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Vitry-sur-Seine, France

Fiaschetti G.,Neuro oncology Group | Abela L.,University of Zurich | Nonoguchi N.,World Health Organization | Dubuc A.M.,Arthur and Sonia Labatt Brain Tumour Research Center | And 9 more authors.
British Journal of Cancer | Year: 2014

Background:microRNA-9 is a key regulator of neuronal development aberrantly expressed in brain malignancies, including medulloblastoma. The mechanisms by which microRNA-9 contributes to medulloblastoma pathogenesis remain unclear, and factors that regulate this process have not been delineated.Methods:Expression and methylation status of microRNA-9 in medulloblastoma cell lines and primary samples were analysed. The association of microRNA-9 expression with medulloblastoma patients' clinical outcome was assessed, and the impact of microRNA-9 restoration was functionally validated in medulloblastoma cells.Results:microRNA-9 expression is repressed in a large subset of MB samples compared with normal fetal cerebellum. Low microRNA-9 expression correlates significantly with the diagnosis of unfavourable histopathological variants and with poor clinical outcome. microRNA-9 silencing occurs via cancer-specific CpG island hypermethylation. HES1 was identified as a direct target of microRNA-9 in medulloblastoma, and restoration of microRNA-9 was shown to trigger cell cycle arrest, to inhibit clonal growth and to promote medulloblastoma cell differentiation.Conclusions:microRNA-9 is a methylation-silenced tumour suppressor that could be a potential candidate predictive marker for poor prognosis of medulloblastoma. Loss of microRNA-9 may confer a proliferative advantage to tumour cells, and it could possibly contribute to disease pathogenesis. Thus, re-expression of microRNA-9 may constitute a novel epigenetic regulation strategy against medulloblastoma. © 2014 Cancer Research UK.

Hassan C.,Catholic University | Gimeno-Garcia A.,University of La Laguna | Gimeno-Garcia A.,Oncology Group | Kalager M.,Telemark Hospital | And 8 more authors.
Alimentary Pharmacology and Therapeutics | Year: 2014

Background Patients with one to two tubular adenomas <1 cm in size without high-grade dysplasia (low-risk group) are considered at low risk for colorectal cancer. However, it is uncertain whether they have the same risk of subsequent advanced neoplasia as those with no neoplasia at baseline colonoscopy. Aim To compare incidence of metachronous advanced neoplasia between patients in the low-risk adenoma group and those without neoplasia at index colonoscopy. Methods Relevant publications were identified by MEDLINE/EMBASE and other databases for the period 1992-2013. Studies comparing the incidence of post-polypectomy advanced neoplasia (adenomas ≥10 mm/high-grade dysplasia/villous or cancer) between the low-risk group and patients without colorectal neoplasia at the first colonoscopy were included. Detection rates for advanced neoplasia at endoscopic surveillance were extracted. Study quality was ascertained according to Newcastle-Ottawa Scale. Forest plot was produced based on random-effect models. Inter-study heterogeneity was assessed using the I2 statistic. Results Seven studies provided data on 11 387 patients. Mean surveillance periods ranged between 2 and 5 years. Altogether, 267 patients with post-polypectomy advanced neoplasia were detected in the two groups. The incidence of advanced neoplasia was 1.6% (119/7308) in those without neoplasia and 3.6% (148/4079) in those with low-risk adenoma, respectively, corresponding to a relative risk of 1.8 (95% CI: 1.3-2.6). Inter-study heterogeneity was only moderate (I2: 37%). No publication bias was present. Conclusions Patients with low-risk adenomas at baseline had a higher risk of metachronous advanced neoplasia than the group with no adenomas at baseline, though the absolute risk was low in both groups. © 2014 John Wiley & Sons Ltd.

News Article | February 2, 2016
Site: www.fastcompany.com

Monday was a big day in the fight against cancer. Vice President Joe Biden convened the first meeting of the Cancer Moonshot Task Force of government departments and other agencies, the White House announced a proposal to spend $1 billion on the effort over the next two years, and in a Q&A with the task force on Twitter specific concerns such as childhood cancer were highlighted. In a fact sheet released on Monday afternoon, the White House proposed funding that includes $195 million this year for the National Institutes of Health (NIH) and a proposed $755 million in the government's 2017 budget for the NIH and the Food and Drug Administration (FDA). The fact sheet largely continues the themes the administration has hammered on since the State of the Union address: genetic analysis of cancers, treatments such as vaccines that harness the immune system to attack tumors, and better data sharing among researchers. On the last item, the fact sheet specifies that this will be a broad effort including not just government and academia, but also philanthropies, patient-advocate organizations, and biotech and pharmaceutical companies. Only government bodies will serve on the task force, but it will convene a "blue ribbon panel" that includes outside experts. There will also be a fund for blue-sky research efforts, what the government calls "high-risk, high-return research." This is a pretty vague area so far. When asked what this meant, NIH director Dr. Francis S. Collins, tweeted, "We don’t know yet, we are counting on wildly creative ideas from the whole community." Childhood cancer hadn't gotten much mention until Monday, which a lot of people mentioned during the Twitter Q&A. The White House fact sheet calls for a new focus on childhood cancer, including analyzing rare cancer tumors and studying how cancer progresses in order to develop better treatments. During the Twitter Q&A, Dr. Douglas Lowy, acting director of the National Cancer Institute (part of NIH) mentioned a program called the NCI-MATCH trial targeted at children with advanced cancer and few treatment options. "Children are special. They deserve treatments that are made for them," Danielle Leach, the director of government relations and advocacy at St. Baldrick’s Foundation, tells Fast Company. "Pediatric cancers don't happen in adults, for the most part," she says. St. Baldrick's, which specializes in child cancer research, put out a press release last week saying that there have been shortages of children's cancer medications (both chemotherapy and medications to treat side effects) in the past and that they expect more shortages in the future. "This is a problem almost exclusively impacting children in the United States and not other developed countries," says Dr. Peter Adamson, chairman of the Children’s Oncology Group (COG), in the press release. COG calls itself the world’s largest organization devoted exclusively to childhood and adolescent cancer research, and St. Baldrick's heavily funds it. The White House fact sheet describes at length the importance of bringing in the U.S. military. (Defense and Veterans Affairs are two of the five federal agencies represented on the task force.) The Pentagon is already spending tens of millions of dollars per year and funding individual centers for breast, prostate, and gynecological cancers. The fact sheet doesn't say what more DOD will do, however, other than allocating more money. The VA, in addition to the 250 cancer research projects it already conducts, will be a source of possible patients for genetic studies. About 140,000 cancer patients are enrolled in the VA Million Veteran Program to contribute biological samples to genetic studies. The Moonshot's massive, multipronged approach seems well suited to the multifaceted nature of cancer. On Twitter, Collins admitted that the moonshot metaphor is not perfect, since there is not a single destination for this effort. "More we study cancer, more we realize that it is a collection of #rarediseases. We want to tackle all of them," he tweeted.

Medina Villaamil V.,Oncology Group | Aparicio Gallego G.,Oncology Group | Valbuena Rubira L.,CHU A Coruna | Garcia Campelo R.,CHU A Coruna | And 5 more authors.
Oncology Reports | Year: 2011

Renal cell carcinomas (RCC) can be subclassified for general purposes into clear cell, papillary cell, chromophobe cell carcinomas and oncocytomas. Other tumours such as collecting duct, medullary, mucinous tubular and spindle cell and associated with Xp 11.2 translocations/TFE 3 gene fusion, are much less common. There is also a residual group of unclassified cases. Previous studies have shown that RCC has high glycolytic rates, and expresses GLUT transporters, but no distinction has been made among the different subtypes of renal cell tumours and their grades of malignancy. In clear renal cell carcinoma (cRCC) glycogen levels increase, glycolysis is activated and gluconeogenesis is reduced. The clear cell subtype of RCC is characterized histologically by a distinctive pale, glassy cytoplasm and this appearance of cRCC is due to abnormalities in carbohydrate and lipid metabolism, and this abnormality results in glycogen and sterol storage. Several isoforms of glucose carriers (GLUTs) have been identified. We show here in a panel of 80 cRCC samples a significant correlation between isoform 5 (GLUT5) and many pathological parameters such as grade of differentiation, pelvis invasion and breaking capsule. GLUT5 expression also appears to associate more strongly with the clear cell RCC subtype. These data suggest a role for the GLUT5 isoform in fructose uptake that takes place in cRCC cells and which subsequently leads to the malignant RCC progression.

Hassan C.,Catholic University | Quintero E.,University of La Laguna | Quintero E.,Oncology Group | Dumonceau J.-M.,University of Geneva | And 15 more authors.
Endoscopy | Year: 2013

This Guideline is an official statement of the European Society of Gastrointestinal Endoscopy (ESGE). The Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system was adopted to define the strength of recommendations and the quality of evidence. Main recommendations: The following recommendations for post-polypectomy endoscopic surveillance should be applied only after a high quality baseline colonoscopy with complete removal of all detected neoplastic lesions. 1 In the low risk group (patients with 1 - 2 tubular adenomas < 10 mm with low grade dysplasia), the ESGE recommends participation in existing national screening programmes 10 years after the index colonoscopy. If no screening programme is available, repetition of colonoscopy 10 years after the index colonoscopy is recommended (strong recommendation, moderate quality evidence). 2 In the high risk group (patients with adenomas with villous histology or high grade dysplasia or ≥10 mm in size, or ≥ 3 adenomas), the ESGE recommends surveillance colonoscopy 3 years after the index colonoscopy (strong recommendation, moderate quality evidence). Patients with 10 or more adenomas should be referred for genetic counselling (strong recommendation, moderate quality evidence). 3 In the high risk group, if no high risk adenomas are detected at the first surveillance examination, the ESGE suggests a 5-year interval before a second surveillance colonoscopy (weak recommendation, low quality evidence). If high risk adenomas are detected at first or subsequent surveillance examinations, a 3-year repetition of surveillance colonoscopy is recommended (strong recommendation, low quality evidence). 4 The ESGE recommends that patients with serrated polyps < 10 mm in size with no dysplasia should be classified as low risk (weak recommendation, low quality evidence). The ESGE suggests that patients with large serrated polyps (≥ 10 mm) or those with dysplasia should be classified as high risk (weak recommendation, low quality evidence). 5 The ESGE recommends that the endoscopist is responsible for providing a written recommendation for the post-polypectomy surveillance schedule (strong recommendation, low quality evidence). © Georg Thieme Verlag KG Stuttgart. New York.

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