I have just learned that a prior post (now removed) depicting the inappropriate habit of parents to try and sue the  school district when their children are not accomplishing well in class merits a “Happy Ending” update!

“This judgment should make parents think twice or three times before attacking the reputation of a teacher in a malicious way” 

Now science tells us that fasting potentiates chemotherapy:  ”fasting can actually make cancerous cells more susceptible to chemotherapy”

Let’s consider these wise words:   “Stop eating while still hungry and do not continue until you are satisfied.”   St. John Cassian

Starving the beast

Feb 9th 2012, 22:02 by T.C

The ECONOMIST

 Chrysin Reverse the Drug Resistance by Targeting Breast Cancer Stem Cell Related Subpopulation

Conclusions:

1) Chrysin can reverse drug resistance of MCF-7/MX cells by targeting BCRP.

2) chrysin can serve as a chemotherapy sensitizer.

Source: Cancer Research

st cisplatin-induced colon. toxicity via amelioration of oxidative stress and apoptosis: Probable role of p38MAPK and p53.

Khan R, Khan AQ, Qamar W, Lateef A, Tahir M, Rehman MU, Ali F, Sultana S.

Toxicol Appl Pharmacol. 2012 Feb 1;258(3):315-29. Epub 2011 Dec 2.

Cisplatin, an antineoplastic drug, is widely used as a foremost therapy against numerous forms of cancer but it has pronounced adverse effects viz., nephrotoxicity, ototoxicity etc. CDDP-induced emesis and diarrhea are also marked toxicities that may be due to intestinal injury.

Chrysin (5,7-dihydroxyflavone), a natural flavone commonly found in many plants possesses multiple biological activities, such as antioxidant, anti-inflammatory and anti-cancer effects. In the present study, we investigated the protective effect of chrysin against CDDP-induced colon toxicity. The plausible mechanism of CDDP-induced colon toxicity and damage includes oxidative stress, activation of p38MAPK and p53, and colonic epithelial cell apoptosis via upregulating the expression of Bak and cleaved caspase-3.

Chrysin was administered to Wistar rats once daily for 14 consecutive days at the doses of 25 and 50mg/kg body weight orally in corn oil. On day 14, a single intraperitoneal injection of cisplatin was given at the dose of 7.5mg/kg body weight and animals were euthanized after 24h of cisplatin injection.

Chrysin ameliorated CDDP-induced lipid peroxidation, xanthine oxidase activity, glutathione depletion, decrease in antioxidant (catalase, glutathione reductase, glutathione peroxidase and glucose-6 phosphate dehydrogenase) and phase-II detoxifying (glutathione-S-transferase and quinone reductase) enzyme activities.

Chrysin also attenuated goblet cell disintegration, expression of phospho-p38MAPK and p53, and apoptotic tissue damage which were induced by CDDP. Histological findings further supported the protective effects of chrysin against CDDP-induced colonic damage.

The results of the present study suggest that the protective effect of chrysin against CDDP-induced colon toxicity was related with attenuation of oxidative stress, activation of p38MAPK and p53, and apoptotic tissue damage.

Chrysin abrogates cisplatin-induced oxidative stress, p53 expression, goblet cell disintegration and apoptotic responses in the jejunum of Wistar rats.

Khan R, Sultana S  et al

Br J Nutr. 2012 Feb 6:1-12. [Epub ahead of print]

Cisplatin (cis-diamminedichloroplatinum (II) (CDDP)) is a commonly used chemotherapeutic drug for the treatment of numerous forms of cancer, but it has pronounced adverse effects, namely nephrotoxicity, ototoxicity, neurotoxicity, hepatotoxicity, diarrhoea and nausea. CDDP-induced emesis and diarrhoea are also marked toxicities that may be due to intestinal injury.

Chrysin (5,7-dihydroxyflavone), a natural flavone commonly found in many plants, possesses multiple biological activities, such as antioxidant and anti-inflammatory properties.

Chrysin ameliorated CDDP-induced lipid peroxidation, increase in xanthine oxidase activity, glutathione depletion, decrease in antioxidant (catalase, glutathione reductase, glutathione peroxidase and glucose-6-phosphate dehydrogenase) and phase-II detoxifying (glutathione-S-transferase and quinone reductase) enzyme activities.

Chrysin attenuated CDDP-induced goblet cell disintegration, enhanced expression of p53 and apoptotic tissue damage. Histological findings further substantiated the protective effects of chrysin against CDDP-induced damage in the jejunum.

The results of the present study demonstrate that oxidative stress and apoptosis are closely associated with CDDP-induced toxicity and chrysin shows the protective efficacy against CDDP-induced jejunum toxicity possibly via attenuating the oxidative stress and apoptotic tissue damage.

Sulforaphane protects against cisplatin-induced nephrotoxicity.

Dr. Weeks’ Comment:    Fish oil component tames cancer STEM cells  -  did your oncologist tell you to take your fish oil?

“Targeting cancer stem cells is of paramount importance in successfully preventing cancer relapse.”

Blood. 2011 Dec 22;118(26):6909-19. Epub 2011 Oct 3.

Δ12-prostaglandin J3, an omega-3 fatty acid-derived metabolite, selectively ablates leukemia stem cells in mice.

Hegde S, Kaushal N, Ravindra KC, Chiaro C, Hafer KT, Gandhi UH, Thompson JT, van den Heuvel JP, Kennett MJ, Hankey P, Paulson RF, Prabhu KS.

Source

Center for Molecular Immunology and Infectious Disease, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, 16802, USA.

Abstract

Targeting cancer stem cells is of paramount importance in successfully preventing cancer relapse. Recently, in silico screening of public gene-expression datasets identified cyclooxygenase-derived cyclopentenone prostaglandins (CyPGs) as likely agents to target malignant stem cells. We show here that Δ(12)-PGJ(3), a novel and naturally produced CyPG from the dietary fish-oil ω-3 polyunsaturated fatty acid eicosapentaenoic acid (EPA; 20:5) alleviates the development of leukemia in 2 well-studied murine models of leukemia. IP administration of Δ(12)-PGJ(3) to mice infected with Friend erythroleukemia virus or those expressing the chronic myelogenous leukemia oncoprotein BCR-ABL in the hematopoietic stem cell pool completely restored normal hematologic parameters, splenic histology, and enhanced survival. More importantly, Δ(12)-PGJ(3) selectively targeted leukemia stem cells (LSCs) for apoptosis in the spleen and BM. This treatment completely eradicated LSCs in vivo, as demonstrated by the inability of donor cells from treated mice to cause leukemia in secondary transplantations. Given the potency of ω-3 polyunsaturated fatty acid-derived CyPGs and the well-known refractoriness of LSCs to currently used clinical agents, Δ(12)-PGJ(3) may represent a new chemotherapeutic for leukemia that targets LSCs.

overview

The University of Michigan has recently emerged as a national leader in the three main types of stem cell research: embryonic, adult, and reprogrammed cells known as iPS cells.

A long-time leader in the study of adult stem cells, U-M has bolstered its human embryonic stem cell program, and added a complementary iPS cell research effort, since the passage of Proposal 2 in November 2008. The state constitutional amendment eased onerous restrictions on the types of embryonic stem cell research allowed in Michigan.

Recent milestones include:

• The launch, in March 2009, of a U-M-led consortium to create new human embryonic stem cell lines to aid the search for disease treatments and cures. The A. Alfred Taubman Medical Research Institute’s Consortium for Stem Cell Therapies (CSCT) is based at the Medical School, and researchers from across campus—including scientists at the Life Sciences Institute, the College of Engineering, the Comprehensive Cancer Center and the Department of Cell and Developmental Biology—participate.

  In addition, collaborations are underway between CSCT and U-M’s University Research Corridor partners—Michigan State University and Wayne State University–as well and other institutions.

• CSCT’s development of the state’s first human embryonic stem cell line in October 2010. The first Michigan line, known as UM4-6, is the product of years of planning and preparation at U-M; the work was made possible by the state constitutional amendment allowing Michigan researchers to derive embryonic stem cell lines using surplus embryos from fertility clinics.
• CSCT’s development, in April 2011, of Michigan’s first human embryonic stem cell lines carrying the genes responsible for inherited diseases. With this accomplishment, U-M joined a small handful of U.S. universities that are producing disease-specific human embryonic stem cell lines. The work will enable scientists here and around the world to study the onset and progression of genetic disorders and to search for new treatments.
• The reprogramming, by CSCT scientists in July 2011, of adult skin cells so they behave like embryonic stem cells. The reprogrammed cells are called induced pluripotent stem cells, or iPS cells. They display many of the most scientifically valuable properties of embryonic stem cells while enabling researchers to bypass embryos altogether.
• The announcement on Feb. 14, 2012, that the U-M’s first human embryonic stem cell line, UM4-6, will be added to the National Institutes of Health’s national registry, joining 146 other cell lines. Inclusion on the national registry makes the U-M-derived cell line available to the scientific community for federally funded embryonic stem cell research projects. Registry listing was a prime CSCT goal since its inception.

In addition to the work underway by the Consortium for Stem Cell Therapies, hubs for U-M stem cell research also exist at the Life Science Institute’s Center for Stem Cell Biology and at the U-M Health System’s Comprehensive Cancer Center. Other groundbreaking stem cell work is being pursued at other units across campus.

The Center for Stem Cell Biology was established in 2005 with $10.5 million provided by the U-M Medical School, the Life Sciences Institute, and the Molecular and Behavioral Neurosciences Institute.

The center’s main goal is to determine the fundamental mechanisms that regulate stem cell function. That knowledge, in turn, provides new insights into the origins of disease and suggests new approaches to disease treatment. Most of the work involves adult stem cells — including blood-forming and nervous system stem cells — but human embryonic stem cells also are studied.

The U-M Comprehensive Cancer Center is one of the few places in North America that has made an institutional commitment to cancer stem cell research. Cancer stem cells are responsible for triggering the uncontrolled cell growth that leads to malignant tumors.

U-M researchers were the first to identify stem cells in solid tumors, finding them in breast cancer in 2003. They were also the first to find pancreatic and head-and-neck stem cells. At the U-M cancer center, scientists are investigating how these cells mutate, causing unregulated growth that ultimately leads to cancer.

SOURCE http://www.stemcellresearch.umich.edu/overview/

Here’s some news about cell phones and cancer which even the mainstream media has found impossible to ignore. The International Agency for Research on Cancer (IARC), an arm of the World Health Organization (WHO), has declared after a review of the research that cell phones are possible cancer-causing agents. The expert panel ruled that there was some evidence that cell phone use was linked to two types of tumors—brain tumors (gliomas) and acoustic neuromas.

Some scientists say the IARC classification is still not strong enough, and that cell phone radiation should have been classified as a “Probable Human Carcinogen” based on the existing science, but evidently there were not enough studies to classify it more strongly at this time.

Alasdair Philips of Powerwatch in the U.K. says,

“The existing science is very clear there is risk of cancer from cell phone use. The warning might have been 2A if there were a larger number of animal studies showing this, or if there were a larger number of up-to-date human studies. It’s important to recognize the Interphone study on which the classification to a large extent relied was completed in 2004, and current studies reflecting usage patterns today would be far more damning, possibly earning a Class 1 “Human Carcinogen.”

However, according to Electromagnetic Health:

“Nonetheless, the IARC opinion is a breath of fresh air to many, and restores some integrity to a badly tarnished IARC … The IARC classification of cell phones as a ‘possible human carcinogen’ will now travel throughout the world, influencing governments far and wide, for the 1st time providing an official scientific basis on which governments, schools and parents can legitimately call for precautionary behavior regarding these radiation-emitting devices.”

Professor Dariusz Leszczynski, of the Radiation and Nuclear Safety Authority in Finland, explains why this should probably be considered big news:

“… for the first time a very prominent evaluation report states it so openly and clearly: RF-EMF is possibly carcinogenic to humans. One has to remember that IARC monographs are considered as ‘gold standard’ in evaluation of carcinogenicity of physical and chemical agents. If IARC says it so clearly then there must be sufficient scientific reason for it, or IARC would not put its reputation behind such claim.”

WHO’s Group 2 Classification of Cancer Risk

“This category includes agents for which, at one extreme, the degree of evidence of carcinogenicity in humans is almost sufficient, as well as those for which, at the other extreme, there are no human data but for which there is evidence of carcinogenicity in experimental animals. Agents are assigned to either Group 2A (probably carcinogenic to humans) or Group 2B (possibly carcinogenic to humans) on the basis of epidemiological and experimental evidence of carcinogenicity and mechanistic and other relevant data.

The terms probably carcinogenic and possibly carcinogenic have no quantitative significance and are used simply as descriptors of different levels of evidence of human carcinogenicity, with probably carcinogenic signifying a higher level of evidence than possibly carcinogenic.”

So as you can see, while some journalists and scientists are now downplaying the IARC decision, saying the IARC classification of cell phones as possibly carcinogenic does not mean cell phones cause cancer, and even preposterously claiming that there is no evidence of this at all, there is no uncertainty that IARC, a highly respected scientific body, is now clearly saying there is evidence of carcinogenicity, otherwise they would not have classified in category 2B.

See Citizens for Health commentary on this, including comments on the 2B classification by 20+ year veteran of the IARC, Dr. Annie J. Sasco of Bordeaux Segalen University, France

Camilla Rees of ElectromagneticHealth.org says,

“We expect to see continued spin from all directions, attempting to confuse the public and raise doubt, for some time to come. Thus it is especially important citizens be able to spot the misinformation and recognize there is an extraordinary propaganda machine in motion. We expect this will get LOUDER until industry is one day forced to cry ‘Uncle” under the landslide pressure from expected lawsuits and governments.”

Already, three senior members of Congress are calling on the General Accounting Office (GAO) to conduct a “thorough review” of the science and “adequacy” of current FCC exposure guidelines. These include Representatives Ed Markey (MA), Henry Waxman (CA) and Anna Eshoo (CA). And Reuters reports the Supreme Court is considering the fate of existing cell phone safety litigation in light of the WHO classification.

The IARC decision came only days after the Council of Europe, elders from 47 European countries, has called for a dramatic reduction in EMF exposure to humans from call phones and wireless technologies.

It is important to realize, however, that cell phones may not all be the same. Although all cell phones emit radiation, CDMA cell phones, such as those used by Sprint and Verizon, do not pulse their signals like the GSM phones used by AT&T and T-Mobile.

According to Dr. Joel Moskowitz, Director of the Center for Family and Community Health at the University of California, Berkeley, “GSM phones emit about 28 times more radiation on average compared to CDMA phones according to one published study.” Dr. Moskowitz recommends switching to a CDMA carrier if you want to reduce your radiation exposure.

Magda Havas, PhD of Trent University, Canada, agrees pulsed radiation is more dangerous:

“Pulsed radiation is much more harmful and the true intensity is not provided as it is “averaged” during a period of time (30 minutes for public exposure in US). The average of the pulse (maximum reading) and the minimum reading
gives a false low reading.  Engineers like to measure averages but living organisms react to extremes so these average readings under estimate the potential for harm if the radiation is pulsed.”

Sources:

Electromagnetic Health May 31, 2011

Gizmodo May 31, 2011

The New York Times May 31, 2011

Associated Press May 31, 2011

Paraben Traces May Be Present In Nearly All Breast Cancer Patients.

Time (1/13, Blue) reports in “Healthland” that “researchers have found that paraben traces are present in the tissue of almost all breast cancer patients, whether or not they use antiperspirants.” The researchers found that “even patients who’d never used underarm products had paraben traces in their breast tissue.” But “that’s not surprising, say the authors, since parabens are found in shampoos, make-up, moisturizers, pharmaceuticals and even some food products,” in addition to some antiperspirants.

HealthDay (1/13, Doheny) reports, “In the study, published online in January in the Journal of Applied Toxicology,” investigators “report that one or more kinds of parabens were found in 158 of the 160 samples taken from the tissue collected from…40 women.” The researchers “found 96 samples contained all five of the most common paraben esters (forms).”

WebMD (1/13, Mann) reports, “Paraben levels did not seem to play a role in the cancer’s location or whether or not the cancer was fueled by estrogen.”