Integrating fields of cancer research through pivotal mechanisms and synthetic final pathways: a unifying and creative overview.
From cancer etiopathogenesis to selective apoptosis, from multiple drug resistance to oncogen activation and from the phenomena of spontaneous regression of cancer to certain aspects of cancer chemotherapy, all these subfields of biology and oncology research share some deep-seated, both basic and clinical, essential features and characteristics. Certain apoptosis-inducing agents of unrelated families, ranging from ether lipids to Na(+)/H(+)-antiporter inhibitors to Delta(9)-tetrahydrocannabinol all have been reported to induce selective cancer-cell death. Behind a wide array of intermediary factors and mechanisms involved in their activity, they seem to share common pivotal and/or final pathways in inducing cell death mediated by a 'pathological' accumulation of intracellular hydrogen ions as a mechanism underlying core changes in intracellular signaling pathways. An H(+)-concentration initial perspective indicates that from pathogenesis to apoptosis and multiple drug resistance, as well as oncogen activity, tumor progression and even the phenomenon of spontaneous regression, all can be interpreted from their deep (H(+))-related basic and clinical essential characteristics. This speculative review discusses the potential integration of these previously disparate subfields of cancer research, through a model which also seems to lead toward improving understanding of the fundamental nature of malignant processes. It is concluded that this synthetic and universal approach allows advancement toward a combining of different areas of oncology into deeper and more comprehensive forms of rational understanding, with the hope of paving the way towards more selective, effective and all-encompassing forms of treatment.
D017209:Apoptosis; D006801:Humans; D009369:Neoplasms / Q000473:pathology; D012106:Research