RESUMO
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that data from the cell adhesion experiment shown in Fig. 11 were strikingly similar to data appearing in different form in Fig. 6B in another article written by different authors at different research institutes [Huang Z, Li J, Du S, Tang Y, Huang L, Xiao L and Tong P: FKBP14 overexpression contributes to osteosarcoma carcinogenesis and indicates poor survival outcome. Oncotarget 7: 3987239884, 2016]. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 21532160, 2018; DOI: 10.3892/mmr.2017.8173].
RESUMO
Lung cancer is the leading cause of global cancerassociated mortality. Genomic alterations in lung cancers have not been widely characterized, however, the molecular mechanism of tumor initiation and progression remain unknown, and no molecularly targeted have been specifically developed for its treatment and diagnosis. The present study observed the upregulation of Aldoketo reductase family 1 member Bio10 (AKR1B10) lung cancer tissues by analyzing two public lung cancer gene expression datasets. Further experiments in silencing AKR1B10 demonstrated that the expression of AKR1B10 was associated with cell proliferation, cell cycle, adhesion and invasion, as well as extracellularsignalregulated kinase/mitogen activated protein kinase signal pathway. The overexpression of AKR1B10 in lung cancer indicates the important role of AKR1B10 in tumorigenesis. These findings suggest that AKR1B10 could be a potential diagnosis and treatment mark of lung cancer.
Assuntos
Aldeído Redutase/genética , Neoplasias Pulmonares/genética , Interferência de RNA , RNA Interferente Pequeno/genética , Aldo-Ceto Redutases , Apoptose/genética , Ciclo Celular/genética , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células , Perfilação da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Redes Reguladoras de Genes , Inativação Gênica , Humanos , Neoplasias Pulmonares/patologiaRESUMO
A better understanding of how solid malignancies arise in an immunocompetent host, avoid immune recognition, and ultimately progress to widely disseminated cancer is essential to effectively harness the immune system against solid tumors. Because of their extra-lymphatic localization, it has been proposed that solid malignancies are just ignored by the immune system, thereby allowing their uncontrolled growth and dissemination. Alternatively, as most of the solid tumors are unable to express costimulatory molecules, the "signal one without signal two" model of tolerance induction has been frequently evoked to account for the failure of the immune system to reject antigenic tumors in vivo. In this study, we showed, however, that the extra-lymphatic growth of solid tumors is not immunologically ignored by the lymphoid compartment, resulting instead in the early induction of antigen-specific CD4(+) T-cell tolerance. Furthermore, analysis of parent-into-F1 bone marrow (BM) chimeras demonstrates that presentation of tumor antigens by BM-derived antigen-presenting cells represents the dominant mechanism in solid tumor-induced CD4(+) T-cell tolerance. Our findings of early development of antigen-specific T-cell unresponsiveness mediated by BM-derived antigen-presenting cells, not only provides a plausible explanation for the failure of the immune system to reject antigenic solid tumors in vivo, but more importantly, they have identified a barrier that, if appropriately manipulated, may lead to approaches to effectively harness the immune system against solid malignancies.
Assuntos
Antígenos de Neoplasias/imunologia , Linfócitos T CD4-Positivos/imunologia , Carcinoma de Células Renais/imunologia , Anergia Clonal/imunologia , Neoplasias Renais/imunologia , Melanoma Experimental/imunologia , Animais , Apresentação de Antígeno/imunologia , Carcinoma de Células Renais/patologia , Divisão Celular/imunologia , Imunoterapia Adotiva , Neoplasias Renais/patologia , Linfonodos/imunologia , Linfonodos/patologia , Masculino , Melanoma Experimental/patologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Camundongos SCID , Camundongos TransgênicosRESUMO
BACKGROUND: The seventh edition of the tumor, node, metastasis Classification of Malignant Tumors is due to be published in 2009. The recommendations of International Association for the Study of Lung Cancer for changes to the T descriptors have been published. We combined this new parameter with other well-established prognostic factors and performed multivariate survival analyses to validate its value in Chinese stage I non-small cell lung cancer (NSCLC). METHODS: We try to validate the new staging project in 325 patients who underwent complete surgical resection for stage I NSCLC in Single Institution of Shanghai Chest Hospital from 1998 to 2003. Variables in the analysis included age, gender, performance status, history of smoking, pathologic type, type of resection (pneumonectomy, lobectomy, and bilobectomy), tumor size (greatest dimension of tumor), T-status (T1 or T2), type of lymph node resection (systematic mediastinal lymphadenectomy or mediastinal lymph node sampling), lymphovascular vessel invasion, and adjuvant chemotherapy. RESULTS: The 5-year overall survival (OS) of patients whose tumor measured no larger than 2 cm in largest diameter or larger than 2 cm but no larger than 3 cm were 75.49 and 74.58%, respectively. For those with tumors measured larger than 3 cm but smaller than 5 cm or larger than 5 cm but smaller than 7 cm were 60.87 and 55.63%. The 5-year OS of patients whose tumor measured larger than 7 cm was 46.15% (p = 0.025). The 5-year disease-free survival rates of patients whose tumor measured no larger than 2 cm in largest diameter or larger than 2 cm but no larger than 3 cm were 67.65 and 66.67%, respectively. For those with tumors measured larger than 3 cm but smaller than 5 cm or larger than 5 cm but smaller than 7 cm were 53.14 and 52.63%. The 5-year disease-free survival rate of patients whose tumor measured larger than 7 cm was 30.77% (p = 0.009). Multivariate analyses revealed that age, gender, type of resection (pneumonectomy, lobectomy, and bilobectomy), tumor size (greatest dimension of tumor), type of lymph node resection (systematic mediastinal lymphadenectomy or mediastinal lymph node sampling), and lymphovascular vessel invasion were significant predictive factors for OS. CONCLUSIONS: The tumor size is a significant independent prognostic factors in stage I NSCLC.