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Biomedical subjects

L Nathanson

Publications and source records attributed to L Nathanson.

At least 55 records · Page 3Linked to original sources
PubMed1987

Bilateral adult Wilms' tumor.

Bilateral Wilms' tumors in children are not uncommon but in the adult are quite rare. A two-mutation theory of oncogenesis has been proposed in which a prezygotic gene mutation and a postzygotic mutation lead to the development of Wilms' tumor. However, the recent discovery of a postzygotic deletion within the 11p13 band of chromosome 11 in adult cases of Wilms' tumor may explain the rarity of the bilateral form in later years. Early diagnosis is difficult because of the nonspecificity of signs and symptoms. Computer tomography, ultrasonography, and arteriography are important modalities in the earlier diagnosis of adult Wilms' tumor. Because of the rarity of these tumors, no definitive guidelines for treatment have emerged. However, a multidisciplinary approach incorporating surgery, chemotherapy and/or radiation therapy has been used most often but with varying success. This report documents the second case of bilateral adult Wilms' tumor presenting as perinephric hematomas which partially resolved.

Female↗
PubMed1987

A first-year medical school pilot program for early clinical exposure.

A weekly out-patient elective in a medical oncology clinic was established for first- and some second-year medical students. Interviews were carried out immediately after the elective experience and two years later to evaluate the degree of success in achieving specific goals in this elective. Such clinical experience appeared to introduce the medical students to some of the major medical and psychosocial issues involved in the clinical care of patients, to be highly motivating for the students with regard to their standard concurrent basic science curriculum, and to relieve the impatience that first-year medical students have for clinical exposure. The usefulness of the elective, as perceived by the participating students, appeared to increase from the first to the second interview, that is as the students entered the clinical teaching program. The clinical setting was perceived by the students as more useful than either their increased understanding of medicine or observation of physicians as role models. The students' perception and understanding of physician-patient communication, and of the problems facing an oncology patient, appeared to be more favorably influenced than increasing confidence in the ability of the student to deal with patient interaction. Thus, a clinical oncology out-patient experience for first-year medical students appears to be sufficiently rewarding to justify the time and effort to develop such an elective.

Clinical Medicine↗
PubMed1985

In vivo and in vitro inhibition of B16 melanoma growth by vitamin B6.

The effect of vitamin B6 on the growth of B16 melanoma cells in vivo and in vitro was studied. B16 melanoma cells grown for three days in medium supplemented with 5.0 mM pyridoxine or 0.5 mM pyridoxal showed an 80% reduction in cell proliferation compared with control culture. Cells cultured for six hours in medium supplemented with 0.5 mM pyridoxal took up and incorporated 13 and 32% less [3H]thymidine, respectively, than did control cultures. A 17% reduction in [3H]glucose uptake was observed at this time point. When the incubation time was decreased to three hours, an inhibition of cellular uptake of [3H]thymidine (22%), [3H]uridine (14%), and [3H]glucose (15%) was observed; however, little or no inhibition in incorporation was detected. In in vivo studies, mice pretreated with pyridoxal for two weeks and then injected with B16 melanoma cells had a 62% reduction in tumor weight compared with controls at the end of a three-week period. If tumors were first established in mice and then treated with pyridoxal for six days, a 39% reduction in tumor growth was observed. There were no differences observed in body weights or liver weights in any of the animal groups. These results indicate that supraphysiological doses of vitamin B6 can inhibit the growth of B16 melanoma cells both in vitro and in vivo. The exact mechanism by which pyridoxal exerts its inhibitory effect was not ascertained, but experiments suggest that the vitamer may be acting on the plasma membrane to reduce precursor transport into the cell.

Adenosine Triphosphate↗
PubMed1985

Thrombotic thrombocytopenic purpura.

This serious disorder of young adults is characterized by fever, hemolytic anemia, hemorrhagic signs, various neurologic abnormalities and renal dysfunction. Laboratory findings include a negative Coombs' test for hemolytic anemia, severe thrombocytopenia, and fragmented erythrocytes on the peripheral blood smear. Without treatment, mortality may exceed 80 percent. Early diagnosis and prompt therapy with high-dose corticosteroids and antiplatelet agents, as well as exchange plasmapheresis when indicated, bring about remission in 60 to 80 percent of patients.

Adrenal Cortex Hormones↗
PubMed1985

Suppression of DNA synthesis in NEL-M1 human melanoma cells by triamcinolone acetonide.

The present study characterizes the biological response of a cloned human melanotic melanoma cell line (NEL-M1) to glucocorticoid treatment. Scatchard analysis of the binding of [3H]-triamcinolone acetonide to the glucocorticoid receptor showed a binding capacity of 170 fmol/mg protein and a dissociation constant (KD) of 1.76 X 10(-9) M. When the 3H-labeled cytosol was warmed to 25 degrees C for 30 min and then incubated with DNA-cellulose at 4 degrees C for 45 min, 32% of the specific glucocorticoid-receptor complexes were bound to DNA-cellulose. Additional studies showed that when NEL-M1 cells were cultured for 72 h with 1 X 10(-7) M triamcinolone acetonide, a 36% reduction in cellular growth was observed compared to the control cultures. The calculated population doubling time for the control cells was 17.5 h compared to 20.3 h for the triamcinolone acetonide-treated cells. Analysis of the effect of triamcinolone acetonide on macromolecular synthesis revealed that, over a 24-h incubation period, triamcinolone acetonide (a) inhibited [3H]thymidine incorporation by 51%; (b) increased the incorporation of the melanin precursor, L-3,4-dihydroxy[3H]phenylalanine, by 59%; and (c) had essentially no effect on [3H]leucine or [3H]uridine incorporation. During this same incubation period, triamcinolone acetonide inhibited [3H]glucose uptake by 19%. Further studies using synchronized NEL-M1 cells clearly show that the earliest detectable action of triamcinolone acetonide was the inhibition [3H]thymidine incorporation during the S phase of the cell cycle. Thus, these findings show that the human melanoma cell line, NEL-M1, is biologically responsive to glucocorticoid treatment. Continued studies using NEL-M1 cells may eventually lead to ascertaining the exact mechanism by which glucocorticoids regulate DNA synthesis.

Cells, Cultured↗
PubMed1984

Mitoxantrone.

Explore the source record for details and available documents.

Animals↗
PubMed1984

Effect of triamcinolone acetonide on tyrosinase activity in a human melanoma cell line.

The synthetic glucocorticoid, triamcinolone acetonide, was found to increase melanogenesis in the human melanoma cell line NEL. Treatment of NEL cells for 24 hr with triamcinolone acetonide (1 X 10(-7) M) increased the activity of the enzyme tyrosinase by 43% and the incorporation of the melanin precursor, L-3,4-dihydroxyphenylalanine, by 23%. Additional studies revealed no change in cyclic AMP levels over an 18-hr test period. A 2-hr preincubation of NEL cells with actinomycin D (10 micrograms/ml) prevented the increase in tyrosinase activity by triamcinolone acetonide. When triamcinolone acetonide was added to a synchronized population of NEL cells, an increase in tyrosinase activity was observed at 16 hr, coinciding with the late S phase of the cell cycle. These results suggest that glucocorticoids are involved in the regulation of melanogenesis in NEL cells by increasing the activity of the rate-controlling enzyme tyrosinase.

Carbon Radioisotopes↗
PubMed1984

Halo nevi and melanoma.

Halo nevi may be associated with occult melanoma or may signify melanoma in a remote location. When a single halo nevus is present, the lesion should be biopsied to exclude melanoma. In addition, the patient's entire skin surface should be examined, and a careful ophthalmologic examination should be performed to exclude intraocular melanoma. Although the pathophysiologic relationship of halo nevus to melanoma is unclear, immunologic mechanisms have been postulated.

Adult↗
PubMed1983

High-dose pyridoxal supplemented culture medium inhibits the growth of a human malignant melanoma cell line.

The in vitro growth characteristics of a human malignant melanoma cell line cultured in 0.5 mM pyridoxal supplemented medium were studied. Experimentation revealed that the high-dose pyridoxal supplemented medium severely inhibited the growth of melanoma cells over a 72-hour growth period. Additional experimentation showed that cells cultured for 6 hours in the pyridoxal supplemented medium took up 25% less and incorporated 20% less [3H]uridine than control cultures. [3H]Glucose uptake was reduced by 23% at this time point. [3H]Thymidine uptake was inhibited by 12%, but no inhibition was detected in [3H]thymidine incorporation. When the vitamin B6 antagonist 4-deoxypyridoxine (which competes with pyridoxal for pyridoxal kinase) was added to the pyridoxal supplemented medium, the inhibition in [3H]uridine incorporation was reduced from 19% to 6%. However, 4-deoxypyridoxine did not reverse the inhibition of [3H]uridine uptake. These results indicate that pyridoxal and its metabolite, pyridoxal 5'-phosphate, may be involved in the growth regulation of a human malignant melanoma cell line.

Cell Division↗
PubMed1983

In vitro growth inhibition of human malignant melanoma cells by glucocorticoids.

The human malignant melanoma cell line, NEL, was found to contain glucocorticoid receptors. When the binding data were analyzed according to the method of Scatchard, results indicated a ligand binding capacity of 247 fmol/mg protein and a Kd of 1 X 10(-9) M. Additional studies show that the continuous incubation of NEL cells with triamcinolone acetonide (TA) for 72 hr results in a 30% inhibition in cell growth. To ascertain the mechanism by which glucocorticoids inhibit the growth of NEL cells, uptake and incorporation studies were carried out using various 3H precursors. Results indicate that, after 4 hr of TA treatment, a modest inhibition in [3H]thymidine uptake was observed, while stimulation of [3H]thymidine incorporation was noted at all steroid concentrations tested. However, cells incubated for 18 hr with TA (concentration, greater than or equal to 10(-8) M) showed a 30% decrease in the amount of [3H]thymidine incorporated into DNA. TA had no effect on [3H]leucine or [3H]glucose uptake after 4 hr of treatment but did inhibit [3H]glucose (42%) uptake after 18 hr of treatment. A slight stimulation (9%) in [3H]leucine incorporation was observed at this time point. When NEL cells were incubated with TA and the antiglucocorticoid, progesterone, the inhibition in [3H]thymidine incorporation was negated. These findings indicate that glucocorticoids exert some influence on the growth of human melanoma cells, and this effect is mediated through the glucocorticoid receptor.

Cell Division↗
PubMed1981

Vinblastine, infusion, bleomycin, and cis-dichlorodiammine-platinum chemotherapy in metastatic melanoma.

A chemotherapy regimen containing vinblastine-bleomycin-platinum has been studied in 42 patients with advanced malignant melanoma. Forty-seven percent of evaluable and 43% of all patients experienced objective response. Complete responses were seen in visceral sites. Median duration of response has not been reached but will exceed 26 weeks. Toxicity is predominantly marrow suppressive, gastrointestinal, pulmonary, and mucocutaneous. Pulmonary toxicity was never severe when bleomycin dose was limited to less than 300 mg/m2 body surface area. Half of the patients relapsed with CNS metastases as a first presenting sign of recurrence. Because hospitalization is required in this program its dollar cost is high.

Adolescent↗
PubMed1981

Radiation therapy of malignant melanomas: an evaluation of clinically used fractionation schemes.

To assess the importance of radiation dose fraction size in the treatment of malignant melanomas, the records of 48 patients (83 sites) treated at Tufts-New England Medical Center from 1971 to 1979 have been retrospectively reviewed. During this period, the dose fractionation schemes evolved from standard fraction size to large-dose techniques. Radiation fraction size was observed to be the major factor in the clinical response of melanoma. Fractions of 600-800 rad resulted in the best overall response (80%). The rapid fractionation scheme of 800-400-400 rad on successive days resulted in intermediate response (58%) and may be useful for the palliative treatment of selected patients.

Dose-Response Relationship, Radiation↗