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1.
Pediatr Blood Cancer ; 70(3): e30118, 2023 03.
Article in English | MEDLINE | ID: mdl-36573297

ABSTRACT

BACKGROUND: A recent survey of pediatric hematology oncology (PHO) physicians identified that a majority believe fellows are struggling to find jobs that align with their goals. Career development for trainees has historically been home institution-specific, limiting fellows' exposures to career path possibilities. The "virtual-Symposium of Pediatric Hematology/Oncology of New York (v-SYMPHONY)" instituted a tristate Career Development Series for PHO trainees to better address their needs and increase awareness of the variety of PHO career opportunities. PROCEDURE: The v-SYMPHONY Career Development Series incorporated three sessions: (a) institutional perspective, (b) individual perspectives, and (c) nuts and bolts of job search. Pre- and post-series surveys were administered to participants to measure impact. RESULTS: Forty-one fellows registered for the series and completed a pre-survey. Over half (54%) were in their third or later year of fellowship. Careers with a clinical focus were the most commonly desired career path (59%). Most had received career development advice only from faculty within their institutions (90%). Post-surveys were completed by 11 PHO fellows. Overall, 100% of respondents reported benefiting from the career sessions and recommended the series should be repeated annually. Over 90% learned new information to prepare for the job search. CONCLUSIONS: The v-SYMPHONY Career Development Series for PHO fellows across multiple institutions was established and was extremely well received by its participants. PHO fellows agreed that these sessions were beneficial in helping prepare them for the job search process. An annual regional Career Development Series is feasible and is strongly suggested to support PHO fellows.


Subject(s)
Hematology , Child , Humans , New York , Fellowships and Scholarships , Surveys and Questionnaires , Medical Oncology , Career Choice
2.
J Pediatr Hematol Oncol ; 43(2): 52-58, 2021 03 01.
Article in English | MEDLINE | ID: mdl-32815877

ABSTRACT

BACKGROUND: Outcome of patients with osteosarcoma (OS) and Ewing sarcoma (EWS) is dependent on presence of metastases. Imaging guidelines for OS and EWS include radiographs, computed tomography (CT), and magnetic resonance imaging for primary tumor evaluation and CT chest and bone scintigraphy (BS) for metastatic detection. 18Fluorodeoxyglucose (18FDG) positron emission tomography (PET)/CT has become more common for disease evaluation, yet there is no consensus for its use in this population. OBJECTIVE: We aimed to compare identification of osseous metastases using BS versus 18FDG PET/CT in our patient population. We hypothesized that 18FDG PET/CT is more likely to detect osseous metastases both at diagnosis and relapse. MATERIALS AND METHODS: We performed retrospective chart reviews of pediatric sarcoma patients treated at our institution from 2008 to 2019. Paired BS and 18FDG PET/CT scans were reviewed. Review of the literature was also performed. RESULTS: Thirty-three patients had paired BS and 18FDG PET/CT during diagnosis or treatment. Fifteen patients had distant osseous metastases. In the OS cohort, 8/16 patients had osseous metastases; 100% of these patients were detected on 18FDG PET/CT and 75% on BS. Thirty-one bony lesions were seen on imaging in OS patients; 100% of these were identified on 18FDG PET/CT but only 29% on BS. In the EWS cohort, 6/15 patients had osseous metastases; 100% of these patients were detected on 18FDG PET/CT and 50% on BS. Eighteen bony lesions were seen on imaging in EWS patients; 94% of these were identified on 18FDG PET/CT, but only 28% on BS. CONCLUSION: For patients in our institution with OS or EWS, osseous metastases were more likely detected using 18FDG PET/CT.


Subject(s)
Bone Neoplasms/secondary , Fluorodeoxyglucose F18/metabolism , Magnetic Resonance Imaging/methods , Osteosarcoma/pathology , Positron Emission Tomography Computed Tomography/methods , Sarcoma, Ewing/pathology , Adolescent , Adult , Bone Neoplasms/diagnostic imaging , Bone Neoplasms/metabolism , Bone Neoplasms/surgery , Child , Child, Preschool , Female , Follow-Up Studies , Humans , Male , Middle Aged , Osteosarcoma/diagnostic imaging , Osteosarcoma/metabolism , Osteosarcoma/surgery , Prognosis , Radiopharmaceuticals/metabolism , Retrospective Studies , Sarcoma, Ewing/diagnostic imaging , Sarcoma, Ewing/metabolism , Sarcoma, Ewing/surgery , Young Adult
3.
J Neurogenet ; 24(1): 18-26, 2010 Mar.
Article in English | MEDLINE | ID: mdl-20131966

ABSTRACT

A mild form of autosomal recessive, nonsyndromal intellectual disability (ARNSID) in humans is caused by a homozygous nonsense mutation in the cereblon gene (mutCRBN). Rodent crbn protein binds to the intracellular C-terminus of the large conductance Ca(2+)-activated K(+)channel (BK(Ca)). An mRNA variant (human SITE 2 INSERT or mouse strex) of the BK(Ca) gene (KCNMA1) that is normally expressed during embryonic development is aberrantly expressed in mutCRBN human lymphoblastoid cell lines (LCLs) as compared to wild-type (wt) LCLs. The present study analyzes the temporal and spatial distribution of crbn and kcnma1 mRNAs in the mouse brain by the quantitative real-time reverse transcriptase-polymerase chain reaction (qPCR). The spatial expression pattern of endogenous and exogenous crbn proteins is characterized by immunostaining. The results show that neocortical (CTX) crbn and kcnma1 mRNA expression increases from embryonic stages to adulthood. The strex mRNA variant is >3.5-fold higher in embryos and decreases rapidly postnatally. Mouse crbn mRNA is abundant in the cerebellum (CRBM), with less expression in the CTX, hippocampus (HC), and striatum (Str) in adult mice. The intracytoplasmic distribution of endogenous crbn protein in the mouse CRBM, CTX, HC, and Str is similar to the immunostaining pattern described previously for the BK(Ca) channel. Exogenous hemagglutinin (HA) epitope-tagged human wt- and mutCRBN proteins using cDNA transfection in HEK293T cell lines showed the same intracellular expression distribution as endogenous mouse crbn protein. The results suggest that mutCRBN may cause ARNSID by disrupting the developmental regulation of BK(Ca) in brain regions that are critical for memory and learning.


Subject(s)
Brain/metabolism , Nerve Tissue Proteins/genetics , Nerve Tissue Proteins/metabolism , Peptide Hydrolases/genetics , Peptide Hydrolases/metabolism , Adaptor Proteins, Signal Transducing , Aging/genetics , Aging/metabolism , Animals , Brain/embryology , Brain/growth & development , Cell Line , Child, Preschool , Developmental Disabilities/genetics , Developmental Disabilities/metabolism , Developmental Disabilities/physiopathology , Gene Expression Regulation, Developmental/genetics , Humans , Immunohistochemistry , Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/genetics , Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/metabolism , Mice , Mice, Inbred C57BL , Mutation/genetics , RNA, Messenger/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Time Factors , Transfection/methods , Ubiquitin-Protein Ligases
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