Medically Induced Euthyroid Hypothyroxinemia May Extend Survival in Compassionate Need Cancer Patients: An Observational Study – Hercbergs – 2015 – The Oncologist – Wiley Online Library

l‐thyroxine (l‐T4) and 3,3′,5‐triiodo‐l‐thyronine (l‐T3) on plasma membrane integrin αvβ3nHighlight:integrin is amply expressed by cancer cells and rapidly dividing endothelial cells and is not well expressed by or activated in quiescent, nonmalignant cellsnHighlight:tumor cell proliferationnHighlight:angiogenesisnHighlight:These actions are inhibited by the deaminated analog of T4, tetraiodothyroacetic acid (tetrac)nHighlight:antiapoptoticnHighlight:Within the cell, T4 serves as a prohormone for T3, and T3 is the metabolically and genomically important form of thyroid hormonenHighlight:At the integrin, in contrast, the thyroid hormone receptor affinity for T4 is higher than that for T3 [7], and T4 is a more potent inducer of tumor cell proliferation than is T3nHighlight:Addition of T3 rapidly reduced serum thyrotropin (TSH) and FT4 levels and was associated with rapid clinical and radiologic improvementnHighlight:Patients were converted to T3 abruptly from l‐T4 (50–88 μg daily). After a 1‐week washout period, exogenous l‐T3 15–37.5 μg/day was begun in 2 or 3 daily divided dosesnSticky notes:Dose: 15 – 37.5 mcg/day in 2 to 3 divided dosesnHighlight:a variety of incurable solid tumors, extended survival was observed in a majority of patients using exogenous T3 to induce and maintain hypothyroxinemianHighlight:T3 administration prevented symptomatic hypothyroidismnSticky notes:T3 allowed suppression of TSH and T4, yet prevented hypothyroid symptoms; must maintain the doses physiologic.nHighlight:In preclinical studies, T4 enhances cancer cell proliferation, migration, invasion, and angiogenesis [3, 10, 17], apparently acting via the thyroid hormone receptor on cell surface integrin αvβ3nHighlight:Supraphysiologic amounts of T3 are required at this receptor to stimulate tumor cell proliferationnHighlight:rapid tumor regression observed following exogenous l‐T4 discontinuationnHighlight:reduced oncogenic potential) of T3 and the pro‐oncogenic actions of T4nHighlight:replacing circulating T4 with exogenous l‐T3 in cancer patients.nSticky notes:And, it reduces the rT3 which also is pro—oncogenicnHighlight:terminal patients with incurable solid tumors, extended survival was observed in a majority of patients using exogenous l‐T3 to simultaneously induce hypothyroxinemia and obviate clinically symptomatic hypothyroidismnHighlight:In a few patients, radiologically documented tumor responses were associated with clinical improvement shortly after discontinuation of exogenous T4 supplementationnSticky notes:Just, the elimination of T4 resulted in tumor regression in a few patients; irregardless of T3 supplementationnHighlight:much‐reduced pro‐oncogenic effects of physiologic T3 from those of T4 on cancer cell growthn]]>

About Dr. Nathan Goodyear
About Dr. Nathan Goodyear

Dr. Nathan Goodyear, a medical doctor with years of experience in the field of integrative cancer care, has announced the launch of an online training program. This program, available on his new website, will provide individuals with access to video trainings led by Dr. Goodyear himself, covering a range of topics related to integrative cancer care. These trainings will include information on the latest research and techniques in the field, as well as guidance on how to incorporate these approaches into a patient’s overall cancer treatment plan. With this online program, Dr. Goodyear hopes to make his expertise and knowledge more widely accessible, and help more people understand the benefits of integrative cancer care.

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