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Ductal carcinoma in situ (DCIS) is a non-obligate precursor to most types of invasive breast cancer (IBC). Although it is estimated only one third of untreated patients with DCIS will progress to IBC, standard of care for treatment is surgery and radiation. This therapeutic approach combined with a lack of reliable biomarker panels to predict DCIS progression is a major clinical problem. DCIS shares the same molecular subtypes as IBC including estrogen receptor (ER) and progesterone receptor (PR) positive luminal subtypes, which encompass the majority (60–70%) of DCIS. Compared to the established roles of ER and PR in luminal IBC, much less is known about the roles and mechanism of action of estrogen (E2) and progesterone (P4) and their cognate receptors in the development and progression of DCIS. This is an underexplored area of research due in part to a paucity of suitable experimental models of ER+/PR + DCIS. This review summarizes information from clinical and observational studies on steroid hormones as breast cancer risk factors and ER and PR as biomarkers in DCIS. Lastly, we discuss emerging experimental models of ER+/PR+ DCIS.

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Results: The results of immunohistochemistry and EBER are shown in the table. Survivin and Bax were expressed strongly in all the cases, and the pattern of staining was both nuclear and cytoplasmic. No apparent correlation was seen between the expression of EBER and p5. CC p5 Bax Survivin Bcl-2 EBER Absent 56% 6% 0% 0% 6% 64% Weak 42% 92% 0% 0% 5%-Strong 2% 2% 100% 100% 2% 6% Conclusions: Our study demonstrates abnormalities in the apoptotic pathways in HRS cells in pediatric cHL. Down-regulation of p53 may contribute to the over-expression of survivin, which then suppresses the final apoptosis effector CC3 and contributes to the resistance of HRS cells to apoptosis, despite the strong expression of the upstream Bax. Survivin may therefore be a potential target for the treatment of pediatric cHL. Background: Neuroblastoma (NB) is a pediatric solid tumour with a poor outcome except in children younger than one year. Based on catecholamines urinary excretion, several mass screening programs have been organised in infants. The AKT pathway contributes to tumor aggressiveness in many cancers. The objective was to analyse expression AKT activation in between mass screening NBs in comparison to standard NBs. Design: A first tissue microarray with standard NB was performed with 101 primary tumors and 39 paired metastases (median age of 30 months (range, newborn to 151 months, 16 stage 1, 7 stage 2, 22 stage 3, 48 stage 4 and 8 stage 4S). A second tissue microarray with mass screening NB coming from Quebec and Japan contained 55 primitive tumors and 21 metastases (median age of 7 months (range 1 to 14 months), 16 stage 1, 15 stage 2, 9 stage 3, 6 stage 4 and 9 stage 4S). Immunohistochemical staining was performed using antibodies against, AKT, phosphoAKT and TRKB which is known as a poor prognosis factor of NB. Immunostaining intensity was evaluated by a semi-quantitative score based on the percentage of positive cells. The t-student test was applied for the comparison of protein expression between standard and mass screening NB. Results: The expression of phosphoAKT was significantly higher in primitive tumors, in metastases, in stage 1 and in patient under one year of standard NB (mean intensity 1.92, 2.1, 1.54 and 1.97 in 96%, 92%, 94% and 100% of tumors cells, receptively) than in mass screening NB (mean intensity 1.18, 1.05, 0.96 and 1.22 in 75%, 68%, 62% and 78% of tumors cells, receptively). AKT was only significantly more present in primitive and metastases of standard NB than in mass screening NB, as for TRKB. Conclusions: The activation of AKT pathway is significantly higher in standard than in mass screening NB independently of age, stage and primitive of metastatic status of the tumor. This confirmed that NB diagnosed through mass sceening differ biologically from standard NB. Background: Ewing's sarcoma (ES), a highly aggressive pediatric tumor is associated with translocations that fuse the EWS gene to one of the ETS family of genes/ transcription factors.The resultant fusion proteins effect transcriptional...

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