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Biomedical subjects

R Lotan

Publications and source records attributed to R Lotan.

At least 271 records · Page 15Linked to original sources
PubMed1975

Labeling of soybean agglutinin by oxidation with sodium periodate followed by reduction with sodium [3-H]borohydride.

Periodate oxidation of soybean agglutinin, a glycoprotein lectin, resulted in destruction of up to 5 out of the 9 mannose residues present in each of its subunits (MW 30,000) without any loss of hemagglutinating activity. The oxidation did, however, abolish the interaction of soybean agglutinin with concanvalin A, as measured by quantitative precipitation. Reduction with sodium [3-H]borohydride of soybean agglutinin in which 4 out of 9 mannose residues per subunit were oxidized, afforded a radioactive product which retained full hemagglutinating activity and was indistinguishable from the native lectin by gel filtration, gel electrophoresis, and affinity chromatography. These results establish that the integrity of the carbohydrate side chain of soybean agglutinin is not essential for the biological activity of the lectin, and suggest a general method for the preparation of radioactive glycoprotein lectins.

Borohydrides↗
PubMed1975

Peanut agglutinin, a new mitogen that binds to galactosyl sites exposed after neuraminidase treatment.

Peanut agglutinin, purified by affinity chromatography, agglutinates lymphocytes from mouse, rat, guinea pig, and man only after their treatment with neuraminidase. However, it stimulates only neuraminidase-treated rat and human cells. A similar number cell surface receptors for peanut agglutinin was found on neuraminidase-treated rat and mouse lymphocytes although the latter cells were not stimulated by the lectin. Galactose specifically inhibited the agglutination and stimulation of lymphocytes by peanut agglutinin. Sequential treatment of lymphocytes with neuraminidase and beta-galactosidase markedly reduced the response of the cells to stimulation by peanut agglutinin, soybean agglutinin, and galactose oxidase. It is suggested that the same galactosyl residue may be the target for the initial step in triggering lymphocytes by the above mentioned mitogens.

Agglutination Tests↗
PubMedDate not supplied

Expression of galectins in head and neck squamous cell carcinoma.

BACKGROUND: Galectins are carbohydrate-binding proteins thought to be important for cell growth and differentiation, whose expression is altered in some tumors with aggressive phenotype. Our objective was to evaluate the expression of galectins in head and neck squamous cell carcinoma (HNSCC). METHODS: Fourteen HNSCC cell lines and four primary tumor specimens were evaluated using immunoblotting, and immunohistochemical analysis was performed on 35 primary HNSCCs. RESULTS: Galectin-1 and galectin-3 were expressed in most HNSCC cell lines and primary tumor specimens. Galectin-1 was detected in the basal layer of normal adjacent mucosa, in connective tissue stroma, and at the periphery of invasive tumor islands. Galectin-3 localized to superficial mucosal layers, and adjacent to keratin pearls in invasive carcinoma. CONCLUSIONS: Galectins are manifested in HNSCC tumors and are localized to the cell surface, where they may participate in cellular interactions. The expression pattern of galectins appears to be associated with degree of squamous differentiation, suggesting a potential role for galectins as biologic and differentiation markers in HNSCC.

Antigens, Differentiation↗
PubMedDate not supplied

Retinoic acid inhibition of a head and neck multicellular tumor spheroid model.

The effects of retinoic acid (RA) on multicellular tumor spheroids (MTS) derived from a head and neck squamous carcinoma cell line, MDA 886Ln, were studied. Growth of MTSs was shown to be inhibited by 10(-5) to 10(-7) M RA; dose response studies demonstrated that by 10(-10) M RA, MTS growth was inhibited by less than 20%. MTSs treated with RA for 10 days had a decreased labeling index (15% compared with 23% for controls). Histologic studies at 10 days showed both an alteration in tissue-like architecture and an inhibition of squamous differentiation in RA-treated spheroids. Morphologic inhibition of differentiation was confirmed by immunohistochemical staining for involucrin. Histologic sections were also probed with a series of biotinylated lectins to search for RA-induced changes in glycosylation. Changes in staining occurred with two lectins, soybean agglutinin and peanut agglutinin. This study showed that RA induced perturbations in biological processes such as growth and differentiation in a new model system for squamous carcinomas of the head and neck, MDA 886Ln MTS.

Carcinoma, Squamous Cell↗
PubMedDate not supplied

Chemoprevention of upper aerodigestive tract cancers: a report of the third Upper Aerodigestive Cancer Task Force workshop.

The National Cancer Institute Organ Systems Program-sponsored Upper Aerodigestive Cancer Task Force workshops are specifically designed to enhance interactions between basic science and clinical investigators and between academic institutions and the community, and ultimately will contribute to more expeditious clinical advances. The third workshop in this series focused on the rapidly expanding area of chemoprevention of upper aerodigestive epithelial cancers. The first two sessions were devoted to discussion of in vitro and animal-model data documenting the multistep process of squamous differentiation and carcinogenesis, associated molecular and biochemical alterations, and modulation by chemopreventive agents. Animal-model studies have identified several promising chemopreventive agents and synergistic combinations for clinical trial. The last two sessions reviewed nutritional epidemiology, major methodologic issues of large intervention studies, and the novel concept of biologic markers as intermediate endpoints for chemoprevention trials.

Animals↗
PubMedDate not supplied

Preventing diversification of malignant tumor cells during therapy.

One of the most difficult problems arising during cancer therapy is the emergence of unique tumor cell subpopulations that express altered malignant and therapeutic properties. In model tumor systems cytotoxic therapies that eliminate all but a few tumor cells seem to stimulate cell diversification to yield heterogeneous cell populations with divergent properties. Clinically the use of repeated cycles of cytotoxic therapies followed by intervening recovery periods often results in the eventual emergence of highly resistant and increasingly malignant tumor cells. To circumvent tumor cell diversification during therapeutic recovery periods we suggest that cytostatic agents might be employed. Although cytostatic agents such as differentiation modulators, hormones, growth factors, vitamins, and other natural products are unlikely to be effective therapeutic agents if used alone, they could be used during therapeutic recovery periods to modulate the diversification of surviving tumor cells so that these periods might be characterized by less extensive tumor cell diversification. At the end of recovery periods after the removal of cytostatic agents, surviving tumor cells could be briefly restimulated by growth factors, hormones or mitogens, just prior to initiation of new cycles of therapy using cytotoxic agents.

Cell Division↗