Janet Hock

B.D.S., PhD
Maine Institute for Human Genetics and Health

Topics (20) View all

Questions and Answers (7) View all

  • Answer added in Science Communication
    53 How important is storytelling and visualization for your science?
    By Sven Schade · Geospatial Information Scientist
    Janet Hock · Maine Institute for Human Genetics and Health
    Sven: what a great video - thanks for posting. 
  • Answer added in Science Communication
    53 How important is storytelling and visualization for your science?
    By Sven Schade · Geospatial Information Scientist
    Janet Hock · Maine Institute for Human Genetics and Health
    Just an anecdote, We have been working for 3 years on software that maps clinical data on cancer patients and their lifestyle exposures with environme... [more]
  • Answer added in Science Communication
    53 How important is storytelling and visualization for your science?
    By Sven Schade · Geospatial Information Scientist
    Janet Hock · Maine Institute for Human Genetics and Health
    Data visualization is incredibly important as a tool of communication - whether for hard or softer data. We used our clinical data on biobanking to li... [more]
  • Answer added in Bone Research
    11 Cryosection or plastic inclusion of mouse femurs for histomorphometry?
    By Camille Bru · Bone Therapeutics
    Janet Hock · Maine Institute for Human Genetics and Health
    Immunohistochemistry on undecalcified plastic embedded bones is very difficult and on mouse bones, is exceptionally difficult. If you want routine his... [more]
  • Answer added in Air Pollution
    16 Mapping Urban vulnerability to air quality
    By Parth Sarathi Mahapatra · Institute of Minerals and Materials Technology
    Janet Hock · Maine Institute for Human Genetics and Health
    In the US, NIH assembled PhenX as a website (https://www.phenxtoolkit.org/) that would provide standardized questions for surveys anywhere in the worl... [more]

Publications (116) View all

  • Article: Hyperactivation of mTOR critically regulates abnormal osteoclastogenesis in neurofibromatosis Type 1.
    Junrong Ma, Mi Li, Janet Hock, Xijie Yu
    [show abstract] [hide abstract]
    ABSTRACT: Individuals with nerofibromatosis Type 1 (NF1) frequently suffer a spectrum of bone pathologies, such as abnormal skeletal development (scoliosis, congenital bowing, and congenital pseudoarthroses, etc), lower bone mineral density with increased fracture risk. These skeletal problems may result, in part, from abnormal osteoclastogenesis. Enhanced RAS/PI3K activity has been reported to contribute to abnormal osteoclastogenesis in Nf1 heterozygous (Nf1+/-) mice. However, the specific downstream pathways linked to NF1 abnormal osteoclastogenesis have not been defined. Our aim was to determine whether mammalian target of rapamycin (mTOR) was a key effector responsible for abnormal osteoclastogenesis in NF1. Primary osteoclast-like cells (OCLs) were cultured from Nf1 wild-type (Nf1+/+) and Nf1+/- mice. Compared to Nf1+/+ controls, there were 20% more OCLs induced from Nf1+/- mice. Nf1+/- OCLs were larger and contained more nuclei. Hyperactive mTOR signaling was detected in Nf1+/- OCLs. Inhibition of mTOR signaling by rapamycin in Nf1+/- OCLs abrogated abnormalities in cellular size and number. Moreover, we found that hyperactive mTOR signaling induced abnormal osteoclastogenesis major through hyper-proliferation. Our research suggests that neurofibromin directly regulates osteoclastogenesis through mTOR signaling pathway. Inhibiting mTOR may represent a viable strategy to treat NF1 bone diseases.
    Journal of Orthopaedic Research 07/2011; 30(1):144-52. · 2.81 Impact Factor
  • Article: Lawrence G. Raisz November 13, 1925-August 25, 2010.
    Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 05/2011; 26(5):903-11. · 6.04 Impact Factor
  • Article: Analyzing spatial and temporal (222)Rn trends in Maine.
    [show abstract] [hide abstract]
    ABSTRACT: Prolonged radon exposure has been linked to lung cancer. Cancer registry data indicates excess risk for age-adjusted lung cancer in Maine. Maine's mean residential radon activity exceeds the EPA maximum contaminant level (MCL). This paper describes the application of spatial autocorrelation methods to retrospective data as a means of analyzing radon activity in Maine. Retrospective air and well water radon activity data, sampled throughout Maine between 1993 and 2008, are standardized and geocoded for analysis. Three spatial autocorrelation algorithms-local Getis-Ord, local Moran, and spatial scan statistic-are used to identify spatial, temporal, and spatiotemporal radon activity clusters and/or outliers. Spatial clusters of high air- and well water-Rn activity are associated with Maine's Lucerne and Sebago granitic formations. Spatial clusters of low air- and well water-Rn activity are associated with Biddeford Granite and the metamorphic bedrock formation Silurian Ordovician Vassalboro. Space-time analysis indicates that most spatial clusters persist over the period of sampling. No significant temporal clusters are identified. Persistent spatial variations in radon may help to better understand and predict radon-related health risks associated with Maine residences.
    Health physics 02/2012; 102(2):115-23. · 0.92 Impact Factor
  • Article: Unmet challenges in cancer disparities--letter.
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    ABSTRACT: Letter to the Editor re "Unmet Challenges in Cancer Disparities" by Gelhert and Colditz. We agree with the paper and offer data from a case series to support their recommendations.
    Cancer Epidemiology Biomarkers &amp Prevention 12/2011; 21(1):248-9. · 4.12 Impact Factor
  • Article: Activation of the p38 MAPK/Akt/ERK1/2 signal pathways is required for the protein stabilization of CDC6 and cyclin D1 in low-dose arsenite-induced cell proliferation.
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    ABSTRACT: Arsenic trioxide (ATO) is a first-line anti-cancer agent for acute promyelocytic leukemia, and induces apoptosis in other solid cancer cell lines including breast cancer cells. However, as with arsenites found in drinking water and used as raw materials for wood preservatives, insecticides, and herbicides, low doses of ATO can induce carcinogenesis after long-term exposure. At 24 h after exposure, ATO (0.01-1 µM) significantly increased cell proliferation and promoted cell cycle progression from the G1 to S/G2 phases in the non-tumorigenic MCF10A breast epithelial cell line. The expression of 14 out of 96 cell-cycle-associated genes significantly increased, and seven of these genes including cell division cycle 6 (CDC6) and cyclin D1 (CCND1) were closely related to cell cycle progression from G1 to S phase. Low-dose ATO steadily increased gene transcript and protein levels of both CDC6 and cyclin D1 in a dose- and time-dependent manner. Low-dose ATO produced reactive oxygen species (ROS), and activated the p38 MAPK, Akt, and ERK1/2 pathways at different time points within 60 min. Small molecular inhibitors and siRNAs inhibiting the activation of p38 MAPK, Akt, and ERK1/2 decreased the ATO-increased expression of CDC6 protein. Inhibiting the activation of Akt and ERK1/2, but not p38 MAPK, decreased the ATO-induced expression of cyclin D1 protein. This study reports for the first time that p38 MAPK/Akt/ERK1/2 activation is required for the protein stabilization of CDC6 in addition to cyclin D1 in ATO-induced cell proliferation and cell cycle modulation from G1 to S phase.
    Journal of Cellular Biochemistry 12/2010; 111(6):1546-55. · 2.87 Impact Factor

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