Balbinot et al. show that intestinal epithelial cells depleted in the homeobox gene Cdx2 acquire an imperfect gastric-type metaplastic phenotype that, through changes in the microenvironment, induces the tumorigenic evolution of adjacent Cdx2-intact cells without themselves becoming cancerous.

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Résumé -Introduction :Le carcinome muco-épidermoïde (CME) est une tumeur maligne rare qui se développe à partir des glandes salivaires. Son traitement comporte la chirurgie associée ou non à la radiothérapie en fonction du grade histologique. Observation : Nous rapportons les cas de découverte fortuite de CME chez deux jeunes filles adressées par leur chirurgien-dentiste traitant. L'examen a mis en évidence une lésion maculaire ou papulaire de couleur violacée localisée au niveau du palais dur. L'examen anatomopathologique a confirmé le diagnostic d'un CME de bas grade dans les deux cas. Une tomographie volumique par faisceau conique, un scanner cervico-thoracoabdomino-pelvien et une imagerie par résonance magnétique ont été réalisés dans le cadre du bilan d'extension. Le traitement a consisté dans les deux cas en une exérèse de la lésion avec marge. Une prothèse obturatrice a été mise en place en per-opératoire pour fermer la communication bucco-nasale. Dans un cas, une reconstruction de la perte de substance par un lambeau de rotation palatin a été effectuée au bout de 2 ans de suivi. Discussion : La découverte d'un CME chez des jeunes patients est rare. Ces deux observations permettent de faire le point sur la prise en charge de ce type de cancer en fonction des caractéristiques histologiques. Abstract -Palatal mucoepidermoid carcinoma: diagnosis and multidisciplinary care. Introduction:Mucoepidermoid carcinoma (MEC) is a malignant tumor of the salivary glands. Depending on the histological grading, treatment requires surgery with or without radiotherapy. Observation: Two cases of MEC in young female patients are described. The clinical examination revealed a purplish lesion located on the hard palate. The histological examination confirmed the diagnosis of a low-grade MEC. Cone beam computed tomography, a cervicothoracic CT scan and a MRI were performed in order to control lesion extension and exclude a metastatic evolution. Resection of the lesion was performed and oro-nasal communication was immediately closed by a prosthetic obturator. In one case, no recurrence was observed, and closure of the oro-nasal communication was performed two years later by a palatal rotation flap. Discussion: MEC in adolescents is rare. These observations are opportunity to review the management of this type of cancer with regard to histological typing.

Most patients with testicular seminoma have been treated with a curative intent for decades. Second cancers after radiotherapy for testicular seminoma before 1990 are a growing issue, and are related to previous generation of dose planning and delineating strategies. Among those cancers, hepatocellular carcinoma is an extremely rare occurrence, especially when affecting patients with healthy, noncirrhotic liver. Here, we describe such a case in a patient of our institution, and subsequently review the relevant literature and large epidemiologic studies. Understanding those late and serious toxicity features may help cancer care teams to screen and treat those patients appropriately. ( J CLIN EXP HEPATOL 2016;6:54-58) M ajor improvement in testicular cancer treatment in the second half of the 20th century made it a curable disease, mainly thanks to platinum-based chemotherapy and radiation therapy. 1,2 Cancer of the testis has one of the best 5-year survival rate. 3,4 Avoiding long-term iatrogenic morbidity is now part of the treatment plan. Among the many malignancies arising from the radiotherapy field of previously treated testicular cancer patients, hepatocellular carcinoma is a rare occurrence. We describe a case of a patient presenting with in-field hepatocellular carcinoma 34 years after radiotherapy for testicular seminoma. CASE REPORTA 62-year-old man presented in April 2013 with dehydration and acute renal failure. Relevant medical history reported a left testicular seminoma in 1979, for which he underwent left orchidectomy, adjuvant platinum-based chemotherapy, and radiotherapy. Other history included transient ischemic attack in 2002. He had lost 8 kg over the past 8 months. On examination, there was no symptom of portal hypertension or chronic liver failure. Abdominal ultrasound (US) found a heterogeneous liver mass. Thoracic and abdominal computerized tomography scan (CT scan) found a 16 cm great axis tumor occupying left liver lobe almost entirely, associated with left portal thrombosis (Figure 1). The thrombus was believed to be of tumorous nature. Angio-CT scan of the liver confirmed the invasion of the left portal vein branch by the tumor. The Right liver lobe was not affected and presented normal radiological features. No distant metastases were found. Gastroscopy and colonoscopy showed no suspicious lesions. Alphafetoprotein level was 374,000 ng/mL. Other tumor markers were within normal range. Liver biopsies were performed. Pathology report came to the conclusion of a well-differentiated hepatocarcinoma (Figure 2). Liver function test were unaffected. Every major cause of cirrhosis and liver disease was ruled out including alcoholic cirrhosis, autoimmune hepatitis, hemochromatosis, Non-Alcoholic Steato-Hepatitis (NASH) or fatty liver disease, primary biliary cirrhosis, sclerosing cholangitis, and Wilson's disease. Viral serologies were negative for hepatitis B (HBs antigen and HBc antibody), hepatitis C, and cytomegalovirus (CMV), and there were no clinical suspicions of viral hepatitis. N...