Deaths From Rare Cancer Linked to Breast Implants


CNN reports that nine deaths have been attributed to breast implants. In each case, a rare form of breast cancer, anaplastic large cell lymphoma (ALCL) was responsible. The FDA responded that this cluster was no cause for alarm as breast implants are linked to only a slightly increased risk of cancer.

Breast cancer is one of the most feared diagnoses a woman can receive. One in 8 women will develop invasive breast cancer in her lifetime. Genetics play a role in breast cancer but there are steps you can take to reduce your risk.

In the largest review of research into lifestyle and breast cancer, the American Institute of Cancer Research estimated that about 40 percent of U.S. breast cancer cases could be prevented by lifestyle choices. I believe this number understates the positive impact of lifestyle modifications.

One of the easiest to implement changes is to improve your diet. Refrain from consuming sugar, especially fructose, and consume only nourishing and whole foods. Processed foods are to be avoided and I recommend limiting protein intake and increasing healthy fat consumption. Obviously, you will want to optimize your gut flora and make sure GMO foods don’t sneak their way onto your menu.

Iodine may also be a crucial player in cancer prevention. Iodine is an essential trace element required for the synthesis of hormones, and the lack of it can also cause or contribute to the development of a number of health problems, including breast cancer. There is evidence that mega doses of iodine are counterproductive.

No matter what health challenges you face, I always recommend optimizing your vitamin D levels. There are hundreds of studies showing the importance of vitamin D. According to Carole Baggerly, founder of GrassrootsHealth, as much as 90 percent of ordinary breast cancer may in fact be related to vitamin D deficiency.

Source:mercola.com

Rare kidney tumor provides insights on role of metabolic changes in cancer


Researchers in The Cancer Genome Atlas (TCGA) Network have made a number of new findings about the biology and development of a rare form of kidney cancer. They found that the disease – chromophobe renal cell carcinoma (ChRCC) – stems in part from alterations in genes in the mitochondria, the cell’s energy supplier. They also discovered that the tumor is characterized by genetic rearrangements near a gene important in DNA repair and in maintaining telomerase, the enzyme which determines a cell’s lifespan. Finally, investigators also found that ChRCC is a distinct disease and shares few genomic characteristics with other kidney cancers.

In the study – the most extensive genomic view of ChRCC to date – investigators led by Chad Creighton, Ph.D., Baylor College of Medicine, Houston, and Kimryn Rathmell, M.D., Ph.D., University of North Carolina, Chapel Hill, performed a complex array of analyses, including examining the entire genomes of 50 of the 66 ChRCC tumors studied, a high number for a rare cancer. The study revealed increased numbers of mitochondria as well as mutations in mitochondrial DNA. This led researchers to discover that ChRCC tumors favor a different energy-generating process than that used by the more common clear cell kidney cancer. In addition, their findings are the first to show specific alterations affecting the TERT gene that could affect cancer development, and might help explain its increased expression – and deregulation – in cancer. Overall, the findings provide new insights into the development of more common forms of kidney cancer, and shed light on the role of mitochondria and metabolic pathways in cancer. The results also support the growing realization that both the cancer’s genomic characteristics and cell of origin matter, as many cancers consist of several individual diseases that require specific therapies. TCGA is a collaboration jointly supported and managed by the National Cancer Institute (NCI) and the National Human Genome Research Institute (NHGRI), both parts of the National Institutes of Health.Cancer Cell.

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