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      Human papillomavirus 16 infection predicts poor outcome in patients with esophageal squamous cell carcinoma

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          Previous studies indicate that human papillomavirus 16 (HPV16) infection plays a pivotal role in the etiology of esophageal squamous cell carcinoma (ESCC). We aim to detect the influence of HPV16 infection on ESCC patient prognosis.

          Patients and methods

          Immunohistochemical staining for HPV16 E6 oncoprotein, the low-affinity p75 neurotrophin receptor (p75NTR), and phosphatidylinositol 3-kinase (PI3K) was performed on 103 archived surgical specimens from patients with ESCC and 54 control samples from patients with benign esophageal tumor or inflammatory lesions. All patients were from the Shaan Xi Province, People’s Republic of China.


          HPV16 E6 expression was significantly higher in the ESCC group ( P<0.05). HPV16 E6 expression was significantly higher in men than in women ( P<0.05). p75NTR expression was higher in those aged >56 years ( P<0.05). PI3K expression was higher in those with a more advanced histopathological grade ( P<0.05). There was a positive correlation between HPV16 E6 and p75NTR expression ( r=0.547, P<0.001) and between p75NTR and PI3K expression ( r=0.364, P<0.001). In 100 evaluable patients, the 5-year overall survival (OS) rate was 11%. In patients with ESCC, HPV16 E6 and PI3K expression were negatively correlated with the 3-year OS ( P<0.05), 5-year OS ( P<0.05), and progression-free survival ( P<0.05).


          HPV16 infection likely contributes to the etiology of ESCC patients in Shaan Xi, People’s Republic of China. HPV16 infection status and PI3K expression levels could be useful for predicting prognosis in patients with ESCC.

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          Most cited references 27

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          EUROCARE-4. Survival of cancer patients diagnosed in 1995-1999. Results and commentary.

          EUROCARE-4 analysed about three million adult cancer cases from 82 cancer registries in 23 European countries, diagnosed in 1995-1999 and followed to December 2003. For each cancer site, the mean European area-weighted observed and relative survival at 1-, 3-, and 5-years by age and sex are presented. Country-specific 1- and 5-year relative survival is also shown, together with 5-year relative survival conditional to surviving 1-year. Within-country variation in survival is analysed for selected cancers. Survival for most solid cancers, whose prognosis depends largely on stage at diagnosis (breast, colorectum, stomach, skin melanoma), was highest in Finland, Sweden, Norway and Iceland, lower in the UK and Denmark, and lowest in the Czech Republic, Poland and Slovenia. France, Switzerland and Italy generally had high survival, slightly below that in the northern countries. There were between-region differences in the survival for haematologic malignancies, possibly due to differences in the availability of effective treatments. Survival of elderly patients was low probably due to advanced stage at diagnosis, comorbidities, difficult access or lack of availability of appropriate care. For all cancers, 5-year survival conditional to surviving 1-year was higher and varied less with region, than the overall relative survival.
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            The role of PTEN/Akt/PI3K signaling in the maintenance and viability of prostate cancer stem-like cell populations.

            Characterization of the molecular pathways that are required for the viability and maintenance of self-renewing tumor-initiating cells may ultimately lead to improved therapies for cancer. In this study, we show that a CD133(+)/CD44(+) population of cells enriched in prostate cancer progenitors (PCaPs) has tumor-initiating potential and that these progenitors can be expanded under nonadherent, serum-free, sphere-forming conditions. Cells grown under these conditions have increased in vitro clonogenic and in vivo tumorigenic potential. mRNA expression analysis of cells grown under sphere-forming conditions, compared with long-term monolayer cultures, revealed preferential activation of the PI3K/AKT signaling pathway. PI3K p110alpha and beta-protein levels were higher in cells grown under sphere-forming conditions, and phosphatase and tensin homolog (PTEN) knockdown by shRNA led to an increase in sphere formation as well as increased clonogenic and tumorigenic potential. Similarly, shRNA knockdown of FoxO3a led to an increase in tumorigenic potential. Consistent with these results, inhibition of PI3K activity by the dual PI3K/mTOR inhibitor NVP-BEZ235 led to growth inhibition of PCaPs. Taken together, our data strongly suggest that the PTEN/PI3K/Akt pathways are critical for prostate cancer stem-like cell maintenance and that targeting PI3K signaling may be beneficial in prostate cancer treatment by eliminating prostate cancer stem-like cells.
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              PI3K pathway regulates survival of cancer stem cells residing in the perivascular niche following radiation in medulloblastoma in vivo.

              Medulloblastomas are brain tumors that arise in the cerebellum of children and contain stem cells in a perivascular niche thought to give rise to recurrence following radiation. We used several mouse models of medulloblastomas in parallel to better understand how the critical cell types in these tumors respond to therapy. In our models, the proliferating cells in the tumor bulk undergo radiation-induced, p53-dependent apoptotic cell death. Activation of Akt signaling via PTEN loss transforms these cells to a nonproliferating extensive nodularity morphology. By contrast, the nestin-expressing perivascular stem cells survive radiation, activate PI3K/Akt pathway, undergo p53-dependent cell cycle arrest, and re-enter the cell cycle at 72 h. Furthermore, the ability of these cells to induce p53 is dependent on the presence of PTEN. These cellular characteristics are similar to human medulloblastomas. Finally, inhibition of Akt signaling sensitizes cells in the perivascular region to radiation-induced apoptosis.

                Author and article information

                Onco Targets Ther
                Onco Targets Ther
                OncoTargets and Therapy
                OncoTargets and therapy
                Dove Medical Press
                05 March 2015
                : 8
                : 573-581
                [1 ]Department of Radiotherapy, The First Affiliated Hospital of Xi’an Jiao Tong University, Xi’an, People’s Republic of China
                [2 ]Department of Radiotherapy, The People’s Liberation Army 323 Hospital, Xi’an, People’s Republic of China
                Author notes
                Correspondence: Shaomin Che, Department of Radiotherapy, The First Affiliated Hospital of Xi’an Jiao Tong University, 76 YanTa West Street, Xi’an, Shaan Xi 710061, People’s Republic of China, Tel +86 189 9123 2572, Fax +86 29 8532 4068, Email chersm@
                © 2015 Xi et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Original Research


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