452 research outputs found
Angaria neglecta Poppe & Goto 1993
No full textneglecta, Angaria Poppe & Goto, 1993 Angaria neglecta Poppe & Goto, 1993: 22 (pl. 6). Gastropoda, Angariidae Paratype: MZSP 95951. Locality: Japan, Wakayama prefecture, Nada-Cho, 510 fms. Preservation: Dry. Remarks: Former Jens Hemmen Collection. The specimen listed above was initially designated as paratype # 12 in the original description. The senior author (Poppe, pers. comm.) confirmed the type status.Published as part of Cavallari, Daniel C., Dornellas, Ana Paula S. & Simone, Luiz Ricardo L., 2016, Second annotated list of type specimens of molluscs deposited in the Museu de Zoologia da Universidade de São Paulo, Brazil, pp. 1-59 in European Journal of Taxonomy 213 on page 38, DOI: 10.5852/ejt.2016.213, http://zenodo.org/record/384012
Eurytemora americana Williams, 1906, not Eurytemora affinis (Poppe, 1880), inhabits the Bahía Blanca estuary, Argentina
No full textThe aim of this report is to clarify the taxonomical identity of the species of Eurytemora (Copepoda, Calanoi- da) present in the Bahía Blanca estuary, Argentina. Observations of taxonomical details were performed and the results led us to conclude that this species is Eurytemora americana Williams, 1906 and not Eurytemora affinis (Poppe, 1880), as pre- viously identified. E. americana is a recent invader in this estuary and could have been accidentally introduced with ballast water of shipsFil: Hoffmeyer, Monica Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto Argentino de Oceanografía. Universidad Nacional del Sur. Instituto Argentino de Oceanografía; ArgentinaFil: Frost, Bruce W. University of Washington; Estados UnidosFil: Castro, María Belén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto Argentino de Oceanografía. Universidad Nacional del Sur. Instituto Argentino de Oceanografía; Argentin
Prolonged recombinant pregnancy hormone use in BRCA1 and BRCA2 mutation carriers
No full textBackground
An early first full-time pregnancy substantially reduces the risk of developing breast cancer later in life. Extensive studies indicate that this protective effect is mediated by the pregnancy hormone human chorionic gonadotrophin (hCG).
Methods
In this proof-of-concept study 33 women with a BRCA mutation received recombinant-hCG (r-hCG). A 4-mm breast biopsy was obtained before (T1) and after 12 weeks of r-hCG injections (T2), as well as 6 months later (T3). The tissue was examined using RNA-sequencing methodology to determine if the 'high-risk' transcriptomic signature was converted to a 'low-risk' signature as in an early first full-time pregnancy. A stringent clinical safety monitoring was performed.
Results
The r-hCG administration was well tolerated in all participants. No clinically relevant changes were observed. In 25 women, the RNA quality was good for RNA sequencing in all three breast tissue biopsies. In response to the r-hCG, we observed 1907 differentially expressed genes (DEGs) (1032 up, 875 down) at T2 vs. T1 and 1065 DEGs (897 up, 168 down) at T3 vs. T1 in the group of women (n = 11) not using any hormonal contraceptives during the study. There was no response at T2 vs. T1 and a small number of DEGs, 260 (214 up, 46 down) at T3 vs. T1 in the group of 14 women using contraceptives.
Conclusions
In summary, r-hCG has a remarkable effect on the gene expression profile of breast tissues from BRCA1/2 carriers who did not use any contraception. This opens an opportunity for a novel preventive strategy to reduce the incidence of breast cancer
Oncogenetic testing for Lynch syndrome and familial adenomatous polyposis : Synthese
No full text7 p.ill.
Oncogenetische testen voor Lynch syndroom en familiale adenomateuze polypose : Samenvatting
No full text7 p.ill.,Het Federaal Kenniscentrum voor de Gezondheidszorg (KCE)ontwikkelde samen met het College voor Genetica en het College voor Oncologie praktijkrichtlijnen voor oncogenetische testen bij colorectale kanker. De richtlijnen beschrijven de selectie van patiënten met een verhoogd risico op een erfelijke vorm van colorectale kanker, met name Lynch syndroom en Familiale adenomateuze polyposis (FAP). Patiënten met een verhoogd risico moeten worden doorverwezen naar een centrum voor menselijke erfelijkheid voor counseling, eventueel gevolgd door genetische testen en gepaste verdere opvolging
Dépistage oncogénétique du syndrome de Lynch et de la polypose adénomateuse familiale : Résumé
No full text7 p.ill.,Dans le classement des tumeurs malignes les plus fréquentes, le cancer du côlon occupe actuellement la troisième place chez les hommes et la deuxième chez les femmes. Une prise en charge multidisciplinaire a toutefois permis d’améliorer sensiblement son pronostic : dans l’état actuel des choses, 60 à 70% des malades sont toujours en vie après 5 ans. Les éléments déterminants de cette approche sont les soins pré-, péri- et postopératoires et le recours à un traitement sur mesure (« personalised care »). Ces conclusions figurent dans les recommandations actualisées rédigées par le Centre Fédéral d’Expertise des Soins de Santé (KCE) en collaboration avec le Collège d’Oncologie et le centre d’expertise néerlandais Integraal Kankercentrum Nederland
Uncovering the microRNA landscape in T-cell acute lymphoblastic leukemia
No full textT-ALL is an aggressive hematological malignancy that develops in the thymus by uncontrolled proliferation of immature T-cells. T-ALL accounts for 10-15% of pediatric and 25% of adult ALL patients. The current T-ALL treatment protocols consist of multiple chemotherapeutics and lead to a 75% survival rate in children and a 50% survival rate for adults with T-ALL. T-ALL patients can be subdivided in different subgroups, each having genetic lesions that define these subgroups. Additionally, targeted and next generation sequencing led to the discovery of various genetic abnormalities that play part in various cellular processes by targeting important genes in NOTCH1 signaling, cell cycle, hematopoiesis, signal transduction, ribosomal machinery and epigenetic regulation. During the last decade, it has been extensively shown that deregulated miRNA expression contributes to tumorigenesis, but in-depth analysis of miRNAs in the context of T-ALL was not performed yet at the beginning of this thesis.
Together with the research group of Prof. Wendel (Memorial Sloan-Kettering Cancer Center, NY, USA), we have demonstrated that known T-ALL tumor suppressor genes are controlled by an extensive network of oncogenic miRNAs, which is presented in the first part of this thesis. We performed miRNA expression profiling on T-ALL patients samples, followed by an independent miRNA library screening finally leading to the identification of five highly expressed miRNAs (miR-19b, miR-20a, miR-26a, miR-92a and miR-223) that are capable of accelerating leukemia onset in a NOTCH1-driven T-ALL mouse model. Furthermore, we also found two less abundantly expressed miRNAs (miR-27a and miR-148a/miR-152) that are able to induce accelerated leukemia onset in this mouse model. All of these miRNAs are part of a cooperative miRNA-tumor suppressive network of important tumor suppressor genes that are involved in T-ALL pathogenesis, namely IKAROS (IKZF1), PTEN, BIM, PHF6, NF1 and FBXW7.
In order to further expand the regulatory miRNA network with oncogenes and novel tumor suppressor genes, we performed a miRNAome wide screen of the 3'UTRs of important tumor suppressor genes (PHF6, FBW7, RB1, EZH2) and oncogenes (NOTCH1, MYC and MYB) implicated in T-ALL using a library of 470 miRNA mimic molecules. During the course of this thesis, we decided to focus on the unraveling of the miRNA-MYB and miRNA-PHF6 networks. Integrated analysis of miRNA and mRNA expression data leads to the selection of different miRNAs for further investigation. We selected miR-128-3p and miR-574-3 as top candidate miRNAs targeting PHF6 and miR-193b-3p as top candidate miRNA targeting MYB. Finally in vitro and in vivo modeling capacitated and confirmed the identification of miR-128-3p as a novel tumor suppressor miR, targeting PHF6, and miR-193b-3p as a novel oncomiR, targeting MYB and MCL1 in T-ALL.
Future experiments will focus on all the other library screening results, to select other candidate miRNAs. These miRNAs will be assessed similarly as miR-128-3p and miR-193b-3p to further extend the miRNA/mRNA network that is implicated in the development of T-ALL
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