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The abnormal membrane glycoprotein that we previously found to be associated with malignancy in a wide range of different tumours is present in the cell membrane as a dimer and appears to have a specific binding site for glucose.
The high potassium, low sodium diet of the Gerson therapy has been observed experimentally to cure many cases of advanced cancer in man, but the reason was not clear. Recent studies from the laboratory of Ling indicate that high potassium, low sodium environments can partially return damaged cell proteins to their normal undamaged configuration. Therefore, the damage in other tissues, induced by toxins and breakdown products from the cancer, is probably partly repaired by the Gerson therapy throught this mechanism.
Single cell suspensions have been prepared, by enzyme digestion, from the mouse preputial gland tumor and separated by flotation centrifugation into populations of different buoyant densities. These populations of cells have been shown by morphological, chemical and biochemical criteria to be in different stages of maturation. Some properties of the separated cells are described.
The cell-surface proteins of 6 different melanoma cell cultures have been labelled with 125I using lactaperoxidase-catalysed iodination. Fractionation of the proteins was achieved using 5--22.5% polacrylamide-gradient gel electrophoresis in the presence of sodium dodecyl sulphate (SDS) and the proteins were detected by autoradiography. Up to 24 labelled proteins were detected in the individual cell cultures, but the proteins labelled differed considerably in the 6 cultures examined. A possible reason for this, involving variation in the glycosylation of cell-surface glycoproteins is discussed. Cells of the same melanoma line had similar cell-surface proteins at different passage levels, but changes in the labelled proteins occurred when the culture conditions were altered. The cell-surface proteins of high molecular weight were cleaved by trypsin, but most of the low mol.-wt. proteins were resistant to trypsin. The "large external transformation sensitive" (LETS) protein detected as a major protein on fibroblasts in culture was not a dominant protein on the melanoma cells. It was detected on only 4/6 cell cultures. Possible relationships of the cell-surface proteins described in this study to morphology, immunological properties and proteolytic activity of human melanoma cells are discussed.
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The distribution on the cell surface of the large external LETS protein that is transformation sensitive of normal, transformed and tumorigenic cells was examined by immunofluorescent staining. A correlation was established between the expression of fibril-like LETS protein and the oncogenic capabilities of a series of adenovirus-transformed cell lines. In cells expressing a transformed phenotype in vitro, LETS protein is only detected in cell-cell contact areas, wheras in "untransformed" cells LETS protein is distributed over the cell surface. Transformed cells capable of inducing invasive tumors, and the cells of established tumor lines, have low or undetectable levels of LETS protein, as measured by this method. The results indicate that LETS protein has a role in cell-cell adhesion and that reduced expression of this protein at the cell surface is related to the oncogenic phenotype. This relationship has been established for experimentally induced and spontaneous tumors.
Human EBV-positive and EBV-negative haematopoietic cell lines were shown to have different and easily distinguishable surface glycoprotein patterns as demonstrated using surface labelling by the galactose oxidase-tritiated sodium borohydride method.
This is a review of the following human gene products which appear in the prenatal period, subsequently are repressed, and reappear in malignant neoplasms: alpha fetal protein; carcinoembryonic antigen; Regan's isoenzyme; fetal sulfoglycoprotein; a fetal liver ferroprotein; beta-S-fetoprotein; gamma-fetoprotein; carcinofetal glial antigen; leukemoembryonic antigens; fetal pancreatic carcinoma antigens; universally reacting oncofetal antigens; and potential oncofetal markers.
Indices of mitotic potential may improve prognostic discrimination in patients with malignant disease. Ki-67 is a monoclonal antibody directed against an unknown proliferation antigen which has been shown to be a measure of mitotic potential. Sixty-four benign and eighty malignant prostatic biopsies were stained with the Ki-67 antibody. Nuclear and cytoplasmic staining was identified in benign and malignant biopsies using immunoalkaline phosphatase and immunoperoxidase staining reactions. Nuclear staining was identified in 14 benign and 44 malignant biopsies. Nuclear staining for Ki-67 was seen in 36% of biopsies with Gleason histological score (GHS) 2-4, 71% with GHS 5-7 and 62% with GHS 8-10. Nuclear staining was associated with advanced local disease stage, but not with metastatic disease stage. Clinical follow-up is required to establish the value of Ki-67 immunostaining as a prognostic determinant in prostatic cancer.
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It is proposed that tumour progression results from the increased mutability of tumour cells and that this mutability leads to the acquisition of a large number of 'neutral' mutations having no significant effects under physiological conditions but capable of lethal expression under different conditions. High temperatures often lead to expression of neutral mutations and this could provide a mechanism for the observed thermosensitivity of tumour cells, and a rational basis for the use of hyperthermia in cancer treatment.
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The studies are presented which demonstrate that smooth endoplasmic membrane of normal liver has a single apparent binding site for cAMP with a KD of 0.6 X 10(-8) M. In contrast to this, however, cyclic AMP binding to the intracellular membrane of hepatoma 7800 exhibit two binding sites; the binding constant of one site on the tumor membrane is comparable to that of the normal liver whereas the value of the second intrinsic association constant differ by a factor of 10. It is suggested that there may be an association between abnormal cyclic nucleotide metabolism and the intracellular membrane modulation of the expression of genetic information in normal and neoplastic cells.
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Human pancreatic exocrine adenocarcinoma cells established in tissue culture expressed both HLA and beta 2-microglobulin (beta 2M). Plasma-membrane components of this pancreatic cancer cell line were purified from plasma membrane fractions enriched by sucrose density-gradient centrifugation, using immunoaffinity chromatography on immobilized anti-human beta 2M antibody. Both rabbit and mouse monoclonal anti-beta 2M IgG were used, with a 20--25-fold overall purification of 5'-nucleotidase. The method was applicable to 5 x 10(7) cells and permitted the solubilization of membranes retained on the column, with the selective desorption of components not associated with beta 2M before the subsequent elution at pH 3 of beta 2M-associated macromolecules. The acid eluate contained one major and two minor bands in the 40--45,000 mol.-wt range with two additional enriched components of 18,000 and 22,000 dalton. A major carbohydrate-containing component of high mol. wt was also found to be associated with the pancreatic cancer-cell plasma membrane.
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