the hospice patients who are imbibing aspirin
and metformin in last efforts to remain alive on this earth, having tried other treatments that have FAILED!!! and are costly.
ASPIRIN AND METFORM, FOR BOOBS AND DICKS WHO BELIEVE THAT THERE IS REASON TO TRY SAME. SEE BELOW.
YOU DON'T THINK ANY BETTER BECAUSE YOU ARE AN MD?
Aspirin may lower ovarian cancer risk, research shows
The research, reported in the current issue of the Journal of the National Cancer Institute, was conducted by institute scientists and adds credence to a provocative notion: The old medicine cabinet standby may possess potent anti-cancer properties.
"Our study suggests that aspirin regimens -- proven to protect against heart attack -- may reduce the risk of ovarian cancer as well," said Dr. Britton Trabert of the NCI's cancer epidemiology and genetics division.
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Dr. Vincent Yang, chairman of medicine at Stony Brook University Hospital, said aspirin and cancer prevention have a long and storied past.
"Aspirin is an anti-inflammatory agent. So by suppressing inflammation, you can reduce the risk," said Yang, who was not involved in the NCI analysis. http://www.stonybrookphysicians.com/doctor/YANG_MD_PHD_VINCENT_3825.asp
He added that while intriguing, the research is not strong enough to recommend aspirin as a preventive. Aspirin can cause side effects, especially gastrointestinal bleeding, Yang said.
Trabert and NCI colleague Dr. Nicolas Wentzensen conducted the type of study known as a meta-analysis. They re-examined previously published data.
From the 12 large studies they reviewed -- nine from the United States -- 8,000 women were involved.
Each participant took one of three types of medications: aspirin; other nonsteroidal anti-inflammatory drugs -- NSAIDs -- such as ibuprofen; or, acetaminophen, a pain reliever that doesn't reduce inflammation.
Aspirin takers had the highest risk reduction. For those who took non-aspirin NSAIDs, the outcome was less clear.
The scientists found only a 10 percent risk reduction among women who took an NSAID at least once per week. Acetaminophen, they said, was not associated with reduced ovarian cancer risk.
Dr. Michael Pearl, director of Stony Brook University Hospital's division of gynecological oncology, said as tantalizing as the study's results seem, he will not recommend aspirin as a preventive.
"When would you start recommending aspirin usage? Age 16 or when a woman is in her forties?" Pearl asked.
"This wasn't a prospective trial," Pearl said, referring to a randomized, placebo-controlled study, in which participants would take specific aspirin doses and results are compared with placebo takers.
Pearl defines ovarian cancer as the most lethal among gynecologic malignancies, its vague symptoms usually translating into late detection.
Trabert noted the study wasn't designed to influence clinical recommendations.
"Dosages [were] not uniform across participants," Trabert said of women who consumed varying aspirin doses. "We saw that participants who used aspirin daily . . . had a 20 percent lower risk of ovarian cancer compared to participants who did not use aspirin regularly."
Trabert's research, however, hails from a deepening well of scientific scholarship, which demonstrates that the pennies-per-dose drug has a powerful impact on cancer prevention.
Two weeks ago, scientists in Boston noted the risk of multiple myeloma -- a cancer involving blood-forming cells in the bone marrow -- also appears lower among aspirin takers.
Malignant melanoma, colorectal and breast cancers also may be lower among aspirin users, studies show.
Cold Spring Harb Symp Quant Biol. 2011;76:155-64. doi: 10.1101/sqb.2011.76.010819. Epub 2011 Nov 9.
Adenosine monophosphate-activated protein kinase: a central regulator of metabolism with roles in diabetes, cancer, and viral infection.
Abstract
Adenosine
monophosphate-activated protein kinase (AMPK) is a cellular energy
sensor activated by metabolic stresses that inhibit catabolic ATP
production or accelerate ATP consumption. Once activated, AMPK switches
on catabolic pathways, generating ATP, while inhibiting cell growth and
proliferation, thus promoting energy homeostasis. AMPK is activated by
the antidiabetic drug metformin,
and by many natural products including "nutraceuticals" and compounds
used in traditional medicines. Most of these xenobiotics activate AMPK
by inhibiting mitochondrial ATP production. AMPK activation by metabolic
stress requires the upstream kinase, LKB1, whose tumor suppressor
effects may be largely mediated by AMPK. However, many tumor cells
appear to have developed mechanisms to reduce AMPK activation and thus
escape its growth-restraining effects. A similar phenomenon occurs
during viral infection. If we can establish how down-regulation occurs
in tumors and virus-infected cells, there may be therapeutic avenues to
reverse these effects.
- PMID:
- 22071265
- [PubMed - indexed for MEDLINE]
Open Biol. 2013 Jan 8;3(1):120144. doi: 10.1098/rsob.120144.
Oxidants, antioxidants and the current incurability of metastatic cancers.
Abstract
The vast majority of all agents used to directly kill cancer
cells (ionizing radiation, most chemotherapeutic agents and some
targeted therapies) work through either directly or indirectly
generating reactive oxygen species that block key steps in the cell
cycle. As mesenchymal cancers evolve from their epithelial cell
progenitors, they almost inevitably possess much-heightened amounts of
antioxidants that effectively block otherwise highly effective oxidant
therapies. Also key to better understanding is why and how the
anti-diabetic drug metformin
(the world's most prescribed pharmaceutical product) preferentially
kills oxidant-deficient mesenchymal p53(- -) cells. A much faster
timetable should be adopted towards developing more new drugs effective
against p53(- -) cancers.
- PMID:
- 23303309
- [PubMed - indexed for MEDLINE]
- PMCID:
- PMC3603456
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