Minimal Recruitment and Activation of Dendritic Cells Within Renal Cell Carcinoma

Troy, Andrew; Summers, Kelly L.; Davidson, Peter; Ch, Atkinson; Hart, Derek N. J.

doi:10.1097/00005392-199905000-00138

Cited by 101 publications

(77 citation statements)

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“…Depending on the cytokine milieu encountered in tumors, DCs can either mediate anti-tumor activity or support tumor growth and metastasis. In fact, increasing evidence from analyses of human ovarian, breast, prostate and renal cell carcinoma reveals the presence of tumor-promoting rather than tumor-suppressing dendritic cells, and altered dendritic cell function and differentiation is likely to be one of the most fundamental mechanisms by which tumors escape immune responses [231][232][233][234][235]. Pro-tumorigenic dendritic cells can favor metastasis by inducing tumor immunotolerance and by promoting tumor angiogenesis.…”

Section: Nks and Dcsmentioning

confidence: 99%

“…Tumor cells, TAMs and tumoral immunosuppressive T cells can secrete high amounts of VEGF-A, IL-6, macrophage colony-stimulating factor (M-CSF), COX2, IL-10, TGFb and gangliosides, which suppress maturation of DCs [192]. Most myeloid DCs found in human ovarian, breast, prostate and renal cell carcinoma are therefore immature and may induce tumor immunotolerance [231][232][233][234]. Tumor-secreted IL-10 and VEGF also induce expression of B7-H1 on myeloid dendritic cells, a ligand for PD-1 receptor expressed on suppressor T cells [238].…”

Section: Nks and Dcsmentioning

confidence: 99%

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Metastasis: cell-autonomous mechanisms versus contributions by the tumor microenvironment

Kopfstein

Christofori

2006

Cell. Mol. Life Sci.

210

160

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Abstract. The fatality of cancer predominantly results from the dissemination of primary tumor cells to distant sites and the subsequent formation of metastases. During tumor progression, some of the primary tumor cells as well as the tumor microenvironment undergo characteristic molecular changes, which are essential for the metastatic dissemination of tumor cells. In this review, we will discuss recent insights into pro-metastatic events occurring in tumor cells themselves and in the tumor stroma. Tumor cell-intrinsic alterations include the loss of cell polarity and alterations in cell-cell and cell-matrix Cell. Mol. Life Sci. 63 (2006) 449-468 1420-682X/06/040449-20 DOI 10.1007/s00018-005-5296-8 © Birkhäuser Verlag, Basel, 2006 adhesion as well as deregulated receptor kinase signaling, which together support detachment, migration and invasion of tumor cells. On the other hand, the tumor stroma, including endothelial cells, fibroblasts and cells of the immune system, is engaged in an active molecular crosstalk within the tumor microenvironment. Subsequent activation of blood vessel and lymph vessel angiogenesis together with inflammatory and immune-suppressive responses further promotes cancer cell migration and invasion, as well as initiation of the metastatic process.

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Section: Nks and Dcsmentioning

confidence: 99%

Section: Nks and Dcsmentioning

confidence: 99%

Metastasis: cell-autonomous mechanisms versus contributions by the tumor microenvironment

Kopfstein

Christofori

2006

Cell. Mol. Life Sci.

210

160

View full text Add to dashboard Cite

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“…DC are found in low numbers in other tumour types (Troy et al, 1998a(Troy et al, ,b, 1999 and the density of CD1a positive DC has been directly correlated with improved overall survival in many solid tumour types. The findings of the present study imply that many breast cancers not only fail to recruit DC but fail to drive DC into either the antigen capture/processing phase (CD1a + ) or the antigen presentation/co-stimulatory phase (CMRF-44/56 + ).…”

Section: Molecular and Cellular Pathologymentioning

confidence: 99%

“…Studies of gastric, thyroid, lung and colorectal carcinomas have shown that the density of putative dendritic cells (DC) (CD1a; S-100 positive) is a predictor of survival (Tsujitani et al, 1987(Tsujitani et al, , 1988(Tsujitani et al, , 1990(Tsujitani et al, , 1992Ambe et al, 1989;Schroder et al, 1988;Zeid and Muller, 1993). Equally, more recent studies suggest minimal recruitment and activation of DC in renal, prostate and bladder cancers (Troy et al, 1998a(Troy et al, ,b, 1999 and that S-100 staining may correlate with an activated DC subset (Troy et al, 1998a). Moreover, it has been shown that there is an inverse correlation between tumour differentiation grade and the DC infiltrate for some tumour types (Becker, 1992).…”

mentioning

confidence: 99%

Dendritic cell density and activation status in human breast cancer – CD1a, CMRF-44, CMRF-56 and CD-83 expression

et al. 2002

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Low CD1a-positive putative dendritic cell numbers in human breast cancer has recently been described and may explain the apparent 'poor immunogenicity' previously reported in breast cancer. Little attention has been given to dendritic cell activation within the tumour microenvironment, which is another reason why the in-situ immune response may be severely deficient. We have therefore examined CD1a expression as a marker for dendritic cells, together with CMRF-44 and -56 as markers of dendritic cell activation status, in 40 human breast cancers. The results demonstrate few or no CD1a-positive putative dendritic cells and minimal or no expression of the dendritic cell activation markers. Both dendritic cell number and dendritic cell activation appear substantially deficient in human breast cancers, regardless of tumour histological grade.

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“…Immunology and immunotherapy approaches E Elkord in antitumour immunity, are functionally impaired in tumour-bearing animals 67,68 and in cancer patients [69][70][71] probably due to their susceptibility to tumour-mediated immunosuppression. Several tumours, such as melanoma, ovarian carcinoma and B-cell lymphoma have been found to produce the immunosuppressive cytokine IL-10, which can reduce DC development and activity.…”

Section: Mechanisms Limiting Cancer Regressionmentioning

confidence: 99%

Immunology and immunotherapy approaches for prostate cancer

Elkord

2007

Prostate Cancer Prostatic Dis

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Several mechanisms that impair the immune response to promote tumour progression are reported. These mechanisms aim to reduce the ability of antigen-presenting cells to present antigen and activate naïve T cells to support an active immune response or to create a suppressive environment that induce non-functional tumour-associated antigen-specific T cells. Prostate cancer (PC) alone accounts for 33% of incident cancer cases and about 9% of all cancer-related deaths among men in the USA during 2006. Whereas androgen deprivation has remained the first line of therapy for advanced PC, other therapies are still required due to progression to an androgen-resistant state and eventually loss of control in patients receiving hormonal therapy. Immunotherapy seems to be a promising approach to enhance tumour-specific T-cell responses in different cancers including prostate. More importantly, clinical trials in advanced PC patients have shown that immunotherapy may generate significant clinical responses. Immunology and immunotherapy aspects of PC with focus on prostate-specific antigen will be presented.

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Minimal Recruitment and Activation of Dendritic Cells Within Renal Cell Carcinoma

Cited by 101 publications

References 0 publications

Metastasis: cell-autonomous mechanisms versus contributions by the tumor microenvironment

Metastasis: cell-autonomous mechanisms versus contributions by the tumor microenvironment

Dendritic cell density and activation status in human breast cancer – CD1a, CMRF-44, CMRF-56 and CD-83 expression

Immunology and immunotherapy approaches for prostate cancer

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