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Biomedical subjects

R Baumal

Publications and source records attributed to R Baumal.

167 records · Page 10Linked to original sources
PubMedDate not supplied

Comparison of growth inhibition of a human ovarian adenocarcinoma cell line by free monoclonal antibodies and their corresponding antibody-recombinant ricin A chain immunotoxins.

Four mouse monoclonal antibodies (mAb) (8C, IgG2a; M2A, IgG2a; M2D, IgG2b; 10B, IgG1) directed against the human ovarian adenocarcinoma cell line HEY were compared for their ability in the free form and as immunotoxins made with recombinant ricin A chain (rRA) to inhibit the growth of HEY cells. For in vitro studies cultured HEY cells were assayed for protein synthesis and plated in agarose to form colonies, and for in vivo studies they were injected intraperitoneally (i.p.) into BALB/c nu/nu (nude) mice at a challenge dose (3 X 10(5) cells) which produced carcinomatosis with ascites, leading to death 30 days following injection. In the free form, mAB 8C was the most potent in inhibiting colony formation in the complement (C)-mediated and ADCC (antibody-dependent cell-mediated cytoxicity) assays in vitro. This mAb was also the only one capable of prolonging survival of mice, both in tumor cell neutralization, and tumor growth inhibition experiments. The four mAb-rRA immunotoxins were effective in inhibiting protein synthesis in vitro in the presence of 10(-7) M monensin. However, in vivo, only 8C-rRA and M2A-rRA were capable of prolonging survival of mice in tumor growth inhibition experiments. Our results suggest that mAb 8C might be useful in the free form and as an 8C-rRA immunotoxin for i.p. immunotherapy of ovarian cancer.

Adenocarcinoma↗
PubMedDate not supplied

IgA nephropathy: Henoch-Schönlein purpura and Berger's disease in one patient.

A patient is described who had an attack of Henoch-Schönlein purpura with no renal dysfunction at 4 years of age. She recovered with conservative management. There were no further episodes of Henoch-Schönlein purpura and her urinalysis remained normal for the next 11 years. At age 15, she developed repeated bouts of gross hematuria and proteinuria, and a renal biopsy was performed 3 years later. Light microscopy showed mesangial proliferative glomerulonephritis with granular, mesangial deposits of IgA by immunofluorescence and numerous, electron-dense deposits in mesangial regions by electron microscopy. These findings were consistent with a diagnosis of Berger's disease. The occurrence of Henoch-Schönlein purpura at 4 years and Berger's disease at 15 years in the same patient suggests that these two conditions are related.

Adolescent↗
PubMedDate not supplied

Inhibition of protein synthesis by monoclonal anti-idiotypic antibody-ricin A chain conjugates in MOPC 315 myeloma cells.

Three monoclonal antiidiotypic antibodies (AIA) to MOPC 315 IgA, G3 (IgG2b), A2 (IgG1) and D10 (a hybrid molecule consisting of gamma 1 and gamma 2a heavy chains), were characterized with respect to their binding constants (Ka) to MOPC 315 mouse myeloma cells. The Ka of G3 and A2 was 10(8)/mole; and that of D10 was 3 X 10(7)/mole. The AIA did not bind to a non-immunoglobulin (Ig) producing subclone of MOPC 315 cells (MOPC 315.36). Immunotoxins derived by conjugating ricin A chain (RTA) to G3 and A2 but not to D10 preferentially inhibited protein synthesis in MOPC 315 over MOPC 315.36 cells. These results suggest that the effectiveness of these immunotoxins assessed on the basis of their targeted cytotoxicity against MOPC 315 cells was dependent on the Ka but not on the Ig subclass of the AIA component of the immunotoxin.

Animals↗
PubMedDate not supplied

Cellular handling of a monoclonal anti-idiotypic antibody in IgA-producing MOPC 315 mouse myeloma cells.

MOPC 315 mouse myeloma cells which produce an IgA (alpha, lambda 2) with dinitrophenol (DNP)-binding capacity were incubated with a [125I]-labeled monoclonal anti-idiotypic antibody (AIA) (D10) to MOPC 315 IgA. AIA D10 bound specifically to the surface of MOPC 315 cells (binding constant 3.0 X 10(7)/mole) but not to cells of a derivative clone which did not produce IgA. Following binding, D10 was taken up intracellularly and localized in a subcellular fraction which sedimented in a Percoll gradient on the light side of the main lysosomal peak. These results indicate that monoclonal AIA to MOPC 315 IgA is selectively bound and internalized by MOPC 315 myeloma cells.

Animals↗