Inhibitory B7-family molecules in the tumour microenvironment

By W. Zou, Lieping Chen. Nature reviews. Immunology, 2008

1,594 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/d737141e2abe50b3422f96fe9006f0014a5d8be7

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. Lieping Chen
2. W. Zou
3. J. Wolchok
4. D. Pardoll
5. S. Topalian
6. Janis Taube
7. E. Buchbinder
8. Anupam M. Desai

In Oncology

1. Lieping Chen
2. J. Wolchok
3. W. Zou
4. D. Pardoll
5. Razelle Kurzrock
6. S. Topalian
7. Janis Taube
8. E. Buchbinder

Citations in the corpus

• CTLA-4 and PD-1 Pathways (2016, background): “PD-L1 expression on tumor cells varies by tumor type and also within a given tumor type, but appears to be particularly abundant in melanoma, non– small cell lung cancer (NSCLC), and ovarian cancer.(27,28,47) In a recent study, PD-L1 expression on tumor cells was shown to be significantly associated”
• Immunology and Immunotherapy of Head and Neck Cancer. (2015, background): “The ligand for PD-1, PD-L1 (B7-H1, CD274), is upregulated in multiple tumor cell lines, including HNSCC,(25) and induces a loss of function of cytotoxic T lymphocytes (CTLs).(26) CTLA-4 is a member of the B7 receptor family expressed by CD4 , CD8 , and Tregs(27) and competes with CD28 to bind to sti”
• Safety and Efficacy of Durvalumab (MEDI4736), an Anti-Programmed Cell Death Ligand-1 Immune Checkpoint Inhibitor, in Patients With Advanced Urothelial Bladder Cancer. (2016, background): “Previous reports from this study in other tumor types demonstrated that durvalumab has a tolerable safety profile and durable antitumor activity.20–22 Herein, we report safety and efficacy of durvalumab in the expansion cohort of patients with UBC.”
• T cell anergy, exhaustion, senescence and stemness in the tumor microenvironment (2013, background): “with low-to-absent expression of B7-1 (CD80) and B7-2 (CD86) [7,8,9 ,10] (Figure 2).”
• Long-term Clinical Outcomes and Biomarker Analyses of Atezolizumab Therapy for Patients With Metastatic Triple-Negative Breast Cancer: A Phase 1 Study (2019, neutral): “(%) [95% CI] 5 (24) [8-47] 10 (11) [5-19] 0 [0-17] 15 (16) [10-26]”
• Colocalization of Inflammatory Response with B7-H1 Expression in Human Melanocytic Lesions Supports an Adaptive Resistance Mechanism of Immune Escape (2012, background): “The B7 Homolog One (B7-H1, also called PD-L1) protein is not detectable in most normal tissues (5, 15–17); however, its expression can be induced to a high level in various cell types by proinflammatory cytokines, particularly interferon-g (IFN-g) (5, 18), and B7-H1 is highly expressed on many human”
• Tumor-infiltrating NY-ESO-1–specific CD8+ T cells are negatively regulated by LAG-3 and PD-1 in human ovarian cancer (2010, background): “These findings are of considerable in vivo significance because expression of PD-L1, the ligand for PD-1, has been observed in ovarian and other human cancers (9, 22).”
• PD-L1 Expression as a Predictive Biomarker in Cancer Immunotherapy (2015, background): “Tumor PD-L1 overexpression confers a poorer prognosis across multiple tumor histologies, making therapeutic intervention on this immunomodulatory axis enticing (24),(25),(26).”
• Targeting the PD-1/B7-H1(PD-L1) pathway to activate anti-tumor immunity (2012, neutral): “The finding that B7-H1/PD-L1 is commonly up-regulated on many different tumor types, where it inhibits local anti-tumor T cell responses [19,20], and that PD-1 is expressed on the majority of tumor infiltrating lymphocytes [21,22] creates an important rationale for mAb blockade of this pathway for c”
• The B7 family member B7-H6 is a tumor cell ligand for the activating natural killer cell receptor NKp30 in humans (2009, background): “Indeed, recent studies have shown that human and rodent cancer cells up-regulate expression of B7 molecules, such as B7-H1, 4IgB7-H3, and B7-H4, but this expression has been proposed to contribute to tumor immune evasion by engaging inhibitory receptors (Castriconi et al., 2004; Zou and Chen, 2008).”
• PD-1 and PD-L1 Checkpoint Signaling Inhibition for Cancer Immunotherapy: Mechanism, Combinations, and Clinical Outcome (2017, background): “Therefore, the function of a tumor overexpressing PD-L1 is to protect itself from cytotoxic T cell (CD8+) mediated cell killing (Zou and Chen, 2008).”