01.08.10
We examine in detail Wilhelm Reich's orgonomic theory of the etiology of cancer and his model of the cytological stages of cancer. The orgonomic model of cancer stands alone in linking the persistence and intensification of social and psychosomatic factors that negatively affect emotional expression with the onset of hypoxic conditions, local and systemic, that select for malignant phenotypes. The rarely broached main novelty of the model suggests that every manifestation of somatic cancer is preceded by increasing RBC dysfunctionality, and that the leukocytosis characteristic of most chronic leukemias is in fact an auto-immune reaction geared against RBC fragments and their (self-)antigens. Even though unproven, these are provocative suggestions that could turn out to be substantially correct. The same cannot be said for the orgonomic model's contention that the real cancer cells are amoeboid cells that arose de novo (heterogenically) from the vesicular byproducts of one or more dying or decaying tissue cells - or for Reich's proposed staging of cancer. In this context, the vesicle-based concept of a PA bion is found to be wanting and unable to acquire a functional sense - as it is employed to designate such widely different biological phenomena as to become merely a catch-all. In contrast, Reich's identification and isolation of his 'T-bacilli', despite some discrepancies, seems to largely coincide with the identification of mycoplasma. His proposed role for these T-bacilli in chronic inflammation and his experimental induction of leukemoid disease in mice injected with T-bacilli isolates are coadunate with current views of the possible role of mycoplasma in the co-induction of leukemia or leukemoid states.
RSS
01.08.10
Rather than writing a review with a limited scope, we attempted to survey the span of medical and molecular biology research in the field of oncology during the last six decades: from the early breakthroughs in viral oncology and the novel notions of virus and viral cancer (onc) genes; to the role of DNA cancer viruses and C retroviruses in experimental carcinogenesis; through the discovery of cellular oncogenes and the biology of growth factors; to the expansion of the concept of oncogene and its types; and, finally, to the realization that cancer is a multiplicity of different disorders that appear to arise through nonviral auto-oncogenic processes involving adaptive changes and epigenetic responses to cancer-promoting pressures in the external and internal environment of the organism. Throughout, we have searched for the integration of an oncogenic vector with different degrees of transformation, seeking the commonality of proliferative disorders, somatic cancer and leukemia. We re-examine what separates transformation, benign and malignant, from differentiation, and how their reversible switch deploys graded responses related to states of hypersensitivity to, or independence from, key physiological growth factors.
RSS
01.08.10
The present communication unites in a novel model of the etiology of cancer very diverse contributions to oncology made since discovery of the Warburg effect. The model proposes a unitarian understanding of acquired malignancy as a neo-lamarckian adaptive disorder whereby a cell escapes organism and tissue regulatory controls to adapt to a condition of energy starvation (embodied in a variety of oncogenic pressures that are hypoxic or hypoxia-like in their effects), by abandoning its normal aerobic metabolism and by altering its growth-factor responses to support hyperplastic and neoplastic proliferation, and block normal differentiation. The multifactorial role of oxygen in normal metabolism is underlined by the biological and biophysical effects of its chronic lack in the initiation and promotion of oncogenesis: via the hypoxia-inducible factors (and especially HIF-1), hypoxia activates glycolysis and shuts down oxidative phosphorylation; and it adversely affects not only the oxygen transport roles of hemoglobin and myoglobin, but also their thermal dissipation of absorbed radiant energy, an essential contribution to temperature regulation in homotherms. Nonhypoxic factors may have similar hypoxia-like effects. Lack of vitamin C and iron can block progression of the Krebs cycle, and shut down aerobic respiration. Copper, according to our model of the respiratory chain, may actually work in vivo as a respiratory poison. Altered growth factor regulation (e.g. decreased plasma concentrations of erythropoietin) or enzymic defects (e.g. lack of citrate synthase) may also induce hypoxia-like effects. Moreover, according to the analysis we present here, poor oxygenation prevents absorption of the radiant energy needed to inject into the respiratory chain. We propose that absorption of solar- sourced radiant energy in the terrestrial environment - with an ambipolar energy spectrum of 28 to 79 keV - is a key modulating function of biological systems involved in the normal activities of hemoglobin, myoglobin, the cytochrome c oxidase complex, skin production of vitamin D3 and the differential radiant energy sensors of pinealocytes. It provides the energy thermally dissipated by hemoglobin and myoglobin, as well as the activation energy needed to initiate and terminate the respiratory chain, and thus the kinetic energy of the electrons and protons shuttled across mitochondrial membranes. Insufficient absorption of ambipolar energy is tied in to the causation of acquired cancer and, as suggested by the present etiological model, also connected to the deregulation of the Pasteur effect that permits manifestation of the Warburg effect. However, the latter is far from being a universal trait of cancer cells. Recent results by Jacques Sonveaux's group have shown that neoplastic phenotypes are distributed inside a tumor according to an oxygen gradient between lactic fermenters and lactic respirers, with their association being symbiotic. Our model suggests that this is best understood as functions of a unitarian auto-oncogenic vector of cumulative transformations for acquired cancers, and that this vector repeatedly invokes a recursive cell-regulatory circuit, the IGF (insulin-like growth factor) axis, in its effort to de-stabilize the autonomic control of the cell cycle. At initiation of cancer, aerobic respiration is shut down substantially or entirely, and glycolysis is activated along with lactate dehydrogenase A (LDHA)-driven fermentation, to sustain hyperplastic proliferation and block differentiation. These metabolic shunts are brought about by the HIF axis (in particular by HIF-1) and modulated by the IGF axis (in particular by IGF-I, its binding proteins and its receptor, IGF-IR). They likely involve specific hypersensitive growth factor responses modulated by the IGF axis, including IGF-I hypersensitivity itself as found in Polycythemia vera. Such responses involve both epigenetic and post-adaptive alterations. With progression of the auto-oncogenic vector from hyperplasia to neoplasia, something akin to a differentiation of malignantly transformed states takes place which appears to require, in either case, changes in the IGF axis that render its operation independent from physiological control by its ligands, in particular from control by IGF-I, so that the orthosympathetic signals of the IGF axis become permanently turned on and the cell now exerts an organism-independent control over its own cycling. At this juncture, the oncogenic vector undergoes a split. The Pasteur effect coupling glycolysis to aerobic metabolism is severed in both instances of "neoplastic differentiation", but while the more aggressive neoplastic cells to which the Warburg effect applies rely solely on further acceleration of lactate production, other neoplastic cells adapt to the acidification of tumors - and blood - by turning on LDHB to employ the lactate as substrate, via conversion to pyruvate, for their mitochondrial Krebs cycle and respiratory chain. In solid tumors, the lactic respirers activate vascular endothelial growth factor production (controlled by the IGF axis) to stimulate tumor angiogenesis and thus acquire direct access to oxygen from the blood. Ultimately, the lactate fermenters become the highly-tumorigenic metastatic elements of terminal cancer. We also suggest that serious clinical investigation with properly staged cancer patients should henceforth target the use of novel, or heretofore improperly-tested, non-cytotoxic treatments based on the presently proposed aetherometric model of auto-oncogenesis.
RSS
01.08.10
In this communication we emphasize the interconnectedness of hematologic neoplasms and their developmental processes, as well as propose new diagnostic classifications for a variety of hematologic disorders. We sought to produce a comprehensive and accurate review of hematologic disorders based on updated medical research, but also connect them as transitional forms of distinct neoplastic processes ("subvectors") that, despite the various lineage-specific phenotypes, repeat a fundamental auto-oncogenic progression (an auto-oncogenic vector) of pre-neoplastic, chronic, subacute and acute (or terminal) stages. Auto-oncogenic theory suggests that the main causation of acquired post-adaptive malignancies involves hypoxic or hypoxia-like factors that chronically impair respiratory metabolism and adversely affect, first and foremost, the red blood cell compartment, both in its functional role and in its formative process (erythropoiesis). In the present communication, we extend the proposed etiology to hematologic neoplasms, to include deregulated humoral and cellular auto-immune responses to RBCs and their precursors as one of the main pathways, if not the dominant one, for the induction of myeloid and lymphoid neoplasms. First, we review the multiplicity of disorders that result in anemia or in erythroid/myeloid polycythemias, with an emphasis on the problems associated with determining the correct etiology of Polycythemia vera(PV) and the so-called myelodysplastic syndrome (MDS) that includes refractory anemias. We suggest that the chronic myeloproliferative disorders (PV; Essential Thrombocytosis, ET; Primary Myelofibrosis, PMF; and other neoplasms, including Refractory Anemia with Ring Sideroblastosis and Thrombocytosis, RARS-T) should be viewed as auto-oncogenic, chronic blood neoplasms, that differ in their phenotype by altered lineage-specific cytokine responses, but are simply variants of a myeloid stem cell neoplasia that has in common the JAK2V617F adaptive mutation. In the second part, we review the myeloid leukemias, and the lymphoid and lymphomatoid neoplasms, but, with a few exceptions, restrict ourselves to auto-oncogenic malignancies - unlike our approach to the anemias and the polycythemias, which included all possible etiologies, not just auto-oncogenic ones. In the domain of the myeloid leukemias, we stress in particular: (1) the existence of an erythroleukemic vector that encompasses chronic phases like PV or Refractory Anemia with Ring Sideroblastosis (or, still, the early stages of typical and atypical CML, which often present a chronic erythroleukemic picture), pre-acute crises like those observed in PMF and MDS, and acute phases like those of acute erythroblastic leukemia and other forms of acute myelogenous leukemia; and (2) the progression of this vector to encompass a wider myeloid leukemic vector, joining in with the auto-oncogenic, Philadelphia chromosome-positive vector linking chronic myeloid leukemias, acute myelogenous leukemias, B cell acute lymphoblastic leukemia and biphenotypic acute leukemia. In the domain of the lymphoid leukemias, we stress their connection, together with the hemolytic anemias caused by cellular or humoral auto-reactivity, to disturbed auto-immunity whose dominant target is the erythroid compartment. We suggest that this anti-RBC reactivity is a neoplastic response to the biological degradation of RBC function and formation. If initiation of disturbed poietic or immunologic auto-oncogenic responses is promoted by hypoxia-induced RBC fragility and dysfunctionality, then it becomes clear why altered erythropoiesis and RBC clearance dominant in the etiology of acquired blood neoplasms. Specific keywords: Growth factors, EPO response, Epigenetic control, Stem Cell Factor (CD117 ligand), all-trans-retinoid acid (ATRA), auto-oncogenic vector, chronic myeloproliferative disorders, Polycythemia vera, essential thrombocytosis, primary myelofibrosis, myelodysplasia, hemolytic anemia, erythroleukemia, chronic myeloid leukemia, actue myelogenous leukemia, chronic lymphocytic leukemia, acute lymphoblastoid leukemia, biphenotypic leukemia, cytogenetics, Philadelphia-positive neoplasms, IGF-I hypersensitivity, cytokine hypersensitivities, JAK2, SOCS and STAT genes, auto-immune neoplasms, hematon, anemias of infection
RSS
15.03.10
In the second part of "Whither Science", the Correas follow the emergence of an eccentric science from the pre-Socratic philosophers to Archimedes, and describe how an eccentric science then went on to become the major source of Royal Science across despotic, imperial and modern social formations. And yet, the problems that properly concern eccentric science have never received conclusive solutions - whether at stake is a consistent treatment of energy as a multiplicity, or of Space and Time as manifolds, or, simply, the question of what it means for a knowledge to be adequate and actual. The authors propose a novel approach to the conceptualization and functional solution of these problems - including that of the relationship between science and art - which arises from the authors' foundational work on a complete physics of energy in both massfree and massbound forms.
RSS
15.03.10
The long-planned and long-awaited Journal of Biophysics, Hematology and Oncology was launched on January 24, 2010. Its primary intent is to serve as an electronic vehicle for the publication of original work carried out at the Aurora Biophysics Research Institute (ABRI) in the fields of biophysics, microbiology, molecular biology, hematology and oncology. However, the Journal will also publish theoretical or experimental contribution from outside authors. Unlike other ABRI publications, this Journal is not restricted to aetherometric research.
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