Elevated serum levels of transforming growth factor-?1 in patients with colorectal carcinoma

Shim, Kang Sup; Kim, Kwang Ho; Han, Woon Sup; Park, Eung Bum

doi:10.1002/(sici)1097-0142(19990201)85:3<554::aid-cncr6>3.0.co;2-x

Cited by 124 publications

(20 citation statements)

References 34 publications

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“…Since pancreatic cancer is characterized by the over-expression of many growth factors, including epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), and transforming growth factor (TGF)-b [6] whether serum levels of these growth factors are predictors of risk is of interest and may offer insights into early detection. Recent clinical studies have reported elevated serum levels of TGF-b1 in patients with prostate [7], colorectal [8], and breast cancer [9], compared with healthy controls. Although enhanced expression of TGF-b1 has been shown in pancreatic tissues or cell lines [10], no study has ever reported a possible link between serum TGF-b1 levels and pancreatic cancer.…”

Section: Introductionmentioning

confidence: 99%

Serum transforming growth factor-β1 levels and pancreatic cancer risk: a nested case–control study (Japan)

Lin

Kikuchi

Tamakoshi

et al. 2006

Cancer Causes Control

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Section: Introductionmentioning

confidence: 99%

Serum transforming growth factor-β1 levels and pancreatic cancer risk: a nested case–control study (Japan)

Lin

Kikuchi

Tamakoshi

et al. 2006

Cancer Causes Control

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“…Likewise, in hepatoma cell lines (HepG2, SMMU7721, LX-2, and L02), cells transfected with CMV-Pro10 had higher capacity for TGF-β1 secretion, greater anti-apoptosis effects, and stronger enhancement of cell proliferation compared with those transfected with CMV-Leu10 in vitro 25 . In vivo , significantly higher serum levels of TGF-β1 have been identified in patients with gastric cancer 10, 26 , hepatocellular carcinoma 25 , and prostate cancer 27 ; however, determining whether there is an association between TGF-β1 rs1982073 serum levels and those specific cancers still requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

A TGF‐β1 genetic variant at the miRNA187 binding site significantly modifies risk of HPV16‐associated oropharyngeal cancer

Tao

Huang

Sun

et al. 2018

Intl Journal of Cancer

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TGF-β1rs1982073 polymorphism at the miRNA-187 binding site may alter TGF-β1 expression and function, and thereby this polymorphism (genotype CT/CC) increases cancer susceptibility. HPV16 L1 seropositivity is associated with the risk of oral squamous cell carcinoma (OSCC), including oropharyngeal squamous cell carcinoma (OPSCC) and oral cavity squamous cell carcinoma (OCSCC). Thus, we hypothesized that TGF-β1rs1982073 polymorphism at the miRNA-187 binding site combined with HPV16 L1 seropositivity may have a joint effect on OSCC susceptibility. We determined the genotypes of TGF-β1rs1982073 and HPV16 status in 325 OSCC subjects and 335 cancer-free controls in the non-Hispanic white population, and used logistic regression models to evaluate the joint effects on OSCC susceptibility. TGF-β1rs1982073 polymorphism (CT/CC genotype) combined with HPV16 L1 seropositivity increased the risk of OSCC via joint effects, particularly in OPSCC subjects who were never-smokers (OR, 165.9; 95% CI, 28.6–960.4) or never-drinkers (OR, 196.0; 95% CI, 28.2–1000.0), respectively. Younger subjects had a higher risk of OPSCC than older subjects (OR, 23.5; 95% CI, 6.3–87.0 vs. OR, 6.0; 95% CI, 1.7–17.9, respectively). The significant associations between this polymorphism and HPV16-associated OSCC and OPSCC were also observed. However, OCSCC subjects did not have similar results. Our findings suggest that the joint effects of TGF-β1rs1982073 and HPV16 L1 seropositivity can increase risk of HPV16-associated oral cancer, particularly in OPSCC subjects who are never-smokers, never-drinkers, and young. This result may help us understand the tumorigenesis process and improve early detection, which are critical for prevention and intervention strategies. However, larger studies are needed to validate our findings.

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“…While TGF-β may suppress cancer initiation, in cancers that do form, increased expression of TGF-β ligands has been broadly reported, including in breast [72, 73], esophageal [74], colorectal [75], gastric [76], lung [77] and pancreatic cancers [78]. In these cancers, increases in TGF-β ligand levels have been demonstrated both locally and systemically, with elevated circulating levels.…”

Section: Tgf-β As a Tumor Promotermentioning

confidence: 99%

“…Higher levels of TGF-β have been demonstrated in lymph node metastasis compared to primary tumors or in tumors that eventually metastasize. High levels of TGF-β also correlate with increased invasiveness, disease progression and a poorer prognosis [72, 75–80]. TGF-β can be produced by the tumor cell itself or other cells in the tumor microenvironment including stromal cells, macrophages and platelets [81–83].…”

Section: Tgf-β As a Tumor Promotermentioning

confidence: 99%

Dichotomous roles of TGF-β in human cancer

Huang

Blobe

2016

Biochemical Society Transactions

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Transforming growth factor-β (TGF-β) mediates/regulates numerous biological processes including embryonic development and maintenance of cellular homeostasis in a context dependent manner. Consistent with its central role in maintaining cellular homeostasis, inhibition of TGF-β signaling results in disruption of normal homeostatic processes and subsequent carcinogenesis, defining the TGF-β signaling pathway as a tumor suppressor. However, once carcinogenesis is initiated, the TGF-β signaling pathway functions to promote cancer progression. This dichotomous function of the TGF-β signaling pathway is mediated both through altered effects on the cancer cells, including via inducing epithelial to mesenchymal transition, as well as through effects on the tumor microenvironment, including via effects on angiogenesis and immunosurveillance. Current studies support inhibition of TGF-β signaling either alone, or in conjunction with anti-angiogenic therapy or immunotherapy as a promising of strategy for the treatment of human cancers.

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Elevated serum levels of transforming growth factor-?1 in patients with colorectal carcinoma

Cited by 124 publications

References 34 publications

Serum transforming growth factor-β1 levels and pancreatic cancer risk: a nested case–control study (Japan)

Serum transforming growth factor-β1 levels and pancreatic cancer risk: a nested case–control study (Japan)

A TGF‐β1 genetic variant at the miRNA187 binding site significantly modifies risk of HPV16‐associated oropharyngeal cancer

Dichotomous roles of TGF-β in human cancer

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