Returning to Ulysses: The Need for Ireland\u27s Higher Education Institutions to Re-imagine the Provision of Entrepreneurship Education

This paper is a detailed analysis of entrepreneurship education in Higher Education Institutions (HEIs) on the island of Ireland based on a survey of all twenty-six institutions. The paper examines the number and types of courses and activities currently being offered to students and concludes that the vast majority of the existing provision is quite traditional in its approach. It is further argued that entrepreneurship education needs to be re-imagined if it is to meet the needs of Ireland’s current economic and social challenges, and that educators should seek inspiration from some of the island’s most creative artists from its rich artistic culture. The efforts to promote entrepreneurship amongst young people on the island of Ireland have become increasingly active over the past fifteen years. According to Hynes (1996) the increased interest in entrepreneurship education and training can also be attributed to the changing structure of the Western economy, the trend in downsizing in large companies, changing business patterns, and developing market economies in other parts of the globe. This paper seeks to examine what has altered in the intervening period, particularly given the background of the devastating economic recession that has hit Ireland, plus the new wave of emigration that has become an increasingly popular choice being made by the younger generation in search of secure employment. These new challenges require newly crafted solutions and entrepreneurship education has a significant role to play in any renewed economy

Risk of second primary tumors in men diagnosed with prostate cancer: A population‐based cohort study

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/108272/1/cncr28769.pd

Rare germline mutations in African American men diagnosed with earlyâ onset prostate cancer

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142420/1/pros23464_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/142420/2/pros23464.pd

Genetic polymorphisms in CYP17 , CYP3A4 , CYP19A1 , SRD5A2 , IGF-1 , and IGFBP-3 and prostate cancer risk in African-American men: The Flint Men's Health Study

BACKGROUND Association studies have examined the significance of several candidate genes based on biological pathways relevant to prostate carcinogenesis, including both the androgen and insulin-like growth factor pathways. Clinical and epidemiologic evidence suggest that androgens, specifically testosterone and dihydrotestosterone (DHT) are important not only in normal prostate growth but in the pathogenesis of prostate cancer. Similarly, the insulin-like growth factor-1 (IGF-1) signaling pathway regulates both cellular proliferation and apoptosis. Therefore, genes involved in the biosynthesis, activation, metabolism and degradation of androgens and the stimulation of mitogenic and antiapoptotic activities of prostate epithelial cells represent important candidates for affecting the development and progression of prostate cancer. METHODS Using resources from the Flint Men's Health Study, a population-based case control study of African-American men aged 40–79, we evaluated the associations between selected single-nucleotide polymorphisms (SNPs) in the CYP17 , CYP3A4 , CYP19A1 , SDR5A2 , IGF1 , and IGFBP3 genes and prostate cancer diagnosis in 473 men (131 prostate cancer cases and 342 disease-free controls). RESULTS We found a significant association between prostate cancer and selected CYP17 SNP genotypes, with the heterozygous genotype conferring decreased risk. Suggestive evidence for association between IGF1 SNPs and prostate cancer were also found. No significant associations were observed between SNPs in the other genes and prostate cancer. CONCLUSIONS These findings suggest that variation in or around CYP17 and/or IGF1 may be associated with prostate cancer development in the African-American population. Additional studies are needed to determine whether these polymorphisms are indeed associated with prostate cancer risk in African Americans. Prostate 68: 296–305, 2008. © 2007 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/57913/1/20696_ftp.pd

Germline genetic variants in men with prostate cancer and one or more additional cancers

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138930/1/cncr30817.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/138930/2/cncr30817_am.pd

Identification of a novel germline SPOP mutation in a family with hereditary prostate cancer

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/106871/1/pros22818.pd

Comprehensive serial molecular profiling of an “N of 1” exceptional non-responder with metastatic prostate cancer progressing to small cell carcinoma on treatment

Abstract Importance Small cell carcinoma/neuroendocrine prostate cancer (NePC) is a lethal, poorly understood prostate cancer (PCa) subtype. Controversy exists about the origin of NePC in this setting. Objective To molecularly profile archived biopsy specimens from a case of early-onset PCa that rapidly progressed to NePC to identify drivers of the aggressive course and mechanisms of NePC origin and progression. Design, setting, and participants A 47-year-old patient presented with metastatic prostatic adenocarcinoma (Gleason score 9). After a 6-month response to androgen deprivation therapy, the patient developed jaundice and liver biopsy revealed exclusively NePC. Targeted next generation sequencing (NGS) from formalin-fixed paraffin-embedded (FFPE)-isolated DNA was performed from the diagnostic prostate biopsy and the liver biopsy at progression. Intervention Androgen deprivation therapy for adenocarcinoma followed by multiagent chemotherapy for NePC. Main outcomes and measures Identification of the mutational landscape in primary adenocarcinoma and NePC liver metastasis. Whether the NePC arose independently or was derived from the primary adenocarcinoma was considered based on mutational profiles. Results A deleterious somatic SMAD4 L535fs variant was present in both prostate and liver specimens; however, a TP53 R282W mutation was exclusively enriched in the liver specimen. Copy number analysis identified concordant, low-level alterations in both specimens, with focal MYCL amplification and homozygous PTEN, RB1, and MAP2K4 losses identified exclusively in the NePC specimen. Integration with published genomic profiles identified MYCL as a recurrently amplified in NePC. Conclusions and relevance NGS of routine biopsy samples from an exceptional non-responder identified SMAD4 as a driver of the aggressive course and supports derivation of NePC from primary adenocarcinoma (transdifferentiation).http://deepblue.lib.umich.edu/bitstream/2027.42/113670/1/13045_2015_Article_204.pd

Mutational landscape of candidate genes in familial prostate cancer

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/108266/1/pros22849-sm-0001-SupTab-S1.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/108266/2/pros22849.pd

R726L androgen receptor mutation is uncommon in prostate cancer families in the united states

Background A mutation in the androgen receptor ( AR ) gene, namely AR R726L, was described in 2% of Finnish men with sporadic or familial prostate cancer and was associated with an approximately sixfold increased risk of prostate cancer. We set out to determine the incidence of this mutation in a sample of men with either early-onset and/or familial prostate cancer in the United States. Methods Five hundred forty-eight men with prostate cancer from 411 unrelated families participating in the University of Michigan Prostate Cancer Genetics Project (PCGP) were studied. Allele-specific oligonucleotide hybridization was used to detect the presence of the AR R726L mutation in germline DNA. Results None of the 548 prostate cancer patients studied, including 513 White, 29 African American, 3 Asian, and 3 Hispanic men, were found to carry the AR R726L allele. Therefore, the prevalence of this allele is significantly less than that observed among Finnish men with prostate cancer (Fisher's exact test, P  = 0.002). Conclusions The AR R726L allele does not account for a significant proportion of early-onset and/or familial prostate cancer in the United States. Prostate 54: 306–309, 2003. © 2003 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/34764/1/10195_ftp.pd