Publications by authors named "J Groden"

Activation of a telomere length maintenance mechanism (TMM), including telomerase and alternative lengthening of telomeres (ALT), is essential for replicative immortality of tumor cells, although its regulatory mechanisms are incompletely understood. We conducted a microRNA (miRNA) microarray analysis on isogenic telomerase positive (TEP) and ALT cancer cell lines. Amongst nine miRNAs that showed difference in their expression in TEP and ALT cancer cells in array analysis, miR-708 was selected for further analysis since it was consistently highly expressed in a large panel of ALT cells.

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Rare biallelic gene mutations cause Bloom syndrome. Whether heterozygous germline mutations () cause human cancer remains unclear. We sequenced the germline DNA of 155 mesothelioma patients (33 familial and 122 sporadic).

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Past research suggests that stress and anxiety are more prevalent in persons with autism as compared to typically developing persons. The Stress Survey Schedule (SSS) was developed in 2001 as a means to measure stressors common to persons with Autism Spectrum Disorder (ASD). The present study compared SSS responses of a sample of students diagnosed with ASD and intellectual disability with a group of typically developing students to explore the divergent validity and internal consistency of this measure, and to assess changes in scores among pre-adolescent and adolescent populations.

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Cell division and organismal development are exquisitely orchestrated and regulated processes. The dysregulation of the molecular mechanisms underlying these processes may cause cancer, a consequence of cell-intrinsic and/or cell-extrinsic events. Cellular DNA can be damaged by spontaneous hydrolysis, reactive oxygen species, aberrant cellular metabolism or other perturbations that cause DNA damage.

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Mutation of the gene occurs in a high percentage of colorectal tumors and is a central event driving tumor initiation in the large intestine. The APC protein performs multiple tumor suppressor functions including negative regulation of the canonical WNT signaling pathway by both cytoplasmic and nuclear mechanisms. Published reports that APC interacts with β-catenin in the chromatin fraction to repress WNT-activated targets have raised the possibility that chromatin-associated APC participates more broadly in mechanisms of transcriptional control.

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