Rising Cost of Anticancer Medications in the United States

Jackson, K. L.; Nahata, Milap C.

doi:10.1177/1060028017702406

Cited by 12 publications

(8 citation statements)

References 14 publications

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“…As there are over 1.6 million new cancer cases annually, it is clear that cancer treatment prescriptions are in high demand. This, in turn, causes corporations that produce said drugs to raise their prices and cost the insurance companies significantly more (Jackson and Nahata, 2017). Due to this fact, many insurance companies have stopped covering cancer treatments, leaving families to pay millions out of pocket.…”

Section: United States Healthcare Structurementioning

confidence: 99%

How United States healthcare can learn from Costa Rica: A literature review

Baker¹,

Gallicchio²

2020

J. Public Health Epidemiol.

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As the development and upkeep of the United States healthcare becomes increasingly debated in society, the systems in place of other successful countries provide opportunities for erudition and comparison. One country's system which seems to be consistently overlooked despite its vast improvement to the country is Costa Rica's universal healthcare. In this comprehensive study of the healthcare systems in both the United States and Costa Rica, there is evidence of a middle ground, as well as areas for improvement to current policies in the United States. Acknowledging the long-term implementation of Costa Rica's universal healthcare, which was split into three unique major reforms, reveals the need for patience and planning. In the midst of heavy debate regarding healthcare reform, this paper seeks to provide an in-depth analysis of Costa Rica's history of reform, their current institutions, and recent statistical improvements in overall health, with the goal of providing a better understanding of how the United States should proceed in order to achieve parity.

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Section: United States Healthcare Structurementioning

confidence: 99%

How United States healthcare can learn from Costa Rica: A literature review

Baker¹,

Gallicchio²

2020

J. Public Health Epidemiol.

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“…273,274 Moreover, the survival benefits of certain newer anticancer drugs may be just a few months more than that of the already existing treatment but at a reasonably higher cost. 271 Considering the complication of this matter, evidently, no single solution will suffice. Adopting approaches like macroeconomic basis of cancer costs' re-engineering, education of policy makers, and a transparent regulatory system might offer some potent solutions to this problem.…”

Section: Costmentioning

confidence: 99%

Cancer drug development: The missing links

Kunnumakkara

Bordoloi

Sailo

et al. 2019

Exp Biol Med (Maywood)

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Although better science and technology has been linked with better health care, however, reality is much different. Although America and most of Europe are equipped with most advanced science and technology, paradoxically cancer incidence is highest in the world. This indicates that science and technology alone is not sufficient in treating diseases like cancer. It is also now well recognized that more than 95% of the drugs/compounds that kill either cancer cells in culture or regress the tumors in animals, fail in phase I clinical trials in humans, indicating that most pre-clinical models of cancer are inadequate. In addition, most of the anticancer drugs that are approved by the regulatory agencies such as FDA either has no effect on the overall survival of the cancer patient or may provide an increase in few months in overall survival. This is despite the fact that most targeted therapies that are currently available are highly expensive; thus suggesting the lack of affordability. This review is meant to focus on some of these problems in detail and then provide potential solutions since most cancers are caused by multiple genes, and thus multi-targeted therapies are needed such as natural products which are inexpensive, safe and have been used for thousands of years for both prevention and treatment of cancer. Impact statement The success rate for cancer drugs which enter into phase 1 clinical trials is utterly less. Why the vast majority of drugs fail is not understood but suggests that pre-clinical studies are not adequate for human diseases. In 1975, as per the Tufts Center for the Study of Drug Development, pharmaceutical industries expended 100 million dollars for research and development of the average FDA approved drug. By 2005, this figure had more than quadrupled, to $1.3 billion. In order to recover their high and risky investment cost, pharmaceutical companies charge more for their products. However, there exists no correlation between drug development cost and actual sale of the drug. This high drug development cost could be due to the reason that all patients might not respond to the drug. Hence, a given drug has to be tested in large number of patients to show drug benefits and obtain significant results.

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“…The slow, very meager progress in prolonging cancer survival, the fact that such survival appears to be at an asymptotic boundary beyond which any further progress may be impossible, and the extreme, accelerating and clearly unsustainable costs of new cancer drugs that only minimally extend life ( Sidduqui & Rajkumar 2012 , Cohen 2017 , Davis et al 2017 , Jackson & Nahata 2017 , Prasad & Mailankody 2017 , Carrera et al 2018 , Dranitsaris et al 2018 ), all indicate the necessity for reappraisal of the current paradigm in which developed tumors are the target for virtually all of our anti-cancer research efforts. It may be time to redirect our labors and research expenditures toward understanding the singularity, the apparent focus of nature’s major effort at tumor suppression.…”

Section: Conclusion: Trouble In Paradigmmentioning

confidence: 99%

Detection of a novel, primate-specific ‘kill switch’ tumor suppression mechanism that may fundamentally control cancer risk in humans: an unexpected twist in the basic biology of TP53

Nyce¹

2018

Endocrine-Related Cancer

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The activation of TP53 is well known to exert tumor suppressive effects. We have detected a primate-specific adrenal androgen-mediated tumor suppression system in which circulating DHEAS is converted to DHEA specifically in cells in which TP53 has been inactivated. DHEA is an uncompetitive inhibitor of glucose-6-phosphate dehydrogenase (G6PD), an enzyme indispensable for maintaining reactive oxygen species within limits survivable by the cell. Uncompetitive inhibition is otherwise unknown in natural systems because it becomes irreversible in the presence of high concentrations of substrate and inhibitor. In addition to primate-specific circulating DHEAS, a unique, primate-specific sequence motif that disables an activating regulatory site in the glucose-6-phosphatase (G6PC) promoter was also required to enable function of this previously unrecognized tumor suppression system. In human somatic cells, loss of TP53 thus triggers activation of DHEAS transport proteins and steroid sulfatase, which converts circulating DHEAS into intracellular DHEA, and hexokinase which increases glucose-6-phosphate substrate concentration. The triggering of these enzymes in the TP53-affected cell combines with the primate-specific G6PC promoter sequence motif that enables G6P substrate accumulation, driving uncompetitive inhibition of G6PD to irreversibility and ROS-mediated cell death. By this catastrophic ‘kill switch’ mechanism, TP53 mutations are effectively prevented from initiating tumorigenesis in the somatic cells of humans, the primate with the highest peak levels of circulating DHEAS. TP53 mutations in human tumors therefore represent fossils of kill switch failure resulting from an age-related decline in circulating DHEAS, a potentially reversible artifact of hominid evolution.

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Rising Cost of Anticancer Medications in the United States

Cited by 12 publications

References 14 publications

How United States healthcare can learn from Costa Rica: A literature review

How United States healthcare can learn from Costa Rica: A literature review

Cancer drug development: The missing links

Detection of a novel, primate-specific ‘kill switch’ tumor suppression mechanism that may fundamentally control cancer risk in humans: an unexpected twist in the basic biology of TP53

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