Learn how you can manage and alleviate your current side effects while actively working to prevent a relapse or secondary cancer using evidence-based, non-toxic therapies.
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If you have just been diagnosed with advanced pancreatic cancer the first issue you must come to terms with is that conventional oncology has little to offer you. Therefore consider therapies that are evidenced-based yet have not been evaluated and approved by the FDA aka conventional oncology.
The study linked and excerpted below is an example of integrative oncology. The studies indicates that gemcitabine chemotherapy works better (aka potentiates anti tumor effect) when the cancer patient is taking Curcumin at the same time the patient is undergoing gemcitibine.
Further, the study shows that Curcumin, by itself, kills pancreatic cancer (aka anti proliferative activity). What is not mentioned in the study below is that many studies cite the ability of Curcumin to reduce the collateral damage caused by toxic chemotherapy.
Most importantly, there are several other therapies that have shown to be either integrative or complimentary for pancreatic cancer patients. While clearly curcumin is a great start, it is only a start.
I am both a long-term cancer survivor and cancer coach. I am alive today due to a host of non-conventional therapies such as curcumin.
Scroll down the page, post a question or a comment and I will reply ASAP.
“Curcumin has a potent antiproliferative activity and can also potentiate the antitumor effect of gemcitabine…
One of 11 evaluable patients (9%) had partial response, 4 (36%) had stable disease, and 6 (55%) had tumor progression. Time to tumor progression was 1-12 mo (median 2½), and overall survival was 1-24 mo (median 5). Low compliance for curcumin at a dose of 8,000 mg/day, when taken together with systemic gemcitabine, may prevent the use of high doses of oral curcumin needed to achieve systemic effect..”
“Pancreatic ductal adenocarcinoma (PDAC) is a highly metastatic malignancy. Approximately 85% of pancreatic cancers are classified as PDACs.
The survival of PDAC patients is very poor and only 5–10% of patients survive 5 years after diagnosis. Mutations at the KRAS and TP53 gene are frequently observed in PDAC patients. The PANC-28 cell line lacks wild-type (WT) TP53.
In the following study, we have investigated the effects of restoration of WT TP53 activity on the sensitivity of PANC-28 pancreatic cancer cells to various drugs which are used to treat PDAC patients as well as other cancer patients.
In addition, we have examined the effects of signal transduction inhibitors which target critical pathways frequently deregulated in cancer.
The effects of the anti-diabetes drug metformin and the anti-malarial drug chloroquine were also examined as these drugs may be repurposed to treat other diseases. Finally, the effects of certain nutraceuticals which are used to treat various ailments were also examined. Introduction of WT-TP53 activity in PANC-28 PDAC cells, can increase their sensitivity to various drugs. Attempts are being made clinically to increase TP53 activity in various cancer types which will often inhibit cell growth by multiple mechanisms…”