cancer Prevention Research Conference, held Dec. 6-9. "It is known that vitamin E provides a degree of protection against certain forms of cancer. Higher intakes of gamma-tocopherol, which is a form of vitamin E, may reduce the risk of lung cancer," said Ladia M. Hernandez, M.S., R.D., L.D., senior research dietitian in the Department of Epidemiology at the University of Texas M. D. Anderson Cancer Center, and doctoral candidate at Texas Woman's University - Houston Center. "Pistachios are a good source of gamma-tocopherol. Eating them increases intake of gamma-tocopherol so pistachios may help to decrease lung cancer risk," she said. Pistachios are known to provide a heart-healthy benefit by producing a cholesterol-lowering effect and providing the antioxidants that are typically found in food products of plant origin. Hernandez and colleagues conducted a six-week, controlled clinical trial to evaluate if the consumption of pistachios would increase dietary intake and serum levels of gamma-tocopherol. A pistachio-rich diet could potentially help reduce the risk of other cancers from developing as well, according to Hernandez. "Because epidemiologic studies suggest gamma-tocopherol is protective against prostate cancer, pistachio intake may help," she said. "Other food sources that are a rich source of gamma-tocopherol include nuts such as peanuts, pecans, walnuts, soybean and corn oils.""

D structure of the virus, known as Seneca Valley Virus-001, reveals that it is unlike any other known member of the Picornaviridae viral family, and confirms its recent designation as a separate genus "Senecavirus." The new study reveals that the virus's outer protein shell looks like a craggy golf ball¬-one with uneven divets and raised spikes-and the RNA strand beneath it is arranged in a round mesh rather like a whiffleball. "It is not at all like other known picornaviruses that we are familiar with, including poliovirus and rhinoviruses, which cause the common cold," says the study's senior author, Associate Professor Vijay S. Reddy, Ph.D., of The Scripps Research Institute. "This crystal structure will now help us understand how Senecavirus works, and how we can take advantage of it." The Senecavirus is a "new" virus, discovered several years ago by Neotropix Inc., a biotech company in Malvern, Pennsylvania. It was at first thought to be a laboratory contaminant, but researchers found it was a pathogen, now believed to originate from cows or pigs. Further investigation found that the virus was harmless to normal human cells, but could infect certain solid tumors, such as small cell lung cancer, the most common form of lung cancer.

Targeted cancer therapy and gene therapy have been mentioned in the blue before, but oncolytic viruses are the hot young thing. For consideration in cancer treatment, an virus must replicate in and kill a high number of exclusively cancer cells, while sparing healthy tissue. A Philadelphia-based company called Neotropix has won awards for its research into a prime contender - the Seneca Valley Virus. It has been the subject of Phase I adult clinical trials, with Phase II adult and Phase I pediatric clinical trials to start this year. SVV has advantages over some other contenders in that it is a naturally occurring (lest we create a race of mutant zombies) organism and studies so far suggest it is not harmful to healthy human cells. While a number of other oncolytic viruses are being examined, NTX-010 seems able to treat a very wide range of common and rare forms of cancer, some of which are now considered uniformly fatal. In addition, unlike some other tested viruses, it can travel through the bloodstream to treat metastatic and not just local disease. Compared to the side-effects and late effects of chemotherapy and radiation treatment, and because many of the cancers ideal for treatment with an oncolytic virus have no surgical options, this may be the next big breakthrough.

...has been the number one Google search term leading people to the blog this week - and that worries me. As I wrote about a week ago, dichloroacetate, or DCA, is the molecule tested recently by a team at University of Alberta for its ability to slow the growth of human lung cancer in immunocompromised rats. Among DCA's action is the ability to prevent cancer cells from producing lactic acid via aerobic glycolysis, a process used by more than half (but not all) tumors. Scientists continue to debate whether this process is a cause of cancer, or just a byproduct of malignant cell transformation. I am deeply concerned that desperate cancer patients may be trying to purchase dichloroacetate (DCA) and self-treat for cancer based on this highly-hyped single paper. To the credit of the researchers and their institution, who have set up a website to address the intense interest, they discourage such practice:

Stem cells are unprogrammed cells in the human body that can be described as "shape shifters." These cells have the ability to change into other types of cells. Stem cells are at the center of a new field of science called regenerative medicine. Because stem cells can become bone, muscle, cartilage and other specialized types of cells, they have the potential to treat many diseases, including Parkinson's, Alzheimer's, diabetes and cancer. Eventually, they may also be used to regenerate organs, reducing the need for organ transplants and related surgeries. "Stem cells are like little kids who, when they grow up, can enter a variety of professions," Dr. Marc Hedrick of the UCLA School of Medicine says. "A child might become a fireman, a doctor or a plumber, depending on the influences in their life -- or environment. In the same way, these stem cells can become many tissues by making certain changes in their environment."

If you want to reduce your risk for getting cancer, heart disease, diabetes and a host of other diseases, the message is clear - eat a nutrient-rich, low-fat, high fiber diet, with plenty of fruit and vegetables. So why is this wisdom forgotten when a person is diagnosed with cancer, and the standard advice becomes: "Eat whatever you want, whatever you can tolerate," even when this may include a diet high in fat and refined sugars. \n\nAccording to two of the country's leading authorities on cancer and nutrition, David Katz, MD and Keith Block, MD, the typical American high-fat, empty calorie diet can set the stage for an inflammatory response that actually fuels a cancer patient's disease, undermines treatment, and promotes malnutrition.

Berberine inhibits human tongue squamous carcinoma cancer tumor growth in a murine xenograft model. Ho YT, Yang JS, Lu CC, Chiang JH, Li TC, Lin JJ, Lai KC, Liao CL, Lin JG, Chung JG. Phytomedicine. 2009 Sep;16(9):887-90. Epub 2009 Mar 20. PMID: 19303753 Our primary studies showed that berberine induced apoptosis in human tongue cancer SCC-4 cells in vitro. But there is no report to show berberine inhibited SCC-4 cancer cells in vivo on a murine xenograft animal model. SCC-4 tumor cells were implanted into mice and groups of mice were treated with vehicle, berberine (10mg/kg of body weight) and doxorubicin (4mg/kg of body weight). The tested agents were injected once per four days intraperitoneally (i.p.), with treatment starting 4 weeks prior to cells inoculation. Treatment with 4mg/kg of doxorubicin or with 10mg/kg of berberine resulted in a reduction in tumor incidence. Tumor size in xenograft mice treated with 10mg/kg berberine was significantly smaller than that in the control group. Our findings indicated that berbeirne inhibits tumor growth in a xenograft animal model. Therefore, berberine may represent a tongue cancer preventive agent and can be used in clinic.

Serum Vitamin D and Risk of Prostate Cancer in a Case-Control Analysis Nested Within the European Prospective Investigation into Cancer and Nutrition (EPIC). Travis RC, Crowe FL, Allen NE, Appleby PN, Roddam AW, Tjønneland A, Olsen A, Linseisen J, Kaaks R, Boeing H, Kröger J, Trichopoulou A, Dilis V, Trichopoulos D, Vineis P, Palli D, Tumino R, Sieri S, Bueno-de-Mesquita HB, van Duijnhoven FJ, Chirlaque MD, Barricarte A, Larrañaga N, González CA, Argüelles MV, Sánchez MJ, Stattin P, Hallmans G, Khaw KT, Bingham S, Rinaldi S, Slimani N, Jenab M, Riboli E, Key TJ. Am J Epidemiol. 2009 Apr 9. [Epub ahead of print] PMID: 19359375 doi:10.1093/aje/kwp022

Vitamin D status and the risk of lung cancer: a cohort study in Finland. Kilkkinen A, Knekt P, Heliövaara M, Rissanen H, Marniemi J, Hakulinen T, Aromaa A. Cancer Epidemiol Biomarkers Prev. 2008 Nov;17(11):3274-8. PMID: 18990771v In conclusion, although there was no overall association between vitamin D and lung cancer risk, women and young participants with a higher level of vitamin D were observed to have a lower lung cancer risk. Although experimental data support the suppressing effect of vitamin D on the development of lung cancer, large epidemiologic studies from different populations with repeated measurements of vitamin D are warranted to confirm this finding. (Cancer Epidemiol Biomarkers Prev 2008;17(11):3274-8)

Aldehyde dehydrogenase 2 and head and neck cancer: a meta-analysis implementing a Mendelian randomization approach. Boccia S, Hashibe M, Gallì P, De Feo E, Asakage T, Hashimoto T, Hiraki A, Katoh T, Nomura T, Yokoyama A, van Duijn CM, Ricciardi G, Boffetta P. Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):248-54. PMID: 19124505 doi: 10.1158/1055-9965.EPI-08-0462

"COLLEGE STATION - Mango. If you know little about this fruit, understand this: It's been found to prevent or stop certain colon and breast cancer cells in the lab. That's according to a new study by Texas AgriLife Research food scientists, who examined the five varieties most common in the U.S.: Kent, Francine, Ataulfo, Tommy/Atkins and Haden. Though the mango is an ancient fruit heavily consumed in many parts of the world, little has been known about its health aspects. The National Mango Board commissioned a variety of studies with several U.S. researchers to help determine its nutritional value. "If you look at what people currently perceive as a superfood, people think of high antioxidant capacity, and mango is not quite there," said Dr. Susanne Talcott, who with her husband, Dr. Steve Talcott, conducted the study on cancer cells. "In comparison with antioxidants in blueberry, acai and pomegranate, it's not even close." But the team checked mango against cancer cells anyway, and found it prevented or stopped cancer growth in certain breast and colon cell lines, Susanne Talcott noted. "It has about four to five times less antioxidant capacity than an average wine grape, and it still holds up fairly well in anticancer activity. If you look at it from the physiological and nutritional standpoint, taking everything together, it would be a high-ranking super food," she said. "It would be good to include mangoes as part of the regular diet." The Talcotts tested mango polyphenol extracts in vitro on colon, breast, lung, leukemia and prostate cancers. Polyphenols are natural substances in plants and are associated with a variety of compounds known to promote good health."

What if we didn't try to cure cancer, but simply kept tumors from growing too big? That's what radiologist Robert Gatenby of the Moffitt Cancer Center proposes this week in the journal Nature. Gatenby argues that high doses of powerful chemotherapies wreak havoc on a patient's immune system and foster the rapid regrowth of chemoresistant cancers that doctors have no hope of fighting.  So instead of curing cancer, he suggests doctors aim to stabilize the tumor at a tolerable size. In practice, this would mean that doctors identify a target size for an individual tumor that gives the patient the best quality of life.  Then, they will regularly monitor the tumor's growth with medical imaging equipment like a PET/CT scanner (see photo), and regulate doses of anticancer drugs to maintain it at a precise volume.

Mechanisms of berberine (natural yellow 18)-induced mitochondrial dysfunction: interaction with the adenine nucleotide translocator. Pereira CV, Machado NG, Oliveira PJ. Toxicol Sci. 2008 Oct;105(2):408-17. Epub 2008 Jul 3. PMID: 18599498 doi: 10.1124/jpet.107.128017 The data from the present work appear to show that berberine also presents some degree of toxicity to "nontumor" systems, which should be carefully understood. ANT inhibition in nontumor cells by berberine would be responsible for a decrease in energy production and could also result in MPT induction. To the best of our knowledge, no full toxicity assessment exists for berberine in humans, although its use in several commercially available supplements suggests that the compound may present a relatively wide safety interval. In fact, a study with patients with congestive heart failure treated with 1.2 g/day of oral berberine revealed low toxicity and resulted into an average plasma concentration of 0.11 mg/l which would translate into 0.3µM (Zeng and Zeng, 1999Go). Repeated cumulative treatments, alternative forms of formulation (e.g., topical application vs. injection) or more importantly, active mitochondrial accumulation due to its positive charge would be expected to increase its concentration in cells into the range of concentrations used in this study. Empirical data from nontraditional medicines plus the use of extensive clinical assays would allow the use of berberine as a promising antimelanoma agent while maintaining its safety for humans. In radial/vertical forms of melanoma, a possible topical application of berberine would also be possible, thus minimizing side effects on other organs. In conclusion, the present work identifies the ANT as an important target for berberine, with clear relevance for its proposed antitumor effects.

In this video, Dr. Ramakant Deshpande explaining How does doctor decide Lung cancer treatment for different stages of Lung cancer. Lung cancer and its adversities can be lethal, if remains undiagnosed or left untreated. A multidisciplinary approach can successfully eliminate the cancer from lungs and patient may resume normal life after recovery, says Dr. Ramakant Dehspande, Chief of Thoracic Surgical Oncology, Asian Institute of Oncology. Lung cancer There are different sizes and stages of lung cancer, which are treated differently. Broadly, specialists categorize various types of lung cancer into two basic forms Non-small cell lung cancer and small cell lung cancer. The staging of lung cancer helps in deciding the severity of the disease, course of treatment, and chances of survival. Detection of cancer at an early stage increases the chances of successful treatment and full recovery of the patient. A small legion located in one area is known as the first stage; a little larger tumor is called stage 2; spread within the lungs is called stage 3, and if it spread to other parts then termed as stage 4. Doctor Profile: Dr. Ramakant Deshpande MS; FICS; FAIS; DHA having experience of 31+ years and is a Chief of Thoracic Surgical Oncology, Asian Institute of Oncology. - Padmashree award by the President of India in 2014 - Lifetime Achievement Award at the Indian National Critical Care Society Annual Meet at Jaipur 2014 - Lifetime Achievement Award by Zee Maaza TV in 2019 - Senior of Robotic surgery at the Asian Cancer Institute - Established the Minimally Invasive method of Thoracoscopy - President of the Indian Society of Oncology - Director - Asian Cancer Institute - Ex Tata Memorial Doctor This video is under the "My Health My Right" Initiative of MedicoExperts - A Global Virtual Hospital. For Inquiry Call or WhatsApp us at +919769516280 #lungcancertreatment​ #MyHealthMyRight​ #lungcancer​ #lungcancerstages​ #MedicoExperts​ #lungcancertreatmen

Our findings suggest that administration of n-3 FA (EPA and DHA) in doses of at least 1.5 g/day for a prolonged period of time to patients with advanced cancer is associated with an improvement in clinical, biological and QoL parameters. N-3 fatty acids, cancer and cachexia: a systematic review of the literature. Colomer R, Moreno-Nogueira JM, García-Luna PP, García-Peris P, García-de-Lorenzo A, Zarazaga A, Quecedo L, del Llano J, Usán L, Casimiro C. Br J Nutr. 2007 May;97(5):823-31. Review. PMID: 17408522 doi:10.1017/S000711450765795X

The relevance of vitamin D receptor (VDR) gene polymorphisms for cancer: a review of the literature. Köstner K, Denzer N, Müller CS, Klein R, Tilgen W, Reichrath J. Anticancer Res. 2009 Sep;29(9):3511-36. Review. PMID: 19667145 CONCLUSION: Significant associations with VDR polymorphisms have been reported in cancer of the breast (Fok1, Bsm1, Taq1, Apa1, poly (A)), prostate (Fok1, Bsm1, Taq1, poly (A)), skin (Fok1, Bsm1, A-1210), colorectum (Fok1, Bsm1), ovary (Fok1, Apa1) and bladder (Fok1), and in renal cell carcinoma (Taq1, Apa1). However, conflicting data have been reported for most malignancies. After careful evaluation of the actual literature, it can be summarized that data indicating an association of VDR polymorphisms and cancer risk are strongest for breast cancer (Bsm1, Fok1), prostate cancer (Fok1) and malignant melanoma (MM) (Fok1). Data indicating an association of VDR polymorphisms and cancer prognosis are strongest for prostate cancer (Fok1), breast cancer (Bsm1, Taq1), MM (Bsm1) and renal cell carcinoma (Taq1).

Mitochondrially targeted effects of berberine [Natural Yellow 18, 5,6-dihydro-9,10-dimethoxybenzo(g)-1,3-benzodioxolo(5,6-a) quinolizinium] on K1735-M2 mouse melanoma cells: comparison with direct effects on isolated mitochondrial fractions. Pereira GC, Branco AF, Matos JA, Pereira SL, Parke D, Perkins EL, Serafim TL, Sardão VA, Santos MS, Moreno AJ, Holy J, Oliveira PJ. J Pharmacol Exp Ther. 2007 Nov;323(2):636-49. Epub 2007 Aug 17. PMID: 17704354 doi: 10.1124/jpet.107.128017 The present work shows that berberine is accumulated by mitochondria of a mouse melanoma cell line, leading to mitochondrial fragmentation and dysfunction, accompanied by decreased cellular energy charge. When the effect was compared with the results obtained on isolated mitochondrial fractions, it is observed that regardless of the system used, berberine is toxic for mitochondria. One major limitation of the present study (as in many others) is the lack of knowledge of the real concentration of berberine that reaches mitochondria in intact cells. Although we do not possess data regarding this aspect, it is wise to speculate that mitochondrial berberine concentrations will be much higher than in the bulk cytosol due to electrophoretic accumulation. We believe that the range of berberine concentrations accumulated by mitochondria in intact cells is within the range of concentrations used on isolated mitochondrial fractions in the present study. The present work not only provides insights on the mechanism by which berberine interferes with tumor cell proliferation, demonstrating previously unknown effects on mitochondrial physiology, but also raises a note of caution on the use of berberine as a nontoxic "natural" over-the-counter medication.

Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells. Mantena SK, Sharma SD, Katiyar SK. Mol Cancer Ther. 2006 Feb;5(2):296-308. PMID: 16505103 doi: 10.1158/1535-7163.MCT-05-0448 The effectiveness of berberine in checking the growth of androgen-insensitive, as well as androgen-sensitive, prostate cancer cells without affecting the growth of normal prostate epithelial cells indicates that it may be a promising candidate for prostate cancer therapy. The evaluation of ancient herbal medicines may indicate novel strategies for the treatment of prostate cancer, which remains the leading cause of cancer-related deaths in American men (1). In our present investigation, we show that a naturally occurring isoquinoline alkaloid, berberine, significantly inhibits the proliferation and reduces the viability of DU145 and PC-3 as well as LNCaP cells (Fig. 1), which suggests that berberine may be an effective chemotherapeutic agent against both androgen-sensitive and androgen-insensitive prostate cancer cells. Importantly, we found that berberine did not exhibit toxicity to nonneoplastic human prostate epithelial cells under the conditions used, except for a moderate reduction in cell viability at higher concentrations when cells were treated in vitro for an extended period of time. In conclusion, the results of the present study indicate that berberine inhibits proliferation and induces G1-phase arrest and apoptosis in human prostate cancer cells but not in normal human prostate epithelial cells. In addition, we provide mechanistic evidence that berberine-induced apoptosis in prostate carcinoma cells, particularly hormone-refractory prostate carcinoma cells, is mediated through enhanced expression of Bax, disruption of the mitochondrial membrane potential, and activation of caspase-3.