Vaccines that induce an antitumour immune response are disappointingly ineffective in treating patients with cancer. Pre-conditioning the vaccination site to induce inflammation might provide a way to improve this therapy. See Letter p.366
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Sabado, R., Bhardwaj, N. Dendritic-cell vaccines on the move. Nature 519, 300–301 (2015). https://doi.org/10.1038/nature14211
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Majid Ali
Augmenting Dendritic-cell Immunotherapy. Clinicians treating cancer eagerly await and enthusiastically accept advances in cancer treatment. The approach of augmenting dendritic-cell (DC) immunotherapy with vaccines spiked with patient?s own tumour antigens is logical. The finding that initial results justify optimism is encouraging. Some of the observed benefits of tumour-enhanced DC immunotherapy may be, as pointed out, due to other elements, including (1) prior resection of tumours; (2) stronger immune response to earlier vaccines; and (3) or altered regulatory T cell functions. These and potentially as yet unrecognized elements should not dampen clinicians? enthusiasm.
A matter that deserves diligent study is how to prevent immunosuppression caused by: (1) fear and anger associated with diagnosis; (2) deep concerns about the potential of serious adverse effects of cancer treatments; (3) doubt about the efficacy of the proposed treatment; (4) and concurrent burdens of cancer biology and comorbidities. Beyond these is the clear need for boosting the immune system in cancer treatment, as is the case in the optimal management of all serious chronic disorders. To address these issues, in 1995, I put forth an oxidative hypothesis of cancer which designated accelerated oxidative injury as the common denominator in all factors implicated in carcinogenesis (ref 1). In a follow-up paper, I described the tumor-host dynamics, focusing on the redox phenomena as the mechanism for sustaining and perpetuating the malignant cellular replication (ref 2). In 2001, looking at the problem through the prism of oxygen homeostasis, I expanded that hypothesis to the dysox model of cancer with the following words: cancer is destructive behavior of cells incited and perpetuated by many factors that cumulatively lead to anomalous oxygen signaling (ref 3). I focused on the following six characteristics: (1) respiratory-to-fermentative (RTF) shift in ATP production; (2) production of prodigious quantities of organic acids ? lactic acid and others; (3) creation of a cocoon of coagulated proteins around malignant cells to exclude functioning host immune cells and their soluble defense molecules; (4) uncontrolled cellular replication that disrupts local tissue architecture; (5) colonization of distant tissues in which the destructive behavior of neoplastic cells continues; and (6) under certain conditions, a cancer cell can be coaxed to alter its behavior (ref 4). In 2004, drawing upon the biochemical rationale provided by Otto Warburg?s observations, I put forth the oxygen model of cancer (ref 5) focusing on stemming and/or controlling the spread of tumour with immune enhancement with optimal food choices, self-regulation (i.e. meditation), and adjuvant oxystatic therapies.
In 2007, I published The Crab, Oxygen, and Cancer in two volumes, the first devoted to theoretical aspects of molecular biology in the context of cancer biology. In the first volume (ref 6), I presented personal morphologic, bio-energetic (altered Krebs cycle dynamics), biochemical, and clinical observations made in patients with a variety of malignant tumors of varying aggressiveness. I coined the term oxystatic therapy for direct and indirect measures that restore oxygen signaling and other dimensions of oxygen homeostasis. I devoted the second volume (ref 7) to therapeutic aspects of an oxygen-based approach to boosting immunity, focusing on issues of altered states of bowel, blood, and liver ecosystems. Recently, one direct evidence of my oxygen model is provided by studies of Simeonov and Himmelstein concerning the lower incidence of lung cancer among people living at high altitudes (ref 8).
There are important philosophic issues in the integrative treatments of malignant neoplasms. It is understandable that in a research and development context, scientists developing specific immunotherapy for specific cancers will seek clarity and objectivity in precise delineation of the benefits of the new treatment. Therefore, the use of concurrent integrative therapies is discouraged. In clinical oncology, however, most patients seek dietary intervention, advice on stress reduction with self-regulation, and related integrative therapies, such as those which I described in my books (ref 6-7) and others have as well. There is substantial number of well-informed and experienced physicians who are able to compare the results of immunotherapy and chemotherapy protocols when administered with or without supportive integrative therapies. Regrettably, there is absence of meaningful discourse between them and oncologists. As for the patients, in the United States, they know that oncologists, in general, do not fully support integrative therapies. This takes away much from the full trust in the patient-physician dynamics that is so necessary for dealing with life-threatening illness.
In closing, I take the good news about augmented dendritic-cell immunotherapy as an opportunity to add a voice for a broader philosophic context of integration in the treatment of individuals encountering malignant tumours.
References
1.	Ali M.RDA:Rats, Drugs, and Assumptions. Denville, New Jersey, Life Span Books 1995.
2.	Ali M. Cancer, Oxygen, and pantotropha ? Part I. Townsend Letter for Doctors and Patients. 2004;256:98-102.
3.	Ali M. The Cancerization?De-cancerization Dynamics of theDysox Model of Cancer- Part II. Townsend Letter for Doctors and Patients. 2005;258:122-131.
4.	Ali M. RDA: Rats, Drugs, and Assumptions. Denville, New Jersey, Life Span Books 1995.
5.	Ali M. Carcinogenesis: The Oxidative-Dysoxygenative Model. J Integrative Medicine 2001;5:9-32.
6.	The Crab, Oxygen and Cancer. Volume I: The Dysox Model of Cancer. 2007. New York, Canary 21 Press.
7.	Ali M. The Crab, Oxygen and Cancer. Volume II: The Oxygen Protocol for Cancer. 2007. New York, Canary 21 Press.
8.	 Kamen P. Simeonov and Daniel S. Himmelstein. Lung cancer incidence decreases with elevation: evidence for oxygen as an inhaled carcinogen. Peer J3:e705.