Stereotactic radiotherapy (SRT) offers a treatment option for hepatocellular carcinoma (HCC) patients that are not eligible for surgery, embolization, chemotherapy, or radiofrequency ablation. We have evaluated the feasibility, tolerance and toxicity of SRT for 25 HCC patients who were not eligible for these other modalities. The patients (6 women and 19 men) were treated with CyberKnife stereotactic radiotherapy using respiratory motion tracking. All patients had liver cirrhosis with an Eastern Cooperative Oncology Group (ECOG) performance score of less than 2 and pre-treatment Child scores ranging from A5 to B9. A total dose of 45 Gy in three fractions of 15 Gy each was prescribed to the 80% isodose line (95% of the PTV received 45 Gy) and delivered to the target volume over 10 to 12 days. Overall the treatment was well tolerated with two Grade 3 acute toxicities and no acute Grade 4 toxicities. Late toxicity was minimal with all observed late toxicities occurring within the first six months of follow-up. Three hepatic recurrences at a distance from the target and one metastasis were observed. The actuarial 1- and 2-year local control rate was 95% (95% CI: 69-95%). At a median overall follow-up of 12,7 months (range, 1-24 months), six of the twenty-five (24%) patients have died. Overall actuarial survival at 1- and 2-years was 79% (95% CI: 52-92%) and 52% (95% CI: 19-78%), respectively. Our results suggest promising therapeutic efficacy and good clinical tolerance to CyberKnife SRT treatment for HCC patients not eligible for other treatment modalities.

Paraffin-embedded sections from a variety of epidermal lesions were stained with fluorescein isothiocyanate-labeled concanavalin A and examined by a fluorescence microscope. Seventy-six normal, hyperplastic, and neoplastic tissues were examined. Lectin binding was demonstrated in all malignant tumors, the fluorescence being confined to the plasma membrane of the tumor cells. Normal and hyperplastic tissues either failed to stain or showed a grossly diminished level of fluorescence. The distinction between malignant and normal of hyperplastic cells was clear-cut and definite.

No abstract

No abstract

No abstract

MANY observers have suggested that the malignant cell differs from its normal counterpart in the loss or modification of a growth-controlling component but it was not until the work of Miller and Miller (1947) that firm experimental support for such an hypothesis was advanced. This work indicated that, at least as far as rat liver is concerned, the cellular constituent involved is protein in nature.The results of Weiler's observations (1952, 1956) provided independent serological and histological support for the concept of the loss of a cellular constituent during aminoazo dye carcinogenesis in the rat liver. Weiler injected particulate antigens prepared from rat liver into rabbits and obtained antisera which, after repeated absorption with rat kidney particulates, still reacted in complement fixation test with the homologous rat liver but failed to react with rat kidney particulates. He found that a serum prepared in this way, which he regarded as a liver " organ-specific antiserum ", did not react with particulate diagnostic ' antigens" prepared from rat hepatomata and concluded that the tumour cells had lost their " organ-specific antigen ". Further support of these results was obtained by application of the fluorescence antibody technique of Coons and Kaplan (1950). Weller found that fluorescein-globulin conjugates prepared from " organspecific anti-rat liver" rabbit globulin stained normal rat liver sections but did not stain sections of rat hepatoma.Hughes, Louis, Dineen and Spector (1957), using Weiler's methods, were unable to obtain an organ-specific antiserum. At the same time the differential staining of normal rat liver and rat hepatoma sections by the use of a fluorescein-conjugated rabbit globulin fraction was completely confirmed (Hughes, 1957). At first serum obtained from rabbits which had previously been injected with homogenates of rat tissues was used. However, it was found that serum from rabbits which had not been so injected was equally effective as a stain. These control sera did not fix complement in the presence of rat liver antigens.The method was applied to naturally-occurring tumours both in man and in animals. At first the sera from rabbits which had been injected with the appropriate tissues were used, but these were soon replaced by sera from uninjected animals. The technique was applied to various tumours and particularly to a series of carcinoma of the colon (Louis, 1957b) and it was also applied to a large series of cases of leukaemia (Louis, 1957c).In view of these results it was clear that the staining could not be attributed to an antibody-antigen reaction and an alternative explanation was sought.In mixtures of proteins, anion-cation salt-like complexes are readily formed within the pH range between the isoelectric points of the components. The formation of these complexes between " stain globulin " and tissue proteins could account for these staining phenomena.

Paraffin‐embedded sections from a variety of breast lesions were stained with a number of lectins labeled with fluorescein isothiocyanate and examined by fluorescence microscopy: 95 non‐neoplastic tissues and 69 malignant tumors were examined. Lectin binding was demonstrated in all malignant tumors, the fluorescence being confined to the plasma membrane of the tumor cells. Normal and hyperplastic tissues either failed to stain or showed a grossly diminished level of fluorescence. The significance of the staining reaction is discussed.

The soluble cytoplasmic proteins isolated from bronchial mucosae and 15 bronchogenic carcinomas of human origin have been examined by agarose-gel electrophoresis and compared with a similar protein preparation isolated from the bronchial mucosa of cynomolgus monkeys (Macaca irus). In all cases, 3 bands were found, 2 (A and B) which migrated to the anode and one (C) which migrated to the cathode. The relative proportions of protein in the 3 bands were similar in smokers and nonsmokers, but there was a significant increase in the proportion of protein in band C in all of the bronchogenic carcinoma material examined. This increase was most pronounced in ‘oat’-cell carcinomas. The finding that basic proteins are increased in bronchogenic carcinoma is in contrast with the decrease in basic proteins in some experimental animal tumors; it is suggested that this difference might be related to functional differences between basic proteins in different tissues. The electrophoretic pattern of human and cynomolgus monkey material was similar, indicating that the cynomolgus monkey may be a suitable model for gaining experimental data of relevance to alterations in these proteins in human material.