Publications by authors named "Hannah Cheung"

Traumatic experiences can impact individuals' oral health and how they experience dental treatment in ways patients and their dental providers may or may not initially anticipate. As approximately half of children and two-thirds of adults in the United States have experienced some type of traumatic event, it is critically important for providers to be aware of patients' trauma histories and to appropriately provide trauma-informed care to their patients when needed. Individuals with a trauma history may experience significant anxiety and distress in the dental setting, even for treatment many providers and patients consider to be "simple," such as a brief intraoral examination, radiographs, or prophylaxis.

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Human colorectal cancer (CRC) is a major cause of cancer mortality and frequently harbors activating mutations in the gene. To understand the role of oncogenic in CRC, we engineered a mouse model of metastatic CRC that harbors an inducible oncogenic allele ( ) and conditional null alleles of and (iKAP). The iKAP model recapitulates tumor progression from adenoma through metastases.

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Multiple synchronous lung cancers (MSLCs) present a clinical dilemma as to whether individual tumours represent intrapulmonary metastases or independent tumours. In this study we analyse genomic profiles of 15 lung adenocarcinomas and one regional lymph node metastasis from 6 patients with MSLC. All 15 lung tumours demonstrate distinct genomic profiles, suggesting all are independent primary tumours, which are consistent with comprehensive histopathological assessment in 5 of the 6 patients.

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Introduction: Although multiple predispositions to hematologic malignancies exist, evaluations for hereditary cancer syndromes (HCS) are underperformed by most hematologist/oncologists. Criteria for initiating HCS evaluation are poorly defined, and results of genetic testing for hereditary hematologic malignancies have not been systematically reported.

Patients And Methods: From April 2014 to August 2015, 67 patients were referred to the Hereditary Hematologic Malignancy Clinic (HHMC).

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Purpose: We applied whole-genome sequencing (WGS) to children diagnosed with neoplasms and found to carry apparently balanced constitutional translocations to discover novel genic disruptions.

Methods: We applied the structural variation (SV) calling programs CREST, BreakDancer, SV-STAT, and CGAP-CNV, and we developed an annotative filtering strategy to achieve nucleotide resolution at the translocations.

Results: We identified the breakpoints for t(6;12)(p21.

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Background: The cellular response to DNA damage is immediate and highly coordinated in order to maintain genome integrity and proper cell division. During the DNA damage response (DDR), the sensor kinases Tel1 and Mec1 in Saccharomyces cerevisiae and ATM and ATR in human, phosphorylate multiple mediators which activate effector proteins to initiate cell cycle checkpoints and DNA repair. A subset of kinase substrates are recognized by the S/T-Q cluster domain (SCD), which contains motifs of serine (S) or threonine (T) followed by a glutamine (Q).

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Aberrant RNA splicing is thought to play a key role in tumorigenesis. The assessment of its specific contributions is limited by the complexity of information derived from genome-wide array-based approaches. We describe how performing splicing factor-specific comparisons using both tumor and cell line data sets may more readily identify physiologically relevant tumor-specific splicing events.

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Point mutations of EHMT1 or deletions and duplications of chromosome 9q34.3 are found in patients with variable neurologic and developmental disorders. Here, we present a child with congenital cataract, developmental and speech delay who developed a metastatic ganglioglioma with progression to anaplastic astrocytoma.

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Clinical cancer genetic susceptibility analysis typically proceeds sequentially, beginning with the most likely causative gene. The process is time consuming and the yield is low, particularly for families with unusual patterns of cancer. We determined the results of in parallel mutation analysis of a large cancer-associated gene panel.

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Polypyrimidine tract-binding protein 1 (PTBP1) is a multi-functional RNA-binding protein that is aberrantly overexpressed in glioma. PTBP1 and its brain-specific homologue polypyrimidine tract-binding protein 2 (PTBP2) regulate neural precursor cell differentiation. However, the overlapping and non-overlapping target transcripts involved in this process are still unclear.

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Previous work has revealed pre-perturbation cortical activity linked to predictably-timed perturbations to upright stability. Because individuals rely on the ability to anticipate perturbations for independent mobility, we sought to determine whether perturbation-evoked cortical potentials elicited by voluntarily-initiated external perturbations were dissociable from those elicited by externally-cued perturbations. Postural instability was evoked under three experimental conditions: cued external perturbations (EXT-CUE), cued self-initiated perturbations (SELF-CUE), and un-cued self-initiated perturbations (SELF-NO CUE).

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Following disturbances to postural stability, balance recovery reactions are evoked by numerous sensory inputs and characterized by motor reactions involving different patterns of activity, depending on postural task conditions. It remains unknown whether well-documented cortical responses to instability share common spatio-temporal characteristics, despite variations in the sensory, motor, and postural components of the reactions. The objective was to explore the spatio-temporal profile of cortical potentials evoked by instability requiring either upper- or lower-limb compensatory responses.

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Background: Tumor-predominant splice isoforms were identified during comparative in silico sequence analysis of EST clones, suggesting that global aberrant alternative pre-mRNA splicing may be an epigenetic phenomenon in cancer. We used an exon expression array to perform an objective, genome-wide survey of glioma-specific splicing in 24 GBM and 12 nontumor brain samples. Validation studies were performed using RT-PCR on glioma cell lines, patient tumor and nontumor brain samples.

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Polypyrimidine tract binding protein (PTB) is expressed in developing mammalian astrocytes, absent in mature adult astrocytes, and aberrantly elevated in gliomas. It is unclear whether PTB is a coincidental marker of tumor progression or a significant mediator of tumorigenesis. In developing Drosophila, the absence of the PTB homolog, hephaestus, results in increased Notch activity.

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