Anne of Green Gables

When aging brother and sister Matthew and Marilla Cuthbert send to the orphanage in Nova Scotia for a boy to help them on the farm, they get more than they bargained for, 11-year-old Anne Shirley. This swift yet theatrical adaptation of the classic novel is an all-ages crowd-pleaser.https://digitalcommons.cedarville.edu/theatre_productions/1050/thumbnail.jp

Silent Sky

Henrietta Leavitt is excited to land a job at the prestigious Harvard Observatory in the early 1900s. Once on the job, she soon realizes she was not hired to be an astronomer, but to serve with a group of female “computers” who merely chart the stars for a man who thinks women are not worthy to be astronomers. Henrietta persists in making her mark within the astronomical society, but finds as she measures the light and distance of stars that she must also take measure of her life on Earth. As a result, she has to choose between her dedication to science, her family, or the possibility of love. Based on the true story of 19th-century astronomer Henrietta Leavitt, the play explores a woman’s place in society during a time of immense scientific discoveries, when women’s ideas were dismissed and credited to men in the field. Leavitt’s story changes the way we see and understand both the glory of the heavens and our purpose on the Earth.https://digitalcommons.cedarville.edu/theatre_productions/1049/thumbnail.jp

The Heiress

Shy and plain young girl Catherine Sloper falls desperately in love with the charming and handsome Morris Townsend. Catherine’s father, a successful doctor, forbids their marriage, fearing that the attraction Morris feels for Catherine may be more for her fortune than for her character. Catherine’s love for Morris is genuine but haunted by doubts regarding her appearance and lack of worldly experience. Her fears are realized when her proposed plan of an elopement fails to succeed, and she retreats into a world of loneliness. But when Morris returns and proposes to her once again, she responds in a shockingly unexpected way. His reaction leaves us to wonder whether Morris is sincere in his love for Catherine, or is rather the fulfillment of Catherine’s fears.https://digitalcommons.cedarville.edu/theatre_productions/1045/thumbnail.jp

Four Comic One-Act Plays

These fast-paced comedies have been collected to be performed together as one entertaining show. All rooted in farce comedy, each explores the frustrating, exasperating, and fun-to-watch situations that happen to people in various social settings. The five short plays are “An Unwilling Martyr,” which presents an overburdened man dealing with ludicrous chores and obligations; “The Anniversary,” which takes a look at frenetic scenes at a bank; “The Wedding,” which depicts a social setting where the mother-of-the-bride causes some awkward but hilarious gaffes; “The Bear,” where a widow unable to pay her rent turns the tables on her landlord; and “The Proposal,” where a suitor winds up in a battle over property. The production will feature Russian music and dancing in a colorful and exciting show set in the social world of the 1890s.https://digitalcommons.cedarville.edu/theatre_productions/1048/thumbnail.jp

Meet Me in St. Louis

It is the summer of 1903, and the Smith family eagerly anticipates the opening of the 1904 World’s Fair. Memorable musical numbers include Have Yourself a Merry Little Christmas, The Boy Next Door, The Trolley Song, and Whenever I’m with You. A delightful show for all ages!https://digitalcommons.cedarville.edu/theatre_productions/1051/thumbnail.jp

Low-risk susceptibility alleles in 40 human breast cancer cell lines

Background: Low-risk breast cancer susceptibility alleles or SNPs confer only modest breast cancer risks ranging from just over 1.0 to 1.3 fold. Yet, they are common among most populations and therefore are involved in the development of essentially all breast cancers. The mechanism by which the low-risk SNPs confer breast cancer risks is currently unclear. The breast cancer association consortium BCAC has hypothesized that the low-risk SNPs modulate expression levels of nearby located genes. Methods: Genotypes of five low-risk SNPs were determined for 40 human breast cancer cell lines, by direct sequencing of PCR-amplified genomic templates. We have analyzed expression of the four genes that are located nearby the low-risk SNPs, by using real-time RT-PCR and Human Exon microarrays. Results: The SNP genotypes and additional phenotypic data on the breast cancer cell lines are presented. We did not detect any effect of the SNP genotypes on expression levels of the nearby-located genes MAP3K1, FGFR2, TNRC9 and LSP1. Conclusion: The SNP genotypes provide a base line for functional studies in a well-characterized cohort of 40 human breast cancer cell lines. Our expression analyses suggest that a putative disease mechanism through gene expression modulation is not operative in breast cancer cell lines

A somatic-mutational process recurrently duplicates germline susceptibility loci and tissue-specific super-enhancers in breast cancers

Somatic rearrangements contribute to the mutagenized landscape of cancer genomes. Here, we systematically interrogated rearrangements in 560 breast cancers by using a piecewise constant fitting approach. We identified 33 hotspots of large (>100 kb) tandem duplications, a mutational signature associated with homologous-recombination-repair deficiency. Notably, these tandem-duplication hotspots were enriched in breast cancer germline susceptibility loci (odds ratio (OR) = 4.28) and breast-specific 'super-enhancer' regulatory elements (OR = 3.54). These hotspots may be sites of selective susceptibility to double-strand-break damage due to high transcriptional activity or, through incrementally increasing copy number, may be sites of secondary selective pressure. The transcriptomic consequences ranged from strong individual oncogene effects to weak but quantifiable multigene expression effects. We thus present a somatic-rearrangement mutational process affecting coding sequences and noncoding regulatory elements and contributing a continuum of driver consequences, from modest to strong effects, thereby supporting a polygenic model of cancer development.DG is supported by the EU-FP7-SUPPRESSTEM project. SN-Z is funded by a Wellcome Trust Intermediate Fellowship (WT100183MA) and is a Wellcome Beit Fellow. For more information, please visit the publisher's website

The landscape of somatic copy-number alteration across human cancers

available in PMC 2010 August 18.A powerful way to discover key genes with causal roles in oncogenesis is to identify genomic regions that undergo frequent alteration in human cancers. Here we present high-resolution analyses of somatic copy-number alterations (SCNAs) from 3,131 cancer specimens, belonging largely to 26 histological types. We identify 158 regions of focal SCNA that are altered at significant frequency across several cancer types, of which 122 cannot be explained by the presence of a known cancer target gene located within these regions. Several gene families are enriched among these regions of focal SCNA, including the BCL2 family of apoptosis regulators and the NF-κΒ pathway. We show that cancer cells containing amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend on the expression of these genes for survival. Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in several cancer types.National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, P50CA90578)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, R01CA109038))National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, R01CA109467)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, P01CA085859)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, P01CA 098101)National Institutes of Health (U.S.) (Dana-Farber/Harvard Cancer Center and Pacific Northwest Prostate Cancer SPOREs, K08CA122833