[Retracted] TGF‑β1 induces peritoneal fibrosis by activating the Smad2 pathway in mesothelial cells and promotes peritoneal carcinomatosis.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the fluorescence microscopy data shown in Fig. 6A and B were strikingly similar to data appearing in different form in Fig. 7 in a previously published paper [Lv Z‑D, Na D, Liu F‑N, Du Z‑M, Sun Z, Li Z, Ma X‑Y, Wang Z‑N and Xu H‑M: Induction of gastric cancer cell adhesion through transforming growth factor‑beta1‑mediated peritoneal fibrosis.

Lymphedema in survivors of breast cancer.

The tremendous improvement of survival in patients with breast cancer can be attributed to several treatment strategies, but these strategies also lead to the occurrence of breast cancer-related lymphedema (BCRL). BRCL is regularly associated with factors such as axillary lymph node dissection and local lymph node radiotherapy and manifests as an increase of >10% in the volume of affected limbs. Being overweight or having obesity (body mass index ≥25 kg/m), an excessive number of positive lymph nodes (>8) and capsular invasion by a tumor are additional risk factors for lymphedema.

Silencing of Prrx2 Inhibits the Invasion and Metastasis of Breast Cancer both In Vitro and In Vivo by Reversing Epithelial-Mesenchymal Transition.

Background/aims: Epithelial-mesenchymal transition (EMT) is recognized as a crucial mechanism in breast cancer progression and metastasis. Paired-related homeobox 2 (Prrx2) has been identified as a new EMT inducer in cancer, but the underlying mechanisms are still poorly understood.

Methods: The expression of Prrx2 was assessed by immunohistochemistry in breast cancer tissues to evaluate the clinicopathological significance of Prrx2, as well as the correlation between Prrx2 and EMT.

Silencing of Prrx1b suppresses cellular proliferation, migration, invasion and epithelial-mesenchymal transition in triple-negative breast cancer.

Triple-negative breast cancer (TNBC) is a highly aggressive tumour subtype associated with poor prognosis. The mechanisms involved in TNBC progression remains largely unknown. To date, there are no effective therapeutic targets for this tumour subtype.

Effects of two different immunotherapies on triple negative breast cancer in animal model.

The ability of immune system to react specifically against tumors inspirited the study of triple negative breast cancer (TNBC) immunotherapies. Sixty spontaneous breast cancer TA2 mice were randomly divided into three groups: GM-CSF group, with therapy of granulocyte-macrophage colony-stimulating factor (GM-CSF) combined with breast cancer stem cells associated antigens and cytosine-phosphorothioate-guanine oligodeoxynucleotides (CpG-ODNs); DC-CIK group, with infusions of dendritic cells/cytokine-induced killer (DC/CIK) cells; and PBS group as controls. After therapy, the cellular immunity of mice in GM-CSF group and DC-CIK group was obviously increased, especially for GM-CSF group (P<0.

Efficacy of combined therapy of goserelin and letrozole on very young women with advanced breast cancer as first-line endocrine therapy.

Breast cancer in young women younger than 35 years old is rare, aggressive and associated with a poor prognosis. Endocrine therapy is a preferred treatment modality in hormone receptor-positive early stage and advanced breast cancer, combined therapy of goserelin and letrozole presents an option for premenopausal women. We reported the efficacy and safety of therapy of goserelin plus letrozole on very young women with advanced breast cancer as first-line endocrine therapy.

Associations of polymorphisms of rs693 and rs1042031 in apolipoprotein B gene with risk of breast cancer in Chinese.

Background: Lipid synthesis is an integrated result of genetic, epigenetic and environmental factors, and also can promote growth and survival of cancer cells. Apolipoprotein B plays a central role in lipid metabolism as the major protein component of very-low-density lipoprotein and low-density lipoprotein.

Methods: We investigated the associations of polymorphisms of rs693 (-7673C>T) and rs1042031 (-12669 G>A) in the APOB gene with risk of breast cancer in 675 blood-unrelated Chinese patients with breast cancer and 712 healthy controls.

Mesothelial cells differentiate into fibroblast-like cells under the scirrhous gastric cancer microenvironment and promote peritoneal carcinomatosis in vitro and in vivo.

Peritoneal metastases are one reason for the poor prognosis of scirrhous gastric cancer (SGC), and myofibroblast provides a favorable environment for the peritoneal dissemination of gastric cancer. The aim of this study was to determine whether myofibroblast originates from peritoneal mesothelial cells under the influence of the tumor microenvironment. Immunohistochemical studies of peritoneal biopsy specimens from patients with peritoneal lavage cytological (+) status demonstrate the expression of the epithelial markers cytokeratin in fibroblast-like cells entrapped in the stroma, suggesting that these cells stemmed from local conversion of mesothelial cells.

Transforming growth factor-β 1 enhances the invasiveness of breast cancer cells by inducing a Smad2-dependent epithelial-to-mesenchymal transition.

Metastasis is unequivocally the most lethal aspect of breast cancer and the most prominent feature associated with disease recurrence, the molecular mechanisms whereby epithelial-to-mesenchymal transition (EMT) mediates the initiation and resolution of breast cancer metastasis remains poorly understood. Transforming growth factor-β1 (TGF-β1) is a multifunctional cytokine that is intimately involved in regulating numerous physiological processes, including cellular differentiation, homeostasis and EMT. Recent findings have implicated high levels of TGF-β1 were associated with poor outcome, whereas inhibition of TGF-β signaling reduces metastasis in breast cancer, suggesting that the chemo-therapeutic targeting of TGF-β1 or TGF-β signaling may offer new inroads in ameliorating metastatic disease in breast cancer patients.

TGF-β1 induces peritoneal fibrosis by activating the Smad2 pathway in mesothelial cells and promotes peritoneal carcinomatosis.

Peritoneal dissemination is one of the main causes of death in gastric cancer patients. Our previous study demonstrated that peritoneal fibrosis induced by transforming growth factor-β1 (TGF-β1) may provide a favorable environment for the dissemination of gastric cancer. The role of Smad3 in the development of dermal fibrosis, subcapsular cataract, and peritoneal fibrosis has been reported.