Expression of E6 and E7 in human cervical carcinoma cell lines and of HBx in hepatocellular carcinoma cell line by Western blot and effect of MG132 proteasome inhibitor treatment on the levels of E6, E7 and HBx in these cell lines:

<p>a) E6 from protein extracts of CasKi cells treated with MG132 for 3 hrs; b) E7 from protein extracts of CasKi cells treated with MG132 for 3 hrs; c) E6 from protein extracts of CasKi cells treated with MG132 for 6 hrs; d) E7 from protein extracts of SiHa cells treated with MG132 for 3 hrs; e) E7 from protein extracts of HeLa S3 cells treated with MG132 for 3 hrs; f) HBX from protein extracts of Hep 3B2.1-7 cells treated with MG132 for 3 hrs.</p

Radioimmunotherapy of Hep 3B2.1-7 tumors in nude mice:

<p>a) changes in tumor volume; b) control untreated mouse; c) mouse treated with 600 µCi ¹⁸⁸Re-4H9 mAb. Both mice shown on Day 18 post-treatment. In b and c lower panels show H&E stained tumors at the completion of the experiment.</p

Scintigraphic images of tumor-bearing mice 24 hours post-injection with: a) CasKi tumor, E6-specific mAb ¹⁸⁸Re-C1P5 mAb; b) CasKi tumor, control ¹⁸⁸Re-18B7 mAb; c) Hep 3B2.1-7 and A2058 human metastatic melanoma tumors, HBx-specific ¹⁸⁸Re-4H9 mAb.

<p>Scintigraphic images of tumor-bearing mice 24 hours post-injection with: a) CasKi tumor, E6-specific mAb ¹⁸⁸Re-C1P5 mAb; b) CasKi tumor, control ¹⁸⁸Re-18B7 mAb; c) Hep 3B2.1-7 and A2058 human metastatic melanoma tumors, HBx-specific ¹⁸⁸Re-4H9 mAb.</p

Detection of viral antigens in tumor cells and in tumors:

<p>a, b) immunofluorescence of fixed and permeabilized tumor cells. Left panels show light microscopy images of the cells. Heavily damaged cells are marked with arrows. Right panels show immunofluorescent images of the same slides treated with viral protein-specific mAbs followed by FTIC-conjugated polyclonal antibody to mouse IgGs: a–CasKi cells and E6-specific C1P5 mAb, b-Hep 3B2.1-7 cells and HBx-specific 4H9 mAb; c) immunohistochemistry of CasKi tumors. Left panel shows binding of E6-specific mAb C1P5. Right panel shows absence of binding of control mAb 18B7; d) western blot of Hep 3B2.1-7 tumor with HBx-specific mAb 4H9.</p

Radioimmunotherapy of CasKi tumors in nude mice:

<p>a) changes in tumor volume; b) mouse treated with 350 µCi ¹⁸⁸Re-C1P5 mAb; c) control mouse (both mice shown on Day 20 post-treatment).</p

Peripheral blood platelet counts from SCID mice used in (a) splenic and (b) peritoneal HIV models and treated with ²¹³Bi-2556 and control mAbs.

<p>Peripheral blood platelet counts from SCID mice used in (a) splenic and (b) peritoneal HIV models and treated with ²¹³Bi-2556 and control mAbs.</p

Targeting and killing of HIV-infected cells in vitro with ²¹³Bi-2556 mAb.

<p>a) binding of “cold” 2556 to chronically-infected ACH-2 cells by flow cytometry. HIV-1-negative A3.01 cells were used as controls; b) killing of HIV-infected hPBMCs with ²¹³Bi-2556 mAb. 246D is an anti-gp41 mAb and 1418 is a negative control; c) killing of chronically-infected ACH-2 cells with ²¹³Bi-2556 mAb. Stimulated - PMA stimulated ACH-2 cells, unstimulated – unstimulated ACH-2 cells. The unlabeled antibodies were present in the same amounts as the radiolabeled antibodies.</p

Immunoreactivity of ²¹³Bi-2556 mAb for gp41 and determination of its K_a by Scatchard analysis.

<p>a) gp41 ELISA of 2556 mAb radiolabeled with high specific activity ²¹³Bi (5 mCi/mg). Binding of ²¹³Bi-2556 to gp41 was compared to that of unlabeled 2556 mAb with (2556-CHXA″) or without (2556 standard) attached CHXA″ ligand. ²¹³Bi-2556 was stored with human serum albumin (HAS) radioprotector (2556-Bi/HAS) or without it (2556-Bi); b) Scatchard plot of ²¹³Bi-labeled 2556 and 246D mAbs binding to HIV-infected hPBMCs.</p

RT-PCR data for two HIV-1 mouse models used in RIT experiments with ²¹³Bi-2556 mAb.

<p>a) splenic model (mice given HIV-1 infected hPBMCs intrasplenically); b) peritoneal model (mice given non-infected hPBMCs followed by i.p. challenge with HIV). “Cold” 2556 – unlabeled 2556; 1418 – isotype-matching irrelevant control.</p

Characterization of 2556 mAb specificity and selectivity.

<p>a) inhibition of binding of biotinylated anti-gp41 mAbs to JR-CSF transfected 293T cells by serum from HIV-1 infected individuals; b) binding of human anti-gp41 mAbs to recombinant gp41_MN protein; c) ELISA reactivity to recombinant gp41_MN of 2556 CHROMOS (made by ACE system) and 2556 (in house) derived from original NYU hybridoma. 246D is an anti-gp41 mAb and 1418 is a negative control.</p