Cancer Center and State Key Laboratory of Biotherapy
Pathak S.,Linköping University |
Ding Z.-Y.,Cancer Center and State Key Laboratory of Biotherapy |
Adell G.,County Council of Ostergotland |
Holmlund B.,County Council of Ostergotland |
And 3 more authors.
Cancer Biology and Therapy | Year: 2015
Our recent study showed the important role of special AT-rich sequence binding protein 1 (SATB1) in the progression of human rectal cancer. However, the value of SATB1 in response to radiotherapy (RT) for rectal cancer hasn't been reported so far. Here, SATB1 was determined using immunohistochemistry in normal mucosa, biopsy, primary cancer, and lymph node metastasis from 132 rectal cancer patients: 66 with and 66 without preoperative RT before surgery. The effect of SATB1 knockdown on radiosensitivity was assessed by proliferation-based assay and clonogenic assay. The results showed that SATB1 increased from normal mucosa to primary cancer, whereas it decreased from primary cancer to metastasis in non-RT patients. SATB1 decreased in primary cancers after RT. In RT patients, positive SATB1 was independently associated with decreased response to preoperative RT, early time to metastasis, and worse survival. SATB1 negatively correlated with ataxia telangiectasia mutated (ATM) and pRb2/p130, and positively with Ki-67 and Survivin in RT patients, and their potential interaction through different canonical pathways was identified in network ideogram. Taken together, our findings disclose for the first time that radiation decreases SATB1 expression and sensitizes cancer cells to confer clinical benefit of patients, suggesting that SATB1 is predictive of response to preoperative RT and clinical outcome in rectal cancer. © 2015 Taylor & Francis Group, LLC.
Luo T.,Cancer Center and State Key Laboratory of Biotherapy |
Chen L.,University of Sichuan |
He P.,Cancer Center and State Key Laboratory of Biotherapy |
Hu Q.-C.,Cancer Center and State Key Laboratory of Biotherapy |
And 5 more authors.
Asian Pacific Journal of Cancer Prevention | Year: 2013
Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis and thereby involved in the development and progression of solid tumours. Associations between three VEGF gene polymorphisms (-634 G/C, +936 C/T, and +1612 G/A) and breast cancer risk have been extensively studied, but the currently available results are inconclusive. Our aim was to investigate associations between three VEGF gene polymorphisms and breast cancer risk in Chinese Han patients. We performed a hospital-based case-control study including 680 female incident breast cancer patients and 680 female age-matched healthy control subjects. Polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) analysis was performed to detect the three VEGF gene polymorphisms. We observed that women carriers of +936 TT genotypes [odds ratio (OR) =0.46, 95% confidence interval (CI) = 0.28, 0.76; P=0.002] or 936 T-allele (OR=0.81, 95% CI= 0.68, 0.98; P=0.03) had a protective effect concerning the disease. Our study suggested that the +1612G/A polymorphism was unlikely to be associated with breast cancer risk. The -634CC genotype was significantly associated with high tumor aggressiveness [large tumor size (OR=2.63, 95% CI=1.15, 6.02; P=0.02) and high histologic grade (OR=1.47, 95% CI= 1.06, 2.03; P=0.02)]. The genotypes were not related with other tumor characteristics such as regional or distant metastasis, stage at diagnosis, or estrogen or progesterone receptor status. Our study revealed that the VEGF -634 G/C and +936 C/T gene polymorphisms may be associated with breast cancer in Chinese Han patients.
He J.,Cancer Center and State Key Laboratory of Biotherapy |
Zhang Y.,Cancer Center and State Key Laboratory of Biotherapy |
Shen Q.,Cancer Center and State Key Laboratory of Biotherapy |
Li Y.,Cancer Center and State Key Laboratory of Biotherapy |
And 5 more authors.
Oncology Letters | Year: 2015
Extramedullary plasmacytoma (EMP) in the vulva is extremely rare. The current study presents, for the first time, a case of EMP in the left labia majora in a 36-year-old patient during pregnancy. A painful 7x4x2-cm mass with ulceration, pus and blood scabs, previously misdiagnosed as vulvar ulcer in a local hosipital, was proven to be an EMP by biopsy. Upon magnetic resonance imaging, the tumor was shown to occur in the left labia majora without lymphadenopathy. A complete multiple myeloma (MM) workup excluded coexistence with MM. The goal of treatment was to eradicate the tumor while synchronously preserving the vulva. Therefore, following the termination of the pregnancy, radiotherapy with a total dose of 4,500 cGy markedly reduced the size of the tumor. An extended local excision of the residual tumor, and anaplasty of the vulva preserved the appearance and function of the vulva to the utmost. No post-operative radiation was administered, as the resection margins were not microscopically involved. There was no relapse, metastasis or progression to MM in a 9-month post-operative follow-up period, but close follow-up and long-term surveillance are required. © Spandidos Publications 2015. All rights reserved.
PubMed | University of Sichuan and Cancer Center and State Key Laboratory of Biotherapy
Type: Journal Article | Journal: International journal of oncology | Year: 2015
Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFRTKIs) have shown promising effects against the growth of non-small cell lung cancer (NSCLC) cells harboring EGFR mutations (EGFRmts). However, many patients with NSCLC that are accepted for EGFRTKI treatment followed by chemotherapy possess an unknown EGFR status including wild-type EGFR (EGFRwt). Little is known about the potential effects of EGFRTKI treatment prior to chemotherapy. We investigated the effects and underlying molecular events of 4 weeks of continuous exposure to EGFRTKIs in the EGFRwt NSCLC line H1299. This treatment dramatically increased the IC50 of several relevant chemotherapeutic agents: cisplatin (DDP) (29.256.1 M for gefitinib, 43.2514.87 M for erlotinib, and 6.921.15 M for parental), paclitaxel (11.163.36 M for gefitinib, 9.161.41 M for erlotinib, and 2.090.44 M for parental), gemcitabine (47.186.2 M for gefitinib, 40.3611.1 M for erlotinib, and 16.003.38 M for parental) and pemetrexed (11.784.07 M for gefitinib, 15.977.23 M for erlotinib, and 4.721.9 M for parental). This chemoresistance was critically dependent on the activation of the mediator signal transducer and activator of transcription 3 (STAT3). In cells exposed to EGFRTKIs for 4 weeks, activation of STAT3 was found to be unrelated to EGFR and to be independent of IL6 and 22. Treatment with the STAT3 inhibitor NSC 74859 was able to reverse the TKI exposure-induced chemoresistance in EGFRwt NSCLC cells. Similar phenomena were observed in H1975 cells harboring EGFR L858R and T790M mutations. Based on the observed molecular events following long exposure of an EGFRwt NSCLC cell line to an EGFRTKI, this study indicates that such drugs should be not recommended for EGFRwt patients who can undergo chemotherapy. This study also suggests that STAT3 inhibitors may aid in the treatment NSCLC patients who exhibit EGFRTKI resistance due to an acquired T790M mutation.