Publications by authors named "E Gugel"

Article Synopsis
  • Co-mutations are linked to worse survival outcomes in various solid tumors, particularly for patients with -mutated advanced non-small cell lung cancer (aNSCLC).
  • A study analyzing data from 356 -mutated aNSCLC patients found that those with co-mutations had significantly shorter progression-free and overall survival compared to those without co-mutations.
  • The negative impact of co-mutations on survival was consistent across different treatment groups, especially among patients receiving first-line targeted therapy.
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Rabbits experimentally infected with HTLV-I and HIV-1 produced antibody to various viral proteins, and viral DNA could be detected by gene amplification using the polymerase chain reaction. HTLV-I genes were detected in cell lines derived from infected rabbits, and in some cases, both HIV-1 and HTLV-I DNA sequences were demonstrated in peripheral blood cells taken from rabbits one year after experimental infection. The polymerase chain reaction procedure was used to demonstrate the presence of HTLV-I gag, env and tax genes and HIV-1 gag and env genes.

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Injection of rabbits with a human T cell line infected with HIV-1 caused seroconversion within 6 wk, and HIV-1 could be isolated from PBL cultures of infected rabbits. Identity of the isolated virus with HIV-1 was shown by analysis of products amplified by the polymerase chain reaction. HIV-1 infection was seen in rabbits injected with HIV-1-infected cells alone as well as in those that were first infected with HTLV-1 and subsequently with HIV-1.

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Although intercellular adhesion molecule-1 (ICAM-1) has been implicated as a ligand in some LFA-1-dependent adhesion, its importance to T cell function has not been established. The present studies investigate the importance of ICAM-1 for human cytotoxic T lymphocytes (CTL), both in their formation of antigen-independent conjugates (AIC) and in their lysis of targets. Analysis of monoclonal antibody (mAb) inhibition of AIC formation indicate that ICAM-1 mAb 1 blocks (a) AIC formation with some but not all targets; (b) the LFA-1 pathway but not the CD2/LFA-3 pathway of adhesion; (c) by binding to the target cell, not the T cell.

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