TGF-β and cancer

Reiß, Michael

doi:10.1016/s1286-4579(99)00251-8

Cited by 121 publications

(108 citation statements)

References 197 publications

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“…Although cellular TGF-b1 inhibits tumour growth, TGF-b1 in extracellular matrix stimulates tumour cell motility and migration, facilitating cancer invasion and metastasis (Arteaga et al, 1990;Reiss, 1999;Barcellos-Hoff, 2005). In mammary gland, TGF-b1 is a potent inhibitor of cell proliferation, and in certain circumstances it can also induce apoptosis (Silberstein and Daniel, 1987;Nguyen et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…In mammary gland, TGF-b1 is a potent inhibitor of cell proliferation, and in certain circumstances it can also induce apoptosis (Silberstein and Daniel, 1987;Nguyen et al, 2000). Studies have shown that when tumour develops, the expression of TbRII by breast cancer cells is diminished, which results in reduced response of tumour cells to TGF-b1 signalling and increased secretion of the ligand (Akhurst and Balmain, 1999;Reiss, 1999). Under this situation, the inhibitory effect of TGF-b1 on tumour cells is diminished or abrogated.…”

Section: Discussionmentioning

confidence: 99%

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TGF-β1 genotype and phenotype in breast cancer and their associations with IGFs and patient survival

Katsaros

et al. 2008

Br J Cancer

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Transforming growth factor-b (TGF-b)-mediated signals play complicated roles in the development and progression of breast tumour. The purposes of this study were to analyse the genotype of TGF-b1 at T29C and TGF-b1 phenotype in breast tumours, and to evaluate their associations with IGFs and clinical characteristics of breast cancer. Fresh tumour samples were collected from 348 breast cancer patients. TGF-b1 genotype and phenotype were analysed with TaqMan s and ELISA, respectively. Members of the IGF family in tumour tissue were measured with ELISA. Cox proportional hazards regression analysis was performed to assess the association of TGF-b1 and disease outcomes. Patients with the T/T (29%) genotype at T29C had the highest TGF-b1, 707.9 pg mg À1 , followed by the T/C (49%), 657.8 pg mg À1 , and C/C (22%) genotypes, 640.8 pg mg À1 , (P ¼ 0.210, T/T vs C/C and C/T). TGF-b1 concentrations were positively correlated with levels of oestrogen receptor, IGF-I, IGF-II and IGFBP-3. Survival analysis showed TGF-b1 associated with disease progression, but the association differed by disease stage. For early-stage disease, patients with the T/T genotype or high TGF-b1 had shorter overall survival compared to those without T/T or with low TGF-b1; the hazard ratios (HR) were 3.54 (95% CI: 1.21 -10.40) for genotype and 2.54 (95% CI: 1.10 -5.89) for phenotype after adjusting for age, grade, histotype and receptor status. For late-stage disease, however, the association was different. The T/T genotype was associated with lower risk of disease recurrence (HR ¼ 0.13, 95% CI: 0.02 -1.00), whereas no association was found between TGF-b1 phenotype and survival outcomes. The study suggests a complex role of TGF-b1 in breast cancer progression, which supports the finding of in vitro studies that TGF-b1 has conflicting effects on tumour growth and metastasis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

TGF-β1 genotype and phenotype in breast cancer and their associations with IGFs and patient survival

Katsaros

et al. 2008

Br J Cancer

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“…It is clear that loss-offunction mutations of components in the TGF-␤ signaling pathway is one route toward loss of TGF-␤ growth control in cancer. 49,50 However, the majority of human tumors has not undergone such mutations but retains a functional TGF-␤ signaling system. Our data suggest that the development of a TRAIL-resistant phenotype of tumor cells may be responsible for the development of resistance toward TGF-␤-induced growth inhibition.…”

Section: Discussionmentioning

confidence: 99%

Transforming growth factor β can mediate apoptosis via the expression of TRAIL in human hepatoma cells

et al. 2005

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Transforming growth factor ␤ (TGF-␤) has been shown to induce apoptotic cell death in normal and transformed hepatocytes. However, the exact mechanism through which TGF-␤ induces cell death is still unknown. We examined a potential role of various death receptor/ ligand systems in TGF-␤-induced apoptosis and identified the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) as a mediator of TGF-␤-induced apoptosis in hepatoma cells. TGF-␤-induced apoptosis is significantly impaired upon blockage of TRAIL. We show that TRAIL is upregulated in hepatoma cells upon treatment with TGF-␤, whereas TRAIL receptor levels remain unchanged. In conclusion, our results provide evidence that the TRAIL system is critically involved in TGF-␤-induced cell death in liver pathology. (HEPATOLOGY 2005;42:183-192.)

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“…TGF-␤1 can be a potent tumor suppressor in the early stages, but increased TGF-␤1 plays a complex role in tumorigenesis by behaving as a tumor promoter through angiogenesis and antitumor immune responses at later stages. 35,36 Mutations in TGF-␤-related genes appear to be closely linked to the progression of human tumors. Mutations in TGF-␤R-I have been identified in prostate cancer, ovarian cancer, glioblastoma, gastric cancer and chronic lymphocytic leukemia.…”

Section: Plasma Tgf-␤1 Levels In Patients With Esophageal Carcinomamentioning

confidence: 99%

Reduced expression of transforming growth factor‐β receptors is an unfavorable prognostic factor in human esophageal squamous cell carcinoma

Fukai

Fukuchi

Masuda

et al. 2003

Intl Journal of Cancer

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TGF-β and cancer

Cited by 121 publications

References 197 publications

TGF-β1 genotype and phenotype in breast cancer and their associations with IGFs and patient survival

TGF-β1 genotype and phenotype in breast cancer and their associations with IGFs and patient survival

Transforming growth factor β can mediate apoptosis via the expression of TRAIL in human hepatoma cells

Reduced expression of transforming growth factor‐β receptors is an unfavorable prognostic factor in human esophageal squamous cell carcinoma

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