879: PD-L1 (B7-H1) Expression by Urothelial Carcinoma of the Bladder and BCG-Induced Granulomata: Associations with Localized Stage Progression

Inman, Brant A.; Sebo, Thomas J.; Frigola, Xavier; Dong, Haidong; Bergstralh, Eric J.; Fradet, Yves; Lacombe, Louis; Kwon, Eugene D.

doi:10.1016/s0022-5347(18)31107-8

Cited by 87 publications

(121 citation statements)

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“…Perhaps this difference in cytokine production is due to the fact that PD-1 typically has greater effects on cytokine production than on cellular proliferation, with significant effects on IFN-c, tumor-necrosis factora and IL-2 production. 21 Another possible explanation is that, in addition to PD-1 upregulation in CD8 1 T cells, higher PD-L1 expression in tumor cells [16][17][18] not in PBMCs, may also have contributed to impaired CD8 1 T-cell function. As a result, it is possible that the PD-1/PD-L1 pathway may have greater effects on CD8 1 T cells in a tumor setting than on peripheral blood CD8 1 T cells.…”

Section: Discussionmentioning

confidence: 99%

“…[6][7][8][9] Involvement of the PD-1 pathway has also been shown during hepatitis B and C virus infection [10][11][12][13] with PD-L1 expression demonstrated in situ on a wide variety of solid tumors including pancreas, lung, ovarian and bladder tumors. [14][15][16][17][18] Studies relating PD-L1 expression on tumors to disease outcome show that PD-L1 expression strongly correlates with unfavorable prognosis in kidney, bladder, gastric and pancreatic cancer. [16][17][18] Such studies indicate that the PD-1/PD-L1 pathway may also play a role in tumor immunity.…”

Section: Introductionmentioning

confidence: 99%

“…[14][15][16][17][18] Studies relating PD-L1 expression on tumors to disease outcome show that PD-L1 expression strongly correlates with unfavorable prognosis in kidney, bladder, gastric and pancreatic cancer. [16][17][18] Such studies indicate that the PD-1/PD-L1 pathway may also play a role in tumor immunity.…”

Section: Introductionmentioning

confidence: 99%

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Programmed death-1 upregulation is correlated with dysfunction of tumor-infiltrating CD8+ T lymphocytes in human non-small cell lung cancer

et al. 2010

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T-cell tolerance is an important mechanism for tumor escape, but the molecular pathways involved in T-cell tolerance remain poorly understood. It remains unknown whether the inhibitory immunoreceptor programmed death-1 (PD-1) plays a role in conditions of human non-small cell lung cancer (NSCLC). In this study, we detected PD-1 expression on CD8 1 T cells from healthy control peripheral blood mononuclear cells (PBMCs) and the PBMCs of NSCLC patients as well as NSCLC tissues. Results showed that tumor-infiltrating CD8 1 T cells had increased PD-1 expression and impaired immune function, including reducing cytokine production capability and impairing capacity to proliferate. Blockade of the PD-1/PD-L1 pathway by the PD-L1-specific antibody partially restored cytokine production and cell proliferation. These data provide direct evidence that the PD-1/PD-L1 pathway is involved in CD8 1 T-cell dysfunction in NSCLC patients. Moreover, blocking this pathway provides a potential therapy target in lung cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Programmed death-1 upregulation is correlated with dysfunction of tumor-infiltrating CD8+ T lymphocytes in human non-small cell lung cancer

et al. 2010

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“…The most frequently altered pathways in bladder cancer include the PI3K/AKT/mammalian target of rapamycin pathway [96,[119][120][121], the FGFR3/RAF/RAS pathway, the TP53/RB1 pathway, immune response checkpoint modulators [122,123], and chromatin-regulating and -remodelling genes [124][125][126]. In general, mutations along a given pathway are mutually exclusive.…”

Section: Genomics Of Urothelial Carcinomamentioning

confidence: 99%

The 2016 WHO Classification of Tumours of the Urinary System and Male Genital Organs—Part B: Prostate and Bladder Tumours

et al. 2016

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It has been 12 yr since the publication of the last World Health Organization (WHO) classification of tumours of the prostate and bladder. During this time, significant new knowledge has been generated about the pathology and genetics of these tumours. Intraductal carcinoma of the prostate is a newly recognized entity in the 2016 WHO classification. In most cases, it represents intraductal spread of aggressive prostatic carcinoma and should be separated from high-grade prostatic intraepithelial neoplasia. New acinar adenocarcinoma variants are microcystic adenocarcinoma and pleomorphic giant cell adenocarcinoma. Modifications to the Gleason grading system are incorporated into the 2016 WHO section on grading of prostate cancer, and it is recommended that the percentage of pattern 4 should be reported for Gleason score 7. The new WHO classification further recommends the recently developed prostate cancer grade grouping with five grade groups. For bladder cancer, the 2016 WHO classification continues to recommend the 1997 International Society of Urological Pathology grading classification. Newly described or better defined noninvasive urothelial lesions include urothelial dysplasia and urothelial proliferation of uncertain malignant potential, which is frequently identified in patients with a prior history of urothelial carcinoma. Invasive urothelial carcinoma with divergent differentiation refers to tumours with some percentage of "usual type" urothelial carcinoma combined with other morphologies. Pathologists should mention the percentage of divergent histologies in the pathology report. PATIENT SUMMARY Intraductal carcinoma of the prostate is a newly recognized entity in the 2016 World Health Organization classification. Better defined noninvasive urothelial lesions include urothelial dysplasia and urothelial proliferation of uncertain malignant potential. v a i l a b l e a t w w w . s c i e n c e d i r e c t . c o m j AbstractIt has been 12 yr since the publication of the last World Health Organization (WHO) classification of tumours of the prostate and bladder. During this time, significant new knowledge has been generated about the pathology and genetics of these tumours.

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“…17 Previous studies have demonstrated that PD-1/PD-L interaction inhibits T-cell growth and cytokine secretion 18 and that tumor cell-borne PD-L1 induces the apoptosis of tumor-specific T-cell clones in vitro, 19 suggesting the potential involvement of PD-Ls in tumor immunity. The expression of PD-L1 in tumors has been reported in melanoma 19,20 ; in cancers of the lung, 19 breast, 21 ovary, 22 kidney, 23 pancreas, 24 esophageus, 25 and bladder 26 ; and even in adult T-cell leukemia/lymphoma. 27 In addition, the involvement of PD-L1 has been demonstrated in the protection of cancer cells from cell lysis by activated T lymphocytes.…”

mentioning

confidence: 99%

Tumor cell expression of programmed cell death‐1 ligand 1 is a prognostic factor for malignant melanoma

Hino

Kabashima

Kato

et al. 2010

Cancer

607

419

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BACKGROUND: Melanoma tends to be refractory to various immunotherapies because of tumor-induced immunosuppression. To investigate the mechanism underlining the immunosuppression of melanoma patients, the authors focused on programmed cell death-1 (PD-1)/PD-1 ligand 1 (PD-L1) interaction between tumor cells and T cells. METHODS: Melanoma specimens were collected from 59 primary tumors, 16 lymph nodes, and 4 lesions of in-transit metastasis. Specimens stained with anti-PD-L1 monoclonal antibodies were digitalized to jpg files. To evaluate the intensity of PD-L1 expression, histograms were used, and the red density (RD) was measured. PD-1 expression on T cells was analyzed in blood samples from 10 patients who had stage IV melanoma and in 4 samples of in-transit metastases. RESULTS: Twenty-five patients comprised the ''low'' PD-L1 expression group (RD value, <90), and 34 patients comprised the ''high'' group (RD value, !90). Breslow tumor thickness in the high-expression group was significantly higher than in the low-expression group. Univariate and multivariate analyses revealed that the overall survival rate of the high-expression group was significantly lower than that of the low-expression group. In all patients with stage IV disease who were examined, both CD8-positive and CD4-positive T cells had significantly higher PD-1 expression levels in the peripheral blood. Tumor-infiltrating T cells expressed high levels of PD-1, and its expression was elevated further during the clinical course. CONCLUSIONS: The current results indicated that there is a correlation between the degree of PD-L1 expression and the vertical growth of primary tumors in melanoma. Multivariate analysis demonstrated that PD-L1 expression is an independent prognostic factor for melanoma. Cancer 2010;116:1757-66.

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879: PD-L1 (B7-H1) Expression by Urothelial Carcinoma of the Bladder and BCG-Induced Granulomata: Associations with Localized Stage Progression

Cited by 87 publications

References 0 publications

Programmed death-1 upregulation is correlated with dysfunction of tumor-infiltrating CD8+ T lymphocytes in human non-small cell lung cancer

Programmed death-1 upregulation is correlated with dysfunction of tumor-infiltrating CD8+ T lymphocytes in human non-small cell lung cancer

The 2016 WHO Classification of Tumours of the Urinary System and Male Genital Organs—Part B: Prostate and Bladder Tumours

Tumor cell expression of programmed cell death‐1 ligand 1 is a prognostic factor for malignant melanoma

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