Self-defense of human sarcoma cells against cytolytic lymphoid cells of their host.

Metastatic human sarcomas temporarily respond to radio-chemotherapy relapse and remain highly resistant to further combination chemotherapy as to a curative effect, including checkpoint control.

Large Granular Lymphoid Cells Discovered First in the Human Blood as "Burnet's Immune Surveillance Cells" (1969) Are Identical with the Late-Designation "Natural Killer Cells" (1975).

The cytolytic large granular lymphoid cells first observed in his own blood by this author "as healthy control" in the late 1960s were referred to as "Burnet's immune surveillance cells". These cells killed autologous/allogeneic malignantly transformed cells close to immediately upon their contact. Healthy individuals and patients with cancers possessed these large granular lymphoid cells.

[Erratum] The cnidarian origin of the proto-oncogenes NF-κB/STAT and WNT-like oncogenic pathway drives the ctenophores (Review).

After the publication of the article, the author noted that there was an error on page 1212, right column, paragraph entitled 'Virus carrier algal symbionts'. The word Hydra virilis should be written as Hydra viridis/viridissima. [the original article was published in the International Journal of Oncology 47: 1211-1229, 2015; DOI: 10.

The cnidarian origin of the proto-oncogenes NF-κB/STAT and WNT-like oncogenic pathway drives the ctenophores (Review).

The cell survival pathways of the diploblastic early multicellular eukaryotic hosts contain and operate the molecular machinery resembling those of malignantly transformed individual cells of highly advanced multicellular hosts (including Homo). In the present review, the STAT/NF-κB pathway of the cnidarian Nematostella vectensis is compared with that of human tumors (malignant lymphomas, including Reed-Sternberg cells) pointing out similarities, including possible viral initiation in both cases. In the ctenophore genome and proteome, β-catenin gains intranuclear advantages due to a physiologically weak destructive complex in the cytoplasm, and lack of natural inhibitors (the dickkopfs).

[Erratum] Virological and immunological connotations of apoptotic and anti-apoptotic forces in neoplasia.

The authors would like to acknowledge that the Coriphosphine O stain shown in the upper panel of Figure 8 was a kind gift from Dr T.P. Loughran of the H.

Molecular biology of oncogenic inflammatory processes. I. Non-oncogenic and oncogenic pathogens, intrinsic inflammatory reactions without pathogens, and microRNA/DNA interactions (Review).

In some inflammasomes tumor cells are generated. The internal environment of the inflammasome is conducive to the induction of malignant transformation. Epigenetic changes initiate this process.

Horizontal gene transfers with or without cell fusions in all categories of the living matter.

This article reviews the history of widespread exchanges of genetic segments initiated over 3 billion years ago, to be part of their life style, by sphero-protoplastic cells, the ancestors of archaea, prokaryota, and eukaryota. These primordial cells shared a hostile anaerobic and overheated environment and competed for survival. "Coexist with, or subdue and conquer, expropriate its most useful possessions, or symbiose with it, your competitor" remain cellular life's basic rules.

Antileukemia and antitumor effects of the graft-versus-host disease: a new immunovirological approach.

In leukemic mice, the native host's explicit and well-defined immune reactions to the leukemia virus (a strong exogenous antigen) and to leukemia cells (pretending in their native hosts to be protected "self" elements) are extinguished and replaced in GvHD (graft-versus-host disease) by those of the immunocompetent donor cells. In many cases, the GvHD-inducer donors display genetically encoded resistance to the leukemia virus. In human patients only antileukemia and anti-tumor cell immune reactions are mobilized; thus, patients are deprived of immune reactions to a strong exogenous antigen (the elusive human leukemia-sarcoma retroviruses).

Horizontal gene transfers and cell fusions in microbiology, immunology and oncology (Review).

Evolving young genomes of archaea, prokaryota and unicellular eukaryota were wide open for the acceptance of alien genomic sequences, which they often preserved and vertically transferred to their descendants throughout three billion years of evolution. Established complex large genomes, although seeded with ancestral retroelements, have come to regulate strictly their integrity. However, intruding retroelements, especially the descendents of Ty3/Gypsy, the chromoviruses, continue to find their ways into even the most established genomes.

Natural and genetically engineered viral agents for oncolysis and gene therapy of human cancers.

Based on personal acquaintances and experience dating back to the early 1950s, the senior author reviews the history of viral therapy of cancer. He points out the difficulties encountered in the treatment of human cancers, as opposed by the highly successful viral therapy of experimentally maintained tumors in laboratory animals, especially that of ascites carcinomas in mice. A detailed account of viral therapy of human tumors with naturally oncolytic viruses follows, emphasizing the first clinical trials with viral oncolysates.

Comments on cultured human sarcoma cells.

Human sarcoma cell populations maintained in culture reflect to the native tumor cells better if the culture retains those nonmalignant cells that comprised the tumor's microenvironment in vivo [Hu M, et al. Characterization of 11 human sarcoma cell strains. Cancer 2002; 95: 1569-76] and thus provide paracrine growth factors and protection from apoptotic death to the tumor cells.

Adult human sarcomas. II. Medical oncology.

Human sarcoma cells can be killed by radio- and chemotherapy, but tumor cells acquiring resistance frequently kill the patient. A keen understanding of the intracellular course of oncogenic cascades leads to the discovery of small molecular inhibitors of the involved phosphorylated kinases. Targeted therapy complements chemotherapy.

Adult human sarcomas. I. Basic science.

When connective tissue undergoes malignant transformation, glioblastomas and sarcomas arise. However, the ancient biochemical mechanisms, which are now operational in sarcomas distorted by mutations and gene fusions in misaligned chromosomes, were originally acquired by those cells that emerged during the Cambrian explosion. Preserved throughout evolution up to the genus Homo, these mechanisms dictate the apoptosis- and senescence-resistant immortality of malignant cells.

Evidence accumulating in support of cancer vaccines combined with chemotherapy: a pragmatic review of past and present efforts.

In the early 1970s supervised clinical trials were initiated at The University of Texas M.D. Anderson Hospital in Houston, TX, for the combination of viral oncolysate-based vaccines and contemporary chemotherapy for the treatment of patients with metastatic melanoma and sarcomas.

Human natural killer cells: a comprehensive review.

The senior author of this comprehensive review observed and reported in 1969 that his lymphocytes killed allogeneic tumor cells in vitro. Some of his research associates and technicians and other healthy individuals also yielded such killer lymphocytes. The team considered pre-immunization to cancer occurring in individuals after in-family or professional exposure to patients with cancer (in an era when the concept of viral etiology of cancer was receiving major support); or that lymphocytes can acquire through blastic transformation immune reactivity to allogeneic cells anew in vitro.

Chondrosarcoma cell differentiation.

A mixed population of lymphocytes from a healthy donor co-existed with an established culture of allogeneic chondrosarcoma cells, during which time the tumor cells changed from malignantly transformed to benign fibroblast-like morphology; from multilayered to a monolayered growth pattern; lost their potency to grow in colonies in soft agar; and showed signs of senescence. A discussion of possible molecular mechanisms for this event is offered. If there are as yet undiscovered lymphokines that can induce reversal of the malignant geno/phenotype, the cognate gene(s) should be cloned for genetic engineering and for the mass production of the corresponding molecular mediators for clinical trials.

Contradictory Concepts in the Etiology and Regression of Kaposi's Sarcoma. The Ferenc Györkey Memorial Lecture.

The Introduction is an overview of 3 decades of works performed by Professor Ferenc Györkey (in many cases in collaboration with the author) and aimed at the elucidation of viral participation in the etiology of arteriosclerosis, SLE, hairy cell leukemia, HD, AIDS and KS. Controversial issues surrounding the etiology, treatment and regression of KS are discussed in terms of paracrine and autocrine loops of growth factors; protooncogene-oncogene activations, immunosuppression and retro- and/or herpesviral etiology. In regressing KS lesions the roles played by Fas, Bcl-2, Bax, TNFß; apoptotic-antiapoptotic events; and antiangiogenesis agents especially that of Hu-r-IFNa are elaborated on.