“Here’s a chart that’s a little disturbing: The interactive graphic above, created by biotechnologist David Taylor and appearing first on his data-visualization blog, illustrates how common and deadly various types of cancer are. Each pie chart represents an organ (matched for color) and is sized according to the incidence of cancer of that organ. The charts are based on data from the American Cancer Society and a 2002 study of long-term survival rates. The red wedges show the proportion of patients who die from the cancer within the selected number of years after diagnosis. As the chart reflects, breast and prostate cancers are the most common, with 235,000 and 239,000 new cases last year respectively. Fortunately, they are relatively survivable cancers, though their mortality rates more than double by the 20-year mark. Pancreatic cancer is the most deadly, killing 96 percent of patients within five years. That’s partly because pancreatic cancer typically does not cause symptoms until it’s at a late stage of progression. For the same reason, liver cancer is the second-deadliest cancer, killing 93 percent of patients within five years
Evidence has to come light.that, instead of arresting Tumor, it increases the risk and actually help growing Tumors!
SVEN HOPPE /SHUTTERSTOCK.COM Healthy cells damaged by chemotherapy secrete more of a protein called WNT16B, which boosts cancer cell survival
“Long considered the most effective cancer-fighting treatment, chemotherapy may actually make cancer worse, according to a shocking new study.
The extremely aggressive therapy, which kills both cancerous and healthy cells indiscriminately, can cause healthy cells to secrete a protein that sustains tumor growth and resistance to further treatment.
Researchers in the United States made the “completely unexpected” finding while seeking to explain why cancer cells are so resilient inside the human body when they are easy to kill in the lab.
They tested the effects of a type of chemotherapy on tissue collected from men with prostate cancer, and found “evidence of DNA damage” in healthy cells after treatment, the scientists wrote in Nature Medicine.
Chemotherapy works by inhibiting reproduction of fast-dividing cells such as those found in tumors.
The scientists found that healthy cells damaged by chemotherapy secreted more of a protein called WNT16B which boosts cancer cell survival.
The protein was taken up by tumor cells neighboring the damaged cells.
“WNT16B, when secreted, would interact with nearby tumor cells and cause them to grow, invade, and importantly, resist subsequent therapy,” said Nelson.
In cancer treatment, tumors often respond well initially, followed by rapid re-growth and then resistance to further chemotherapy.
Rates of tumor cell reproduction have been shown to accelerate between treatments.
“Our results indicate that damage responses in benign cells… may directly contribute to enhanced tumor growth kinetics,” wrote the team.
“Public and private funds have been thrown around like confetti at a country fair to close up and destroy clinics, hospitals, and scientific research laboratories which do not conform to the viewpoint of medical associations,” stated Benedict Fitzgerald. [1]
Fitzgerald was special counsel to the Senate Interstate and Foreign Commerce Committee in 1953. He was commissioned by Congressman Charles Tobey of Massachusetts to investigate the obstruction of natural cancer treatments by the American Medical Association.
His report to the committee is known as “The Fitzgerald Report” of 1953.
Alone, this information is a bombshell. But, to my knowledge the information you are about to read hasn’t been put into the same or connect-the-dots context before.
If anything else, know this simple fact: While the AMA was actively suppressing natural cures for cancer, millions of Americans were being injected with vaccines contaminated with a cancer-causing monkey virus, SV40.
Before I tell you what Fitzgerald concluded, you may be thinking this information is from the 1950s so it is outdated and can be discredited.
Please realize, though, the ‘success’ of the Rockefeller-funded polio vaccine program set the precedent for the entire U.S. vaccine program, which apparently is being followed to this day. With the explosion of cancer in the United States, this information deserves serious consideration and further investigation.
Fitzgerald vividly described what he uncovered stating,
“…There is reason to believe that the AMA (American Medical Association) has been hasty, capricious, arbitrary, and outright dishonest, and of course if the doctrine of ‘respondeat suprior‘ to be observed, the alleged machinations of Dr. J.J. Moore (for the past 10 years the treasurer of the AMA, could involve the AMA and others in an interstate conspiracy of alarming proportions.” [2]
And if that’s not enough, Fitzgerald continues…
“Behind and over all this is the weirdest conglomeration of corrupt motives, intrigue, selfishness, jealousy, obstruction, and conspiracy that I have ever seen.” [3]
Over 75 years ago, in the summer of 1934 in California USA, under the auspices of the University of Southern California, a group of leading American bacteriologists and doctors conducted the first successful cancer clinic. At this clinic they discovered the cure for cancer. Their clinical research found that:
a) cancer was caused by a micro-organism;
b) the micro-organism could be painlessly destroyed in terminally ill cancer patients; and
c) the effects of the disease could be reversed.
The technical discovery leading to the cancer cure had been published in Science magazine in 1931. In the decade following the 1934 clinical success, the technology and the subsequent, successful treatment of cancer patients was discussed at medical conferences, disseminated in a medical journal, cautiously but professionally reported in a major newspaper, and technically explained in an annual report published by the Smithsonian Institution.
Cancer is such that any attempt to glean an insight into its treatment is often visited by tragedy.
However a step ahead.
English: Gross appearance of the cut surface of a pneumonectomy specimen containing a lung cancer, here a Squamous cell carcinoma (the whitish tumor near the bronchi). (Photo credit: Wikipedia)
But isn’t the price great?
Yet these tragedies can not be avoided.
Let’s Pray that the price paid is compensated by the Greatest Good.
Story:
In 2005, after she had spent more than a year going from specialist to specialist, a dermatologist figured it out. Mrs. McDaniel, then 62, had Sezary syndrome, a rare T cell lymphoma, in which white blood cells become cancerous and migrate to the skin. All her doctors could tell her was that the disease was incurable, that there was no standard treatment, and that on average patients at her stage die within a few years.
“Of course I was shocked,” Mrs. McDaniel said in an interview last September.
She wept that day as her husband drove her home. And she asked God to help her cope.
Before cancer, she had had a vibrant life, hiking in the mountains, traveling the world, entertaining her wide network of friends. Her disease destroyed all of that. She could not even enjoy her luxuriant garden because sun on her inflamed skin was agony.
Although there is no standard treatment, for five years chemotherapy held her disease at bay. But in the summer of 2010, she got worse, much worse, with hundreds of tumorspopping up under her skin. Some grew as large as kiwi fruits and split open.
Her son, Dr. McDaniel, decided he would orchestrate the use of the most advanced techniques of gene sequencing and analysis to take on her cancer. Because of his job — he works for Illumina, a company that does DNA sequencing — Dr. McDaniel had read scientific reports and gone to medical conferences where he heard talks on whole genome sequencing. He noticed that the patients all seemed to have rare cancers.
“Every time I heard one of those stories, I thought, ‘That’s my mom,’ ” he said.
For now, there are not many drugs that can target specific gene mutations in cancer cells.
But the hope is that when more is known and more drugs are developed, doctors will treat cancer by blocking several major genes at once. With several escape routes barred, the cancer will not be able to break free of the drugs stopping its growth.
……..
He worked all night, found a paper by scientists who had deliberately fused those very genes and discovered that, yes, the genetically altered T cells had their growth signals reversed.
At 5:45 a.m. Dr. McDaniel sent an e-mail to his collaborators.
“I was so tired at that point that, believe it or not, I had forgotten about the drug,” he said.
He fell asleep and woke at 11 a.m., rushing back to his computer. The melanoma drug he had forgotten in his exhaustion should hit that target. And that could stop his mother’s cancer from growing. “My jaw was just hanging open,” Dr. McDaniel said. “The implications were so tantalizing that I didn’t dare believe them.”
A Remarkable Turnaround
Mrs. McDaniel had her first infusion on July 28, and the result seemed remarkable. Her oncologist, Dr. Gohmann, was overwhelmed. Her son, who had been terrified that he and the doctors might have made a terrible mistake, was overjoyed.
Mrs. McDaniel, who had not left her house for several months except to see her doctors, began going to movies and restaurants every day.
On Sept. 2, she and her husband went to the Heirloom Restaurant, in the middle of horse country, to celebrate their 50th wedding anniversary.
She had given away so many of her clothes when she thought she was dying that she puzzled over what to wear. She had a favorite blouse that was loosefitting and comfortable, but Mr. McDaniel recalled, “It was long gone.” She could not drink wine with the medicines she was taking, so she and her husband sipped iced tea in the quiet dining room.
“We reminisced, but also talked about the future as we hoped it would be,” Mr. McDaniel said.
But the reprieve lasted only weeks. By the end of September, the cancer was back.
Dr. McDaniel did not want to give up. Mrs. McDaniel’s tumor was sequenced again, looking for a new mutation, but there was nothing striking. As Dr. McDaniel sifted through the data, he called his parents every day. They began calling him the governor, hoping he would bring his mother another stay of execution.
The doctors considered a less appealing target, a mutated gene that T cells use to stop growing. Unpublished studies in mice suggested that a kidney cancer drug might stop the growth of T cells with this mutation.
By then, Mrs. McDaniel’s body was ravaged by the cancer and her treatments. She had entered hospice care, with a hospital bed in her home and a nurse and an assistant to help.
“We had this shaky evidence, based on the genome and on unpublished data,” Dr. McDaniel said.
But the drug’s side effects were mild, and her family and doctors decided she should try it.
“If we do nothing, she will be dead in one to six weeks,” Dr. McDaniel explained.
Mrs. McDaniel took the drug on Nov. 26. But she was so ill that she was unable to get out of bed, unable to drink from a straw. Her son Tim took his children to her bedroom one at a time so they could say goodbye.
“She wasn’t talking, but her eyes were open, and she acknowledged each one with a weak chuckle,” Dr. McDaniel said.
Three days later, she briefly rallied. Her husband held her hand.
“She said, ‘I love you,’ ” Mr. McDaniel said. “She then repeated it twice more. I kissed her forehead and told her that I loved her. Those were our last words to each other.”
The next morning, Nov. 30, Mr. McDaniel woke early and went to his wife’s room. Her breathing had become erratic. Worried, he stepped out and asked the hospice nurse to call the doctor. “In the seconds that I was absent, she died,” Mr. McDaniel said.
The team that tried to save her was heartbroken too, and was left with a long list of what-ifs. “If you really look at it, what did we buy her?” Dr. de Castro asked. Mrs. McDaniel was dying last January. Yet would she have survived as long even without the sequencing or the drugs? Did the team make a difference?
“I hope we did,” Dr. de Castro said, “but it’s hard to know.”.
Daily aspirin reduces the long-term incidence of some adenocarcinomas, but effects on mortality due to some cancers appear after only a few years, suggesting that it might also reduce growth or metastasis. We established the frequency of distant metastasis in patients who developed cancer during trials of daily aspirin versus control.
Methods
Our analysis included all five large randomised trials of daily aspirin (≥75 mg daily) versus control for the prevention of vascular events in the UK. Electronic and paper records were reviewed for all patients with incident cancer. The effect of aspirin on risk of metastases at presentation or on subsequent follow-up (including post-trial follow-up of in-trial cancers) was stratified by tumour histology (adenocarcinoma vs other) and clinical characteristics.
Findings
Of 17 285 trial participants, 987 had a new solid cancer diagnosed during mean in-trial follow-up of 6·5 years (SD 2·0). Allocation to aspirin reduced risk of cancer with distant metastasis (all cancers, hazard ratio [HR] 0·64, 95% CI 0·48—0·84, p=0·001; adenocarcinoma, HR 0·54, 95% CI 0·38—0·77, p=0·0007; other solid cancers, HR 0·82, 95% CI 0·53—1·28, p=0·39), due mainly to a reduction in proportion of adenocarcinomas that had metastatic versus local disease (odds ratio 0·52, 95% CI 0·35—0·75, p=0·0006). Aspirin reduced risk of adenocarcinoma with metastasis at initial diagnosis (HR 0·69, 95% CI 0·50—0·95, p=0·02) and risk of metastasis on subsequent follow-up in patients without metastasis initially (HR 0·45, 95% CI 0·28—0·72, p=0·0009), particularly in patients with colorectal cancer (HR 0·26, 95% CI 0·11—0·57, p=0·0008) and in patients who remained on trial treatment up to or after diagnosis (HR 0·31, 95% CI 0·15—0·62, p=0·0009). Allocation to aspirin reduced death due to cancer in patients who developed adenocarcinoma, particularly in those without metastasis at diagnosis (HR 0·50, 95% CI 0·34—0·74, p=0·0006). Consequently, aspirin reduced the overall risk of fatal adenocarcinoma in the trial populations (HR 0·65, 95% CI 0·53—0·82, p=0·0002), but not the risk of other fatal cancers (HR 1·06, 95% CI 0·84—1·32, p=0·64; difference, p=0·003). Effects were independent of age and sex, but absolute benefit was greatest in smokers. A low-dose, slow-release formulation of aspirin designed to inhibit platelets but to have little systemic bioavailability was as effective as higher doses.
Interpretation
That aspirin prevents distant metastasis could account for the early reduction in cancer deaths in trials of daily aspirin versus control. This finding suggests that aspirin might help in treatment of some cancers and provides proof of principle for pharmacological intervention specifically to prevent distant metastasis.
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