Cancer

Cancer

Microbes and Cruciferous Vegetables : Cancer Cure

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It confirms once more that:

  1. the inflamed organs end into cancer
  2. Prana heals (Here, in form of microbes that releases chemical to stop the cancer proliferation signals

Cruciferos-Vegetable


Research


With these special bacteria, a broccoli a day can keep the cancer doctor away

Colorectal cancer is one of the most common cancers in the world, especially the developed world. Although the 5-year survival rates for earlier stages of this cancer are relatively good, at later stages survival goes down and the risk of cancer recurrence goes up considerably.

At the heart of this cancer-targeting system is an engineered form of E. coli Nissle, a harmless type of bacteria found in the gut. Using genetic techniques, the team engineered the bacteria into a probiotic that attached to the surface of colorectal cancer cells and secreted an enzyme to convert a substance found in cruciferous vegetables (like broccoli) into a potent anticancer agent. The idea was for the cancer cells in the vicinity to take up this anticancer agent and be killed. Normal cells cannot do this conversion, nor are they affected by the toxin, thus the system should be targeted only to colorectal cancer cells.

True enough, the mixture of engineered probiotics with a broccoli extract or water containing the dietary substance killed more than 95% of colorectal cancer cells in a dish. Moreover, the mixture had no effect on cells from other types of cancer such as breast and stomach cancer. Strikingly, the probiotics-veggie combination reduced tumour numbers by 75% in mice with colorectal cancer. Also, the tumours that were detected in these mice were 3 times smaller than those in control mice which were not fed with the mixture.

https://www.nature.com/articles/s41551-017-0181-y

Dietary Sulforaphane in Cancer Chemoprevention: The Role of Epigenetic Regulation and HDAC Inhibition

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4432495/

Significance: Sulforaphane, produced by the hydrolytic conversion of glucoraphanin after ingestion of cruciferous vegetables, particularly broccoli and broccoli sprouts, has been extensively studied due to its apparent health-promoting properties in disease and limited toxicity in normal tissue. Recent Studies: Recent identification of a sub-population of tumor cells with stem cell-like self-renewal capacity that may be responsible for relapse, metastasis, and resistance, as a potential target of the dietary compound, may be an important aspect of sulforaphane chemoprevention. Evidence also suggests that sulforaphane may target the epigenetic alterations observed in specific cancers, reversing aberrant changes in gene transcription through mechanisms of histone deacetylase inhibition, global demethylation, and microRNA modulation. Critical Issues: In this review, we discuss the biochemical and biological properties of sulforaphane with a particular emphasis on the anticancer properties of the dietary compound. Sulforaphane possesses the capacity to intervene in multistage carcinogenesis through the modulation and/or regulation of important cellular mechanisms. The inhibition of phase I enzymes that are responsible for the activation of pro-carcinogens, and the induction of phase II enzymes that are critical in mutagen elimination are well-characterized chemopreventive properties. Furthermore, sulforaphane mediates a number of anticancer pathways, including the activation of apoptosis, induction of cell cycle arrest, and inhibition of NFκB. Future Directions: Further characterization of the chemopreventive properties of sulforaphane and its capacity to be selectively toxic to malignant cells are warranted to potentially establish the clinical utility of the dietary compound as an anti-cancer compound alone, and in combination with clinically relevant therapeutic and management strategies. Antioxid. Redox Signal. 22, 1382–1424.

Fatty Acids Or Lipids, Estrogen and Cancer

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Highfat estrogen

Everyone knows that modern high-fat processed diet lead to obesity. Obesity is associated with several health issues, including cancer.

But since this fact is popular, even doctors, now prescribe low-fat diet. They force patients to get rid of even traditional fat-focused diet like Ghee.

At this juncture, it is important to know different dietary fat and their role in health and diseases.

Different Types of Dietary Fats

Fatty acids are long, straight-chain molecules categorized as:

  1. Saturated : Animal far
  2. Monosaturated
  3. Polyunsaturated

Difference between them is their chemistry. Since our focus is cancer, we will consider only those fat types which affects cancer etiology upto some extent (In reality, there is no single cause for cancer. There are always multiple factors working together, causing cancer).

Omega-6 fat, Estrogen and Cancer

In 1982, National research council, USA, identified fats (Omega-6 fatty acids) as the single dietary component most strongly related to cancer risk. This report was based on studies that suggested correlations between fats consumption and incidence of GI, Prostate and breast cancers.

But these reports did not provide specific detail. Later it was realized from more studies that intake of omega-6 fatty acids may promote cancer progression partly by increasing the production of availability of estrogen. [1][2][3][4][5][6]

Estrogen is a growth factor for a number of cancers, including breast cancer. High-fat diets and associated increase in fat tissuecan increase estrogen by number of ways:

  1. Fat tissue is a major source of estrogen production in postmenopausal women.
  2. Obesity and insulin resistance can decrease the levels of sex hormone binding globulin in men and women and increase cancer risk. Decreased binding protein means more biologically active estrogen.
  3. Obesity can alter estrogen metabolism in the liver
  4. High-fat diet may reduce the amount of estrogen excreted through the feces.

If you have not read old post, we have covered here (http://prachodayat.in/fast-food-estrogen-storm/), how fast-food diet leads to high serum estrogen level. And as per this post, it plays critical role in cancer progression.

Make your teen kids aware about this and help them love their life. Stop being suicidal. Stop fast food, processed food and high-fat diet full of Omega-6 fat.

Solution is to replace Omega-6 fat by Omega-3 fat. In Indian context, it is desi cow ghee.

 


References


[1] Dwyer JT. Dietary fat and breast cancer: Testing interventions to reduce risks. In Exercise, calories, fat and cancer. Jacobs MM, ed. New York: Plenum Press, 1992.

[2]

Possible Mechanisms through which Dietary Lipids, Calorie Restriction, and Exercise Modulate Breast Cancer

Though the exact cause of breast cancer still remains a mystery, years of investigations have suggested that several dietary and endocrine-related factors may induce and/or could modulate the growth of breast cancer. Epidemiologic and experimental evidence have indicated a close association between high-fat diets and increased incidence of breast cancer.1–3 Furthermore, several immunologic functions, including the levels of growth factors, cytokines, and sex steroid hormones, may be altered or regulated by dietary lipids.4,5 Excessive fat in the diet has been reported to enhance the growth of both spontaneously occurring and chemically induced colon and mammary tumors, as well as accelerated growth of transplantable carcinomas.6–8 Diets containing high levels of ω-6 fatty acids derived from vegetable fats appear to enhance tumorigenesis, while ω-3-containing lipids, either from vegetable or marine origin, or low levels of fat in the diet can diminish tumorigenesis. Recently, a number of mechanisms have been proposed to explain the modulation of mammary tumorigenesis in experimental animals by increasing the levels of dietary fats.9,10 Initiation and promotion have been linked to immune suppression,11 prostaglandin production,12,13 free radical formation,14 membrane fluidity changes,15 intracellular transport system modulation,16 increased caloric utilization,17 increased mammotrophic hormone secretion,18and cytokine changes.19,20 Over-expression of oncogenes and certain growth factors are other mechanisms that have been linked to dietary changes that may influence mammary tumori-genesis.

https://link.springer.com/chapter/10.1007%2F978-1-4684-7953-9_15

[3]

Meta-analysis: Dietary Fat Intake, Serum Estrogen Levels, and the Risk of Breast Cancer

Abstract

BACKGROUND: There is compelling evidence that estrogens influence breast cancer risk. Since the mid-1980s, dietary fat intervention studies have been conducted to investigate the effect of fat intake on endogenous estrogen levels. To further our understanding of the possible relationship between dietary fat and breast cancer, we conducted a meta-analysis of dietary fat intervention studies that investigated serum estradiol levels, and we reviewed the nature of the evidence provided by prospective analytic studies of fat consumption and breast cancer risk. METHODS: A computerized search of the English language literature on estrogen/estradiol and dietary fat intervention studies published from January 1966 through June 1998 was conducted using the MEDLINE® database. Pooled estimates were derived from the change in estradiol levels associated with fat reduction from 13 studies. Analyses were conducted separately for premenopausal and postmenopausal women and in both groups combined. RESULTS AND CONCLUSIONS: Statistically significant reductions in serum estradiol levels of − 7.4% (95% confidence interval [CI] = − 11.7% to −2.9%) among premenopausal women and − 23.0% (95% CI = −27.7% to −18.1%) among postmenopausal women were observed, with an overall −13.4% (95% CI = −16.6% to −10.1%) reduction observed. The greatest reductions occurred in two studies in which dietary fat was reduced to 10%-12% of calories compared with 18%-25% of calories in the other studies. A statistically significant reduction in estradiol levels of −6.6% (95% CI = −10.3% to −2.7%) remained after exclusion of these two studies. Review of prospective analytic epidemiologic studies that allowed for dietary measurement error suggests that the possibility that reducing fat consumption below 20% of calories will reduce breast cancer risk cannot be excluded. IMPLICATIONS: Dietary fat reduction can result in a lowering of serum estradiol levels and such dietary modification may still offer an approach to breast cancer prevention.

https://academic.oup.com/jnci/article/91/6/529/2549361

[4]

Western nutrition and the insulin resistance syndrome: a link to breast cancer.

https://www.ncbi.nlm.nih.gov/pubmed/10099938

[5] https://www.ncbi.nlm.nih.gov/pubmed/8391818

[6]

Sex hormone-binding globulin, its membrane receptor, and breast cancer: a new approach to the modulation of estradiol action in neoplastic cells.

The role of human Sex Hormone-Binding Globulin (SHBG), the plasma carrier of sex steroids, and its membrane receptor, SHBG-R, in estrogen-dependent breast cancer has been investigated in our laboratory in the past few years. SHBG-R is expressed in MCF-10 A cells (not neoplastic mammary cells), MCF-7 cells (breast cancer, ER positive) and in tissue samples from patients affected with ER positive breast cancer, but not in estrogen-insensitive MDA-MB 231 cells. The SHBG/SHBG-R interaction, followed by the binding of estradiol to the complex protein/receptor, causes a significant increase of the intracellular levels of cAMP, but does not modify the amount of estradiol entering MCF-7 cells. The estradiol-induced proliferation of MCF-7 cells is inhibited by SHBG, through SHBG-R, cAMP and PKA. Similarly, the proliferation rate of tissue samples positive for SHBG-R was significantly lower than the proliferation rate of negative samples. SHBG and SHBG-R could thus trigger a ‘biologic’ anti-estrogenic pathway. In order to get a more detailed knowledge of this system, we first examined the frequence of the reported mutated form of SHBG in 255 breast cancer patients. The mutated SHBG is characterized by a point mutation (Asp 327 –> Asn) causing an additional N-glycosylation site, which does not affect the binding of steroids to SHBG. The frequence of the mutation was significantly higher (24.5%) in estrogen-dependent breast cancers than in healthy control subjects (11.6%). This observation confirms the close relationship between SHBG and estrogen-dependent breast cancer and suggests that the mutation could modify SHBG activity at cell site. Lastly, the possibility of using SHBG to modulate the estradiol action in breast cancer was further studied by transfecting MCF-7 cells with an expression vector carrying the SHBG cDNA (study in collaboration with G.L. Hammond). Transfected cells are able to produce significant amount of SHBG in their medium, but their SHBG-R is reduced to undetectable levels. The SHBG produced by transfected MCF-7 cells is, however, able to inhibit estradiol-induced proliferation of MCF-7 cells expressing a functional receptor. Thus, the local production of SHBG obtained with transfection could be a useful tool to control cell growth in estrogen-dependent breast cancer.

https://www.ncbi.nlm.nih.gov/pubmed/10419027

Pill Now? Cancer Later

Pills

Don’t panic if you have taken in past. Avoid in future and take measures to reverse the effect in body by living stress-free life.

I have been vocal against idiotic Pill obsession. Mindless birth control pills in your young age will invite grave danger in menopausal age. Not only obesity but also diabetes, cancer and hormonal disorders.

It is grave mistake on govt side to promote contraceptives as birth control tools.

Not only females, newborns also suffer due to pills. Early in fetal life, nutrient deficiencies may result in severe impairments. For example, folate. Or as popularly known as : B Vitamin. Pill obsession will make your child devoid of folate in growth period as mother’s folate level reduces due to pill-intake.

Take care. Spread awareness. Save Nation.

ACCORDING TO A LOT OF DOCTORS:

Got acne? Take the pill.
Got PMS? Take the pill.
Got irregular cycles? Take the pill.
Don’t want to get pregnant? Take the pill.

All thanks parents’ pre-planning sexual indulgence and avoidance of progeny by modern pills. Folate is a vitamin that may become depleted with the use of birth control pills. Aside from the long list of potential side effects birth control pills can deplete important nutrients. These nutrients include: Vitamin B2, Vitamin B6, Vitamin B12, Folic Acid, Vitamin C, Magnesium and Zinc.

Once the pills become regular bedroom utility, body start denying absorption of nutrients. No matter how sophisticated supplements you take.

Such information is never passed-on to teens and young married couples. And so sex becomes pleasure machine for them. Instant, handy and under control. What a toxic delusion! 🙁🙁 And and top of that Idiot Chetan Bhagat tribe cry for porn freedom rights!! Ghor Kaliyug !! 🙁🙁

Spread the awareness. Save the future of Bharat.

More here : http://prachodayat.in/belong-pill-tribe/

 


Research


Contemporary Hormonal Contraception and the Risk of Breast Cancer

http://www.nejm.org/doi/full/10.1056/NEJMoa1700732

Background

Little is known about whether contemporary hormonal contraception is associated with an increased risk of breast cancer.

Methods

We assessed associations between the use of hormonal contraception and the risk of invasive breast cancer in a nationwide prospective cohort study involving all women in Denmark between 15 and 49 years of age who had not had cancer or venous thromboembolism and who had not received treatment for infertility. Nationwide registries provided individually updated information about the use of hormonal contraception, breast-cancer diagnoses, and potential confounders.

Results

Among 1.8 million women who were followed on average for 10.9 years (a total of 19.6 million person-years), 11,517 cases of breast cancer occurred. As compared with women who had never used hormonal contraception, the relative risk of breast cancer among all current and recent users of hormonal contraception was 1.20 (95% confidence interval [CI], 1.14 to 1.26). This risk increased from 1.09 (95% CI, 0.96 to 1.23) with less than 1 year of use to 1.38 (95% CI, 1.26 to 1.51) with more than 10 years of use (P=0.002). After discontinuation of hormonal contraception, the risk of breast cancer was still higher among the women who had used hormonal contraceptives for 5 years or more than among women who had not used hormonal contraceptives. Risk estimates associated with current or recent use of various oral combination (estrogen–progestin) contraceptives varied between 1.0 and 1.6. Women who currently or recently used the progestin-only intrauterine system also had a higher risk of breast cancer than women who had never used hormonal contraceptives (relative risk, 1.21; 95% CI, 1.11 to 1.33). The overall absolute increase in breast cancers diagnosed among current and recent users of any hormonal contraceptive was 13 (95% CI, 10 to 16) per 100,000 person-years, or approximately 1 extra breast cancer for every 7690 women using hormonal contraception for 1 year.

Conclusions

The risk of breast cancer was higher among women who currently or recently used contemporary hormonal contraceptives than among women who had never used hormonal contraceptives, and this risk increased with longer durations of use; however, absolute increases in risk were small. (Funded by the Novo Nordisk Foundation.)

For 50 years, Sugar Industry cartel hid the link between Processed Sugar and Cancer

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Sugar Cancer

When a like-minded friend shared below comment with me, I started thinking about the correlation.

 “It looks like Sugar is doing all the Vata Disorder even in remote areas like hilly states of Uttarakhand and Himachal.

Thyroid disorders, blood pressure, heart attack, diabtes in remote areas is unjustifiable. 
Sugar is taking a great toll”

I think my friend is right. If you observe last 20-25 years, due to easy road transport technology and electricity everywhere, modern utensils and processed food has reached even remote area. They did play critical role in bringing life-style disorders to the remote hill area.

Tips from personal experience, learning and observations:

  1. Avoid processed polished sugar in regular diet
  2. Best if you can stop having it
  3. Replace sugar by jaggery prepared without chemicals
  4. Unprocessed Sugar – once in a while

Here are  research paper showing how sugar industry never allowed to publish health impact reserch.


Sugar industry sponsorship of germ-free rodent studies linking sucrose to hyperlipidemia and cancer: An historical analysis of internal documents

https://doi.org/10.1371/journal.pbio.2003460


In 1965, the Sugar Research Foundation (SRF) secretly funded a review in the New England Journal of Medicine that discounted evidence linking sucrose consumption to blood lipid levels and hence coronary heart disease (CHD). SRF subsequently funded animal research to evaluate sucrose’s CHD risks. The objective of this study was to examine the planning, funding, and internal evaluation of an SRF-funded research project titled “Project 259: Dietary Carbohydrate and Blood Lipids in Germ-Free Rats,” led by Dr. W.F.R. Pover at the University of Birmingham, Birmingham, United Kingdom, between 1967 and 1971. A narrative case study method was used to assess SRF Project 259 from 1967 to 1971 based on sugar industry internal documents. Project 259 found a statistically significant decrease in serum triglycerides in germ-free rats fed a high sugar diet compared to conventional rats fed a basic PRM diet (a pelleted diet containing cereal meals, soybean meals, whitefish meal, and dried yeast, fortified with a balanced vitamin supplement and trace element mixture). The results suggested to SRF that gut microbiota have a causal role in carbohydrate-induced hypertriglyceridemia. A study comparing conventional rats fed a high-sugar diet to those fed a high-starch diet suggested that sucrose consumption might be associated with elevated levels of beta-glucuronidase, an enzyme previously associated with bladder cancer in humans. SRF terminated Project 259 without publishing the results. The sugar industry did not disclose evidence of harm from animal studies that would have (1) strengthened the case that the CHD risk of sucrose is greater than starch and (2) caused sucrose to be scrutinized as a potential carcinogen. The influence of the gut microbiota in the differential effects of sucrose and starch on blood lipids, as well as the influence of carbohydrate quality on beta-glucuronidase and cancer activity, deserve further scrutiny.


Supporting research material


Scientists’ Study Sweetens Connection Between Cancer, Sugar

http://www.utdallas.edu/news/2017/5/30-32567_Scientists-Study-Sweetens-Connection-Between-Cance_story-wide.html?WT.mc_id=NewsHomePageCenterColumn

Excessive sugar consumption is not only a problem that can lead to complications like diabetes, but also, based on our studies and others, the evidence is mounting that some cancers are also highly dependent on sugar.

Dr. Jung-whan “Jay” Kim,
assistant professor
of biological sciences

 

“As a culture, we are very addicted to sugar,” Kim said. “Excessive sugar consumption is not only a problem that can lead to complications like diabetes, but also, based on our studies and others, the evidence is mounting that some cancers are also highly dependent on sugar. We’d like to know from a scientific standpoint whether we might be able to affect cancer progression with dietary changes.”

The research was supported by the National Institutes of Health, the American Lung Association, the Japan Agency for Medical Research and Development, the Takeda Science Foundation, the Welch Foundation and the Cancer Prevention and Research Institute of Texas.

The research team, which included a Dallas high school student who interned in Kim’s lab, first tapped into a large government database called The Cancer Genome Atlas, which maps information about 33 types of cancer gathered from more than 11,000 patients.

Based on that data, they found that a protein responsible for transporting glucose — a kind of sugar — into cells was present in significantly higher levels in lung SqCC than in lung ADC. The protein, called glucose transporter 1, or GLUT1, takes up glucose into cells, where the sugar provides a fundamental energy source and fuels cell metabolism. GLUT1 is also necessary for normal cell functions, such as building cell membranes.

“Prior to this study, it was thought that the metabolic signatures of these two types of lung cancers would be similar, but we realized that they are very different,” Kim said. “These findings lend credence to the idea that cancer is not just one disease, but many diseases that have very different characteristics.”

With elevated GLUT1 implicated in SqCC’s appetite for sugar, the researchers looked for additional evidence by examining human lung tissue and isolated lung cancer cells, as well as animal models of the disease.

 

Sugar in Western diets increases risk for breast cancer tumors and metastasis

https://www.mdanderson.org/newsroom/2015/12/sugar-in-western-diets.html

“We found that sucrose intake in mice comparable to levels of Western diets led to increased tumor growth and metastasis, when compared to a non-sugar starch diet,” said Peiying Yang, Ph.D., assistant professor of Palliative, Rehabilitation, and Integrative Medicine. “This was due, in part, to increased expression of 12-LOX and a related fatty acid called 12-HETE.”

Previous epidemiological studies have shown that dietary sugar intake has an impact on breast cancer development, with inflammation thought to play a role.

“The current study investigated the impact of dietary sugar on mammary gland tumor development in multiple mouse models, along with mechanisms that may be involved,” said co-author Lorenzo Cohen, Ph.D., professor of Palliative, Rehabilitation, and Integrative Medicine. “We determined that it was specifically fructose, in table sugar and high-fructose corn syrup, ubiquitous within our food system, which was responsible for facilitating lung metastasis and 12-HETE production in breast tumors.”

Cohen added that the data suggested that dietary sugar induces 12-LOX signaling to increase risks for breast cancer development and metastasis.

Identifying risk factors for breast cancer is a public health priority, say the authors.  The researchers state that moderate sugar consumption is critical, given that the per capita consumption of sugar in the U.S. has surged to over 100 lbs. per year and an increase in consumption of sugar-sweetened beverages has been identified as a significant contributor to an epidemic of obesity, heart disease and cancer worldwide.

Cancer and Death : Two Biological events

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Would you call ‘Death’ as disease? No, right? Death is not a disease. It is biological event. Similarly, cancer is also a biological event. Sometimes, it surfaces on life early. Most of the times, it does in last stage of life. Game of circadian clocks. Time driven events.

diagram-showing-how-cancer-cells-keep-on-reproducing-to-form-a-tumour_0

Cancer is a property of each cell. It is the faulty clock that leads to cell into Cancer pathway than Cell Death pathway.

We all take birth with a probability of normal cells turned cancer cells.

Once you die, the cells in your body think that you are an embryo….so all the genes which remain up in embryo (and that never again become active in your life time after birth) become active again.

Body cells also think that there is something wrong, that’s why there is no signal of cell proliferation, development etc. So, the cells start expressing the genes that are generally overexpressed during cancer. I.e. signal is given to cell to proliferate (multiply).

People who get organ donation from dead body are more prone to cancers. This is explanation!!
Or in other words, Cancer is a sign of early death or rapid aging.

 


Research


http://www.scripps.edu/news/press/2016/20161116lamia.html

TSRI Researchers Show How Circadian ‘Clock’ May Influence Cancer Pathway

A new study led by scientists at The Scripps Research Institute (TSRI) describes an unexpected role for proteins involved with our daily “circadian” clocks in influencing cancer growth.

The research, published recently in the journal Molecular Cell, suggests that disruptions in circadian rhythms might leave levels of an important cancer-linked protein, called cMYC, unchecked.

“This appears to have big implications for the connection between circadian rhythms and cancer,” said TSRI biologist Katja Lamia, senior author of the study.

There is growing evidence that shift work and frequent jet lag can raise a person’s risk of cancer, suggesting a link between daily rhythms and cell growth. “We know this connection exists, but we haven’t known why,” said Lamia.

The researchers focused on proteins called cryptochromes, which evolved from bacterial proteins that sense light and repair DNA damage caused by sunlight. In humans, these proteins, called CRY1 and CRY2, regulate our circadian clocks, which influence what times of day we become tired, hungry and much more.

Using cells from mouse models, the researchers demonstrated that deleting the gene that expresses CRY2 reduced the cells’ ability to degrade a protein called cMYC. Without CRY2 keeping cMYC at normal levels, the researchers saw increased cell proliferation—similar to the abnormal growth seen in cancers.

Further studies of protein structures suggested that CRY2 is a key player in a process to “mark” cMYC for degradation. The researchers said it is significant that this process occurs after gene transcription—once the proteins are already produced—rather than during transcription, as in many other cryptochrome functions.

“This is a function of a circadian protein that has never been seen before,” said TSRI Research Associate Anne-Laure Huber, who served as first author of the study.

The researchers say more studies are needed to confirm this connection between circadian clocks and cancer in human tissues.

In addition to Lamia and Huber, authors of the study, “CRY2 and FBXL3 Cooperatively Degrade c-MYC,” were Stephanie J. Papp, Alanna B. Chan, Sabine D. Jordan, Anna Kriebs and Madelena Nguyen of TSRI; Emma Henriksson of TSRI and Lund University; Martina Wallace and Christian M. Metallo of the University of California, San Diego; and Zhizhong Li of the Genomics Institute of the Novartis Research Foundation and Novartis Institutes for Biomedical Research.

This study was supported by the National Institutes of Health (grants DK090188, DK097164, CA188652 and NIGMS P41-GM103311), the Searle Scholars Program through the Kinship Foundation, the Sidney Kimmel Foundation, the Lung Cancer Research Foundation, the Swedish Research Council, the Deutsche Forschungsgemeinschaft and the American Heart Association (grant 15POST22510020).

 

 

Ginger :10000 times more effective than Chemotherapy

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Ginger Cancer

What is cancer cell?

Some dirty cell of your body? No. This body is wonderful gift. Nature does not act dirty. You and me do. Cancer cell is ordinary cell with cancerous tendency. Such tendency is expected due to cellular level stress. This stress is due to mental stress, physical stress (Food, water, air pollution) and environmental stress. Prolonged stress.

No cell loves to act cancerously. If you help them reduce local and global stress, they prefer to live happy life for you.

Cancer stem cells is a step before Cancer Cells. Cancer stem cells (CSCs) pose a serious obstacle to cancer therapy as they can be responsible for poor prognosis and tumour relapse.

It is shown by this research paper that Ginger compounds act against CSCs and inhibits them.

So is this the solution? No! Why should we even invite cancer? Prevention is always better than cure. Having ginger in diet can help but more than that stress-free life is more important! The root of all sicknesses start with weak mind!

Beware! Ginger and Turmeric are found 10000 times more effective than Chemotherapy. Now, we will have flood industrial farming of ginger and turmeric. That will follow genetically modified Ginger and Turmeric. That is how species are destroyed by Idiot science.


Research


6-Shogaol Inhibits Breast Cancer Cells and Stem Cell-Like Spheroids by Modulation of Notch Signaling Pathway and Induction of Autophagic Cell Death

http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0137614

Abstract

Cancer stem cells (CSCs) pose a serious obstacle to cancer therapy as they can be responsible for poor prognosis and tumour relapse. In this study, we have investigated inhibitory activity of the ginger-derived compound 6-shogaol against breast cancer cells both in monolayer and in cancer-stem cell-like spheroid culture. The spheroids were generated from adherent breast cancer cells. 6-shogaol was effective in killing both breast cancer monolayer cells and spheroids at doses that were not toxic to noncancerous cells. The percentages of CD44+CD24/low cells and the secondary sphere content were reduced drastically upon treatment with 6-shogaol confirming its action on CSCs. Treatment with 6-shogaol caused cytoplasmic vacuole formation and cleavage of microtubule associated protein Light Chain3 (LC3) in both monolayer and spheroid culture indicating that it induced autophagy. Kinetic analysis of the LC3 expression and a combination treatment with chloroquine revealed that the autophagic flux instigated cell death in 6-shogaol treated breast cancer cells in contrast to the autophagy inhibitor chloroquine. Furthermore, 6-shogaol-induced cell death got suppressed in the presence of chloroquine and a very low level of apoptosis was exhibited even after prolonged treatment of the compound, suggesting that autophagy is the major mode of cell death induced by 6-shogaol in breast cancer cells. 6-shogaol reduced the expression levels of Cleaved Notch1 and its target proteins Hes1 and Cyclin D1 in spheroids, and the reduction was further pronounced in the presence of a γ-secretase inhibitor. Secondary sphere formation in the presence of the inhibitor was also further reduced by 6-shogaol. Together, these results indicate that the inhibitory action of 6-shogaol on spheroid growth and sustainability is conferred through γ-secretase mediated down-regulation of Notch signaling. The efficacy of 6-shogaol in monolayer and cancer stem cell-like spheroids raise hope for its therapeutic benefit in breast cancer treatment.

 

 

Muladhara(मूलाधार) and Cancer : Prevent and Cure

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MicrobesCancer

Tvam muladhara sthitosi nityam |
त्वं मूलाधार स्थितोऽसि नित्यं।
Lord Ganesha! You always dwell in muladhara chakra!

मूलाधार : शक्ति Center near Gut & anus : Abode of मरुत गण (Microbes) and their leader गणपति

It does not only control microbes in GUT but of entire body.

He is the lord of muladhara chakra. In other words, he rules our microbial flora (मरुत गण) and make sure only body-friendly मरुत गण resides in the abode.

मरुत गण (Microbes) : गण पति (Ganesha) : गण (Citizens) & पति (Protector) live together @ Muladhara

Awakening गण पति शक्ति is critical for maintaining health (which is critical for self-realization). Only he can protect and act as gatekeeper of Muladhara (Gut) so that body is kept protected from pathogens & aasuri shakti.

Here are two interesting researchers focuses on Muladhara for cancer-cause and cancer recovery.


Research


Cleveland Clinic Researchers Find Link Between Bacterial Imbalances and Breast Cancer

In a newly published study, Cleveland Clinicresearchers have uncovered differences in the bacterial composition of breast tissue of healthy women vs. women with breast cancer. The research team has discovered for the first time that healthy breast tissue contains more of the bacterial species Methylobacterium, a finding which could offer a new perspective in the battle against breast cancer.

Bacteria that live in the body, known as the microbiome, influence many diseases.

Most research has been done on the “gut” microbiome, or bacteria in the digestive tract. Researchers have long suspected that a “microbiome” exists within breast tissue and plays a role in breast cancer but it has not yet been characterized. The research team has taken the first step toward understanding the composition of the bacteria in breast cancer by uncovering distinct microbial differences in healthy and cancerous breast tissue.

“To my knowledge, this is the first study to examine both breast tissue and distant sites of the body for bacterial differences in breast cancer,” said co-senior author Charis Eng, M.D., Ph.D., chair of Cleveland Clinic’s Genomic Medicine Institute and director of the Center for Personalized Genetic Healthcare. “Our hope is to find a biomarker that would help us diagnose breast cancer quickly and easily.  In our wildest dreams, we hope we can use microbiomics right before breast cancer forms and then prevent cancer with probiotics or antibiotics.”

Published online in Oncotarget on Oct. 5, 2017, the study examined the tissues of 78 patients who underwent mastectomy for invasive carcinoma or elective cosmetic breast surgery. In addition, they examined oral rinse and urine to determine the bacterial composition of these distant sites in the body.

newsroom.clevelandclinic.org/2017/10/05/cleveland-clinic-researchers-find-link-between-bacterial-imbalances-and-breast-cancer/

Good-guy bacteria helps in cancer therapies

Researchers found he had the beneficial gut bacteria and suspect this microbiome contributed to the outcome. As a group, patients who responded well to the immunotherapy had three specific bacteria:

  • Bacteroides thetaiotaomicron
  • Faecalibacterium prausnitzii
  • Holdemania filiformis

All three are common normal flora in the human intestinal tract.

After identifying the link, researchers looked for a potential reason for the association between the helper bacteria and immunotherapy effectiveness. “Is it something the bacteria are making? We examined metabolites in these subjects and found the strongest correlation between anacardic acid, present in cashews and mangoes, and the beneficial bacteria,” Dr. Koh said.

Researchers plan to follow up on the current research, which appears in the journal Neoplasia, with larger clinical studies.

http://www.utsouthwestern.edu/newsroom/articles/year-2017/bacteria-immunotherapy-koh.html

 

Desi Cow Ghee against Cancer and Coronary Heart Diesease

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cowghee

Note 1

Ghee is medicine but modern doctors blame it for all life style diseases. They even prescribe ban at home.

Well, urban dwellers disconnected from Gau based villages must not consume ghee available in their super markets. It is indeed deadly.

But this does not mean all variety of ghee is bad. Rural India is where we can find ideal case studies. A study on a rural population in India showed a significantly lower prevalence of coronary heart disease in men who consumed higher amounts of ghee.

“Asian Indians previously had a low incidence of coronary heart disease and for generations had been using ghee in their cooking, which is low in PUFAs such as linoleic acid and arachidonic acid. The epidemic of coronary heart disease in India began two to three decades ago when traditional fats were replaced by oils rich in linoleic and arachidonic acid, as well as trans fatty acids which comprise 40% of vanaspati. Adulteration of commercially prepared ghee with vanaspati is also prevalent in India.”

Ghee prepared from desi Gau’s milk by churning is an elixir. If you can avail it, get it at any cost! Yes, at any cost! It will be cheaper than your medical bills. 😛 Be wise, at least health-wise. 😉

Association of dietary ghee intake with coronary heart disease and risk factor prevalence in rural males.

https://www.ncbi.nlm.nih.gov/pubmed/9212571

Abstract

To determine the association between intake of dietary fat, specifically Indian ghee, and prevalence of coronary heart disease (CHD) and risk factors as study was undertaken on a rural population in Rajasthan. Total community cross-sectional survey was done using a physician administered questionnaire; 1982 males aged 20 years and more were studied. The dietary questionnaire focused on the amount and type of fat consumed. Staple dietary fat in this area is mustard/rapeseed oil and Indian ghee. To define the role of ghee, the average amount consumed in a month was determined; 782 males (39%) consumed 1 kg or more ghee per month (group 1) and 1200 (61%) consumed less than 1 kg per month (group 2). To elicit details of fatty acid composition of the diet consumed, detailed dietary history was acquired from a random 460 (23%) males; 220 from group 1 and 240 from group 2. Group 1 males were significantly younger, more literate and had more weight and body-mass index. This group consumed significantly more calories, saturated and mono-unsaturated fats while the consumption of polyunsaturated fats was similar in the two groups. Fatty acid intake analysis showed that group 1 males consumed more mono-unsaturated (n-9) fatty acids than group 2. Intake of polyunsaturated n-3 and n-6 fatty acids was similar. There was significantly lower prevalence of CHD in men who consumed > kg ghee per month (odds ratio = 0.23, 95% confidence limits 0.18-0.30, p < 0.001). Multivariate analysis confirmed this association (p < 0.001). The prevalence of hypertension and other coronary risk factors was similar in the two groups.


Note 2

So your doctor asks you to stop having Ghee and start having Soyabean oil. Right?

Well, study suggests contradictory findings. You should actually stop eating genetically modified Soya oil and start consuming ethically procured desi Gau’s ghee (*What is it?).

As per this study:

“Dietary cow ghee compared to soybean oil downregulates the enzyme activities responsible for carcinogen activation in liver and upregulates carcinogen detoxification activities in liver and mammary tissues.”

*Ethically procured desi Gau’s ghee is produced by Gau shala that treats Gau as mother, never tortures her by hormone injections, processed food, allows calves to have milk as much they want, allows Gau to live freely and graze green grass daily.

Effects of cow ghee (clarified butter oil) & soybean oil on carcinogen-metabolizing enzymes in rats.

https://www.ncbi.nlm.nih.gov/pubmed/23041740

INTERPRETATION & CONCLUSIONS:

Our findings show that dietary cow ghee compared to soybean oil downregulates the enzyme activities responsible for carcinogen activation in liver and upregulates carcinogen detoxification activities in liver and mammary tissues.

Cow Milk, BAMLET and Cancer Prevention

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Cow Milk Cancer

We cut short feeding duration for petty things like career, beauty and money.
We also don’t have access to ethically procured A2 milk from lovable mother Gau.

Mother’s milk has HAMLET. Cow’s raw milk has BAMLET.

Both can control cancerous nature of the cell.

And we cry increasing numbers of cancer cases. 🙁

“Breast-feeding has also been reported to protect against development of immunological diseases, such as allergy (Ahmed & Fuchs, 1997; Saarinen & Kajosaari, 1995), infantile diabetes mellitus (Gerstein, 1994; Mayer et al., 1988) and inflammatory gastrointestinal disease (Koletzko et al., 1989). These results imply that factors in milk may help optimise the function of the immune system and regulate cell populations that results in les risk of tumor development and less risk for abberant immunity in the rapidly growing neonatal intestinal tract.”

 

“These data indicate that BAMLET triggers lysosomal cell death pathway in cancer cells, thereby clarifying the ability of alpha-lactalbumin:oleate complexes to kill highly apoptosis-resistant tumor cells.”


Research


Breast-feeding, HAMLET, and cancer

http://www.acsu.buffalo.edu/~andersh/research/milkcancer.asp

HAMLETs effect against tumors in vivo

To date several studies have addressed the ability of HAMLET to kill tumor cells in vivo. Early attempts in mouse models were thwarted as we realized that serum (especially serum albumin) induces a partial inactivation of HAMLET based on binding to the fatty acid in HAMLET. The attempts that have since been done have addressed topical or mucosal administration of HAMLET.

Walter Fischer, then in Bergen, Norway, used HAMLET in a model where tumor tissue from patients with glioblastomas were transplanted under the skull of rats. In this model one dose of HAMLET was infused in the brain through a pump and tissue was tested for apoptosis induction and the rats were monitored for survival. HAMLET treatment delayed death of the rats and the most important finding was that when investigating the brain tissue they found that apoptosis was only induced in tumor cells, no healthy brain cells were affected (Fischer Cancer Res 2004). This indicated what we already know in vitro, that the protein only attacks tumor cells, and indicated that little side effects may be expected should this be used for treatment purposes. Walter, now in Copenhagen, Denmark, is currently planning a patient study in patients with glioblastomas.

In a second study, Lotta Gustafsson together with Irene Leijonhufvud conducted a study on benign papilloma virus warts. Papillomas are a benign tumor form where the skin cells are transformed by virus infection and the hypothesis was that this transformation may make them susceptible to HAMLET treatment. A population of individuals having a major problem with recurrent warts were treated topically with HAMLET and it was found that HAMLET was effective in eliminating warts and that this effect had a long lasting effect (Gustafsson NEJM 2004).

Recently, Anki Mossberg together with Bjorn Wullt performed a study on 9 patients with transitional bladder carcinomas (tumor of the urinary bladder) (Mossberg Int J Cancer 2007). They instilled HAMLET in the bladder of patients in the week preceding surgery and evaluated the tumor morphology by endoscopic photography and apoptosis-induction in biopsy tissue. They found that a reduction in tumor size was seen in 8 of 9 patients and that apoptosis was detected in the tumor tissue but not in the adjacent healthy tissue, indicating that HAMLET is specifically tumorigenic also in vivo. This study was followed up by a study in mice (Mossberg, J Urol, 2010) using the MB49 bladder carcinoma model. In this model they showed a delay in tumor development when HAMLET was instilled in the bladder.

In a study from 2014 Puthia et al (Gut January issue, 2014) it wa shown that HAMLET could be used to prevent and treat colon cancer in APC/Min-mice. HAMLET was given perorally and showed a reduced progression of tumor growth and an increased survival when given as a prophylaxis and reduction of established tumors when given as treatment. HAMLEt accumulated only in tumor tissue and only healthy cells were observed to be apoptotic.


BAMLET activates a lysosomal cell death program in cancer cells.

https://www.ncbi.nlm.nih.gov/pubmed/20053771

A complex of human alpha-lactalbumin and oleic acid (HAMLET) was originally isolated from human milk as a potent anticancer agent. It kills a wide range of transformed cells of various origins while leaving nontransformed healthy cells largely unaffected both in vitro and in vivo. Importantly, purified alpha-lactalbumins from other mammals form complexes with oleic acid that show biological activities similar to that of HAMLET. The mechanism by which these protein-lipid complexes kill tumor cells is, however, largely unknown. Here, we show that complex of bovine alpha-lactalbumin and oleic acid (BAMLET), the bovine counterpart of HAMLET, kills tumor cells via a mechanism involving lysosomal membrane permeabilization. BAMLET shows potent cytotoxic activity against eight cancer cell lines tested, whereas nontransformed NIH-3T3 murine embryonic fibroblasts are relatively resistant. BAMLET accumulates rapidly and specifically in the endolysosomal compartment of tumor cells and induces an early leakage of lysosomal cathepsins into the cytosol followed by the activation of the proapoptotic protein Bax. Ectopic expression of three proteins known to stabilize the lysosomal compartment, i.e. heat shock protein 70 (Hsp70), Hsp70-2, and lens epithelium-derived growth factor, confer significant protection against BAMLET-induced cell death, whereas the antiapoptotic protein Bcl-2, caspase inhibition, and autophagy inhibition fail to do so. These data indicate that BAMLET triggers lysosomal cell death pathway in cancer cells, thereby clarifying the ability of alpha-lactalbumin:oleate complexes to kill highly apoptosis-resistant tumor cells.


Raw Milk Fights Cancer? Who is Hamlet and Bamlet?

Raw Milk Fights Cancer? Who is Hamlet and Bamlet?

Milk Protein Kills Cancer Cells and Antibiotic-Resistant Bacteria

Milk Protein Kills Cancer Cells and Antibiotic-Resistant Bacteria

Cell Phone Radiation and Cancer

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CancerCellphone

When the technology is not safe in controlled environment, imagine the havoc it will create in country like India where rampant loopholes runs across all levels of tech implementations.

We are passing through toxic clouds of EMF.

❝ The unsettling findings are the result of a US$25 million study by the National Toxicology Program (NTP) – a division of the National Institutes of Health (NIH) – which has been underway for the past 2.5 years.
Although a full report on the study is not yet finished, the NTP has released its partial results early.
The research studied rats to determine whether the radio-frequency (RF) radiation emitted by mobile phones can cause cancer. To do so, pregnant rats were placed in special chambers. Once their pups were born, they were treated with RF radiation for approximately nine hours per day. ❞


News


The radiation received by rats was “not very different” from what humans are exposed to when they use mobile phones, said Chris Portier, a former associate director of the NTP and the person who commissioned the study, as cited by Mother Jones.

As researchers increased the intensity of the radiation, the incidence of cancer in the rats also increased. The highest level of radiation was five to seven times as strong as what humans typically receive while using a mobile phone.

I think this is a game changer,” Portier said. “We seriously have to look at this issue again in considerable detail.”

https://www.rt.com/usa/344640-mobile-phones-cancer-radiation/

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