Ruminations of a Taco-Obsessed Philly Native

The Effects of Naloxone on Human Breast Cancer Regression

Naloxone, more known for functioning as an opioid antagonist, and playing the role of opioid adversary at the opioid receptor level, is now finally being properly studied; with respects to its role in tumor cell growth and human cancer cell lines. Reported studies and findings from the in vitro and in vivo experiments evaluate the effects of naloxone on human breast cancer cell growth and progression.

In vitro experiments consisted of estrogen receptor (ER)-negative human breast carcinoma cells, MDA.MB231, being treated with naloxone at different dosages(10-100µM). In vivo experiments were conducted with mice being subcutaneously injected with human triple negative breast cancer, TNBC, formulated by using MDA.MB231. For 2 weeks, mice were injected daily with naloxone, then injected with double the dosage for another two weeks. Due to injection of Fluorescein isothiocyanate (FITC)-dextran (100 μL) into the tail vein of the mice and the confirmation by immunohistochemistry with CD31 on mice tumor sections, microvessel formation were detected in the mice.

Vitro results showed that the cell proliferation MDA.MB231, was inhibited by naloxone, depending upon the volume of doses, whereas the cell death was increased. The vivo experiments revealed that mice treated with naloxone, had greatly decreased in size than those observed in the control groups, with naloxone being the constant factor. Check the journal at SCImago Journal & Country Rank.

Although naloxone wasn’t able to impair the microvessel formation in tumors of treated mice, for the first time, scientific data and research has proven that naloxone reduces breast cancer progression without causing damage to the angiogenesis process.

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Improved Therapeutic Strategies for Drug Resistant Thyroid Cancers

At the Harvard Medical School, new studies(published first on Oncotarget) have revealed that patients suffering from papillary thyroid carcinoma(PTC), the most common form of thyroid cancer, can now find relief; as it has been found that palbociclib, a FDA approved drug that treats breast cancer, is a far more effective treatment of PTC in patients, than the usual treatments of the drug, vemurafenib. The problem with vemurafenib is its inability to aggressively and permanently keep cancer in remission, allowing cancer to go into remission for a brief period, only to return stronger and incurable.

Research conducted in the past, suggested that the lab-grown vemurafenib-resistant thyroid cancer cells produces a loss of the P16 gene, a gene that keep cells from dividing too frequently. This discovery brought forth the possibility of reasons as to why vemurafenib is so ineffective with PTC. Follow Oncotarget journal on Twitter.

The protein complex, CDK4/6, which is a requirement for DNA to replicate inside cells, was targeted as the key component to treating PTC, as it would act as the P16 gene and mimic the replicating effects. This is when Harvard medical researchers realized that treating the vemurafenib-resistant cells with vemurafenib combined with palbociclib, form a synergistic duo that induces stronger cell deaths, than when treated alone.

Although additional studies further revealed that cancer cells harbor a secondary unit of drug-resistant treatment cells that can potentially override the already vemurafenib-resistant cells, researchers have confirmed that the therapy of vemurafenib combined with palbociclib is the most efficient and effective treatment for PTC cells, whether primary or secondary.

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Make sure to check out the Oncotarget podcast, which can be found on Stitcher, Player.FM and iTunes.

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