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Purpose: To assess radiation oncologists' perceptions of training and research opportunities in the fields of genomics, bioinformatics, and immunology. Materials and Methods: A 13-item electronic survey was sent to 101 radiation oncology department chairs and administrators. A separate 30-item electronic survey was sent to 132 members of the American Society for Radiation Oncology Science Council as well as to 565 members of the Association of Residents in Radiation Oncology. Survey responses were collected, and results were analyzed using descriptive statistics. Results: Twenty-six department chairs and 91 general respondents submitted responses. Among general respondents, 69% were current trainees and 31% had completed training. The majority of respondents (92%) were affiliated with an academic/university main campus. Approximately half of respondents (43% to 53%) reported no prior formal training in bioinformatics, genomics, or immunology. More than half of department chairs (54% to 58%) and general respondents (57% to 63%) thought that current training opportunities in these areas were absolutely or moderately insufficient. A majority of respondents (53% to 65%) thought that additional training in these areas would provide opportunity for career advancement, and 80% could identify a current or future research project that additional training in these fields would allow them to pursue. More than half of respondents expressed interest in attending a formal training course, and the majority of department chairs (22 of 26 [85%]) reported that they would probably or definitely send trainees or faculty members to a formal training course. Conclusion: Among radiation oncologists surveyed, there is a perceived lack of current training opportunities in bioinformatics, genomics, and immunology. A majority of respondents reported an interest in obtaining additional training in these areas and believed that training would provide opportunity for career advancement. [ABSTRACT FROM AUTHOR]

The expression of protein phosphatase 32 (PP32, ANP32A) is low in poorly differentiated pancreatic cancers and is linked to the levels of HuR (ELAV1), a predictive marker for gemcitabine response. In pancreatic cancer cells, exogenous overexpression of pp32 inhibited cell growth, supporting its long-recognized role as a tumor suppressor in pancreatic cancer. In chemotherapeutic sensitivity screening assays, cells overexpressing pp32 were selectively resistant to the nucleoside analogs gemcitabine and cytarabine (ARA-C), but were sensitized to 5-fluorouracil; conversely, silencing pp32 in pancreatic cancer cells enhanced gemcitabine sensitivity. The cytoplasmic levels of pp32 increased after cancer cells are treated with certain stressors, including gemcitabine. pp32 overexpression reduced the association of HuR with the mRNA encoding the gemcitabine-metabolizing enzyme deoxycytidine kinase (dCK), causing a significant reduction in dCK protein levels. Similarly, ectopic pp32 expression caused a reduction in HuR binding of mRNAs encoding tumor-promoting proteins (e.g., VEGF and HuR), while silencing pp32 dramatically enhanced the binding of these mRNA targets. Low pp32 nuclear expression correlated with high-grade tumors and the presence of lymph node metastasis, as compared to patients' tumors with high nuclear pp32 expression. Although pp32 expression levels did not enhance the predictive power of cytoplasmic HuR status, nuclear pp32 levels and cytoplasmic HuR levels associated significantly in patient samples. Thus, we provide novel evidence that the tumor suppressor function of pp32 can be attributed to its ability to disrupt HuR binding to target mRNAs encoding key proteins for cancer cell survival and drug efficacy. [ABSTRACT FROM AUTHOR]

Although interleukin 13 (IL-13) is an important mediator of asthma and allergic diseases, the molecular mechanisms regulating IL-13 gene expression are not well understood. This study was designed to define the molecular mechanisms governing IL-13 gene expression in T cells. IL-13 expression was examined in human peripheral blood T cells and in the EL-4 T-cell line by enzyme-linked immunosorbent assay and reverse-transcription polymerase chain reaction. An IL-13 promoter deletion analysis was performed using luciferase-based reporter plasmids transiently transfected into EL-4 cells by electroporation. DNA binding factors were investigated using electrophoretic mobility shift assays. In contrast to IL-4 expression, which required concomitant activation of calcium- and protein kinase C- (PKC-) dependent signalling pathways, PKC activation alone was sufficient for IL-13 protein secretion in mitogen-primed (but not resting) peripheral blood T cells, and for IL-13 mRNA expression and promoter activity in EL-4 T cells. Promoter deletion analysis localized a phorbol 12-myristate 13-acetate (PMA) -sensitive element to a proximal promoter region between − 109 and − 79 base pairs upstream from the IL-13 transcription start site. This promoter region supported the binding of both constitutive and PMA-inducible nuclear factors in gel shift assays. [ABSTRACT FROM AUTHOR]