Escape of human solid tumors from T-cell recognition: molecular mechanisms and functional significance.

By F. Marincola, E. Jaffee, D. Hicklin, S. Ferrone. Advances in Immunology, 2000

1,238 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/61f1c483df903862c1cb275d24a2a40cb2bfa33c

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Citations in the corpus

Interferons, immunity and cancer immunoediting (2006, background): “In addition, many tumours that lack expression of immunologically relevant genes that are regulated by IFNs — such as MHC molecules, TAP1 (transporter associated with antigen processing 1) and LMP2 (low-molecular-mass protein 2) — have been identifie”
Genetics and biology of prostate cancer (2018, background): “…β-2 microglobulin that is involved in human leukocyte antigen class I folding and transport, or the major histocompatibility complex itself (Marincola et al. 2000; Sucker et al. 2014); these defects contribute to the lack of T-cell responses observed in patients with primary resistance…”
Human T-lymphocyte cytotoxicity and proliferation directed by a single chimeric TCRζ /CD28 receptor (2002, background): “Furthermore, malignant cells may escape from tumor-specific effector T cells by downregulating major histocompatibility complex (MHC) and/or antigen expression, or by establishing an immunosuppressive microenvironmen”
Selective cytotoxic T-lymphocyte targeting of tumor immune escape variants (2006, background): “Indeed, impairment of TAP is frequently observed in human cancer”
Inhibition of indoleamine 2,3-dioxygenase, an immunoregulatory target of the cancer suppression gene Bin1, potentiates cancer chemotherapy (2005, background): “To survive in this environment, however, cancer cells expressing recognizable tumor antigens must evolve strategies to thwart immune detection and destructio”
Interaction of PD-L1 on tumor cells with PD-1 on tumor-specific T cells as a mechanism of immune evasion: implications for tumor immunotherapy (2005, background): “Initial work has shown that most human tumors express tumor-associated antigens (TAAs) that can be recognized by T cells and thus are potentially capable of inducing immune responses [8].”
Cancer immunotherapy: moving beyond current vaccines (2004, background): “Inadequate numbers or avidity of the immune cells, the inability of the tumor to activate quiescent or precursor lymphocytes, tolerance mechanisms including anergy, and suppressor influences produced by the tumor or the immune system itself are among the mechanisms that can prevent tumor destruction”
Mechanisms of resistance to immune checkpoint inhibitors (2018, background): “…which can be thought of in three simple categories: (1) insufficient generation of anti-tumour T cells, (2) inadequate function of tumour-specific T cells (Marincola et al, 2000; Bronte et al, 2005), or (3) impaired formation of T-cell memory (O’Donnell et al, 2017; Sharma et al, 2017) (Figure 1).”
Mechanisms of immune evasion by tumors. (2006, background): “of tumor types, such as breast cancer, prostate cancer, and lung cancer (Cabrera et al., 1996, 1998; Esteban et al., 1989, 1990, 1996; Ferrone and Marincola, 1995; Marincola et al., 2000; Natali et al., 1983, 1984, 1985, 1989; Perez et al., 1986; Ruiz‐Cabello et al., 1989, 1991; van den Ingh et al.,”
Evidence for a tumoral immune resistance mechanism based on tryptophan degradation by indoleamine 2,3-dioxygenase (2003, background): “Pharmacological inhibition of IDO IDO expression is not the only mechanism by which tumors can resist immune rejectio”