Cytokine Variations in Patients With Hormone Treated Prostate Cancer

Wise, Gilbert J.; Marella, Venkata K.; Talluri, Giridhar; Shirazian, Djamshid

doi:10.1016/s0022-5347(05)67289-8

Cited by 127 publications

(69 citation statements)

References 14 publications

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“…Accordingly, patients affected by a variety of human tumors express high levels of T H 2 cytokines in the periphery and in the tumor microenvironment, which correlate with the stage and grade of malignancy. 21,22 Particularly, IL-4 plays a major role in inducing T H 2 responses acting through IL-4Ra and activating the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling cascade. 17,23 Recently, IL-4 has been shown to induce apoptosis in hepatocarcinoma cells 24 and a similar finding has been reported in renal cell carcinoma (RCC), where in vitro treatment of tumor cells with IL-4 and tumor necrosis factor-a is shown to increase RCC apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Apoptosis resistance in epithelial tumors is mediated by tumor-cell-derived interleukin-4

et al. 2008

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We investigated the mechanisms involved in the resistance to cell death observed in epithelial cancers. Here, we identify that primary epithelial cancer cells from colon, breast and lung carcinomas express high levels of the antiapoptotic proteins PED, cFLIP, Bcl-xL and Bcl-2. These cancer cells produced interleukin-4 (IL-4), which amplified the expression levels of these antiapoptotic proteins and prevented cell death induced upon exposure to TRAIL or other drug agents. IL-4 blockade resulted in a significant decrease in the growth rate of epithelial cancer cells and sensitized them, both in vitro and in vivo, to apoptosis induction by TRAIL and chemotherapy via downregulation of the antiapoptotic factors PED, cFLIP, Bcl-xL and Bcl-2. Furthermore, we provide evidence that exogenous IL-4 was able to upregulate the expression levels of these antiapoptotic proteins and potently stabilized the growth of normal epithelial cells rendering them apoptosis resistant. In conclusion, IL-4 acts as an autocrine survival factor in epithelial cells. Our results indicate that inhibition of IL-4/IL-4R signaling may serve as a novel treatment for epithelial cancers.

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Section: Discussionmentioning

confidence: 99%

Apoptosis resistance in epithelial tumors is mediated by tumor-cell-derived interleukin-4

et al. 2008

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“…Elevated IL-6 levels have been associated with advanced stage and metastasis-related morbidity (Adler et al, 1999;Nakashima et al, 2000;Wise et al, 2000). Thus, it has been recently reported that patients with metastatic ovarian cancer and patients with metastatic renal cell carcinoma have higher serum IL-6 levels than those without disseminated disease (Blay et al, 1992;Scambia et al, 1995).…”

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confidence: 99%

Serum levels of IL-6 and TNF-α correlate with clinicopathological features and patient survival in patients with prostate cancer

et al. 2004

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Interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-a) are important multifunctional cytokines involved in tumour growth and metastasis. In this study, we have measured serial levels of serum IL-6 and TNF-a in prostate cancer patients. A total of 80 patients with carcinoma of the prostate and 38 controls were studied. Three patient groups, with small bulk localised, large volume localised and metastatic prostate cancer, were assessed. Serum IL-6 and TNF-a levels were measured and correlated with clinicopathological variables and patient survival. Serial changes in these cytokines were also assessed and related to disease progression in 40 patients with recurrent prostate cancer. Serum IL-6 levels in patients with metastatic disease (9.377.8 pg ml À1 ) were higher than those in patients with localised disease (1.370.8 pg ml À1 , Po0.001). Significantly elevated levels of TNF-a were found in metastatic disease (6.373.6 pg ml À1 ) compared with localised disease (1.170.5 pg ml À1 , Po0.001). The levels of both cytokines were directly correlated with the extent of the disease. Serial analysis in 40 patients with recurrent tumours showed that both cytokines became elevated at the point of prostate-specific antigen progression. In conclusion, these results suggest that IL-6 and TNF-a correlate with the extent of disease in patients with prostate cancer and may be monitored in conjunction with other disease markers.

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“…Clinical data showed that the levels of IL-4 are significantly elevated in serum of patients with ablation resistant prostate cancer [17,18]. Previous studies demonstrated that IL-4 activates AR-mediated gene expression by activation of the AR in a ligandindependent manner or in the presence of very low levels of androgen [19].…”

Section: Introductionmentioning

confidence: 99%

Interleukin‐4 stimulates androgen‐independent growth in LNCaP human prostate cancer cells

et al. 2007

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BACKGROUND. Clinical data showed that the levels of interleukin-4 (IL-4) are significantly elevated in serum of patients with ablation resistant prostate cancer. Previous studies demonstrated that IL-4 enhances androgen receptor (AR) activation mediated by NF-kB in the absence or in the very low levels of androgen in prostate cancer cells. In this study, the role of IL-4 in promoting the growth of androgen-independent prostate cancer cells was examined.

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Cytokine Variations in Patients With Hormone Treated Prostate Cancer

Cited by 127 publications

References 14 publications

Apoptosis resistance in epithelial tumors is mediated by tumor-cell-derived interleukin-4

Apoptosis resistance in epithelial tumors is mediated by tumor-cell-derived interleukin-4

Serum levels of IL-6 and TNF-α correlate with clinicopathological features and patient survival in patients with prostate cancer

Interleukin‐4 stimulates androgen‐independent growth in LNCaP human prostate cancer cells

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