Publications by authors named "G A Hallenbeck"

163 Publications

DEK promotes HPV-positive and -negative head and neck cancer cell proliferation.

Oncogene 2015 Feb 10;34(7):868-77. Epub 2014 Mar 10.

Cancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.

Head and neck squamous cell carcinoma (HNSCC) is the sixth most common malignancy worldwide, and patient outcomes using current treatments remain poor. Tumor development is etiologically associated with tobacco or alcohol use and/or human papillomavirus (HPV) infection. HPV-positive HNSCCs, which frequently harbor wild-type p53, carry a more favorable prognosis and are a biologically distinct subgroup when compared with their HPV-negative counterparts. HPV E7 induces expression of the human DEK gene, both in vitro and in vivo. In keratinocytes, DEK overexpression is sufficient for causing oncogenic phenotypes in the absence of E7. Conversely, DEK loss results in cell death in HPV-positive cervical cancer cells at least in part through p53 activation, and Dek knockout mice are relatively resistant to the development of chemically induced skin papillomas. Despite the established oncogenic role of DEK in HPV-associated cervical cancer cell lines and keratinocytes, a functional role of DEK has not yet been explored in HNSCC. Using an established transgenic mouse model of HPV16 E7-induced HNSCC, we demonstrate that Dek is required for optimal proliferation of E7-transgenic epidermal cells and for the growth of HNSCC tumors. Importantly, these studies also demonstrate that DEK protein is universally upregulated in both HPV-positive and -negative human HNSCC tumors relative to adjacent normal tissue. Furthermore, DEK knockdown inhibited the proliferation of HPV-positive and -negative HNSCC cells, establishing a functional role for DEK in human disease. Mechanistic studies reveal that attenuated HNSCC cell growth in response to DEK loss was associated with reduced expression of the oncogenic p53 family member, ΔNp63. Exogenous ΔNp63 expression rescued the proliferative defect in the absence of DEK, thereby establishing a functional DEK-ΔNp63 oncogenic pathway that promotes HNSCC. Taken together, our data demonstrate that DEK stimulates HNSCC cellular growth and identify ΔNp63 as a novel DEK effector.
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http://dx.doi.org/10.1038/onc.2014.15DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160430PMC
February 2015

Pyloric and duodenal motor contributions to duodenogastric reflux.

Scand J Gastroenterol Suppl 1984 ;92:13-6

The motor mechanisms of duodenogastric reflux were identified in 4 healthy, conscious dogs using electromyographic and fluoroscopic recordings of stomach, duodenum and upper jejunum. A barium suspension was injected via a pre-placed cannula in the orad jejunum, during the interdigestive period. Under normal conditions, reflux was uncommon. It was produced by duodenal segmental contractions occurring when the pylorus was open, or forced open by the duodenal contractions. Reflux was more common during retrograde electrical pacing of the duodenal pacesetter potential. It was then also produced by duodenal segmental contractions associated with an open, or opening, pylorus. During intravenous administration of apomorphine, reflux occurring early in the vomiting complex, was again produced by duodenal segmental contractions associated with an open, or opening, pylorus. The major apomorphine reflux event, however, occurred later when an emetic antiperistaltic contraction, originating in the duodenum or orad jejunum swept the contents before it into the stomach.
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August 1984

Nonsurgical pneumoperitoneum.

Am J Surg 1977 Sep;134(3):411-4

Free intraperitoneal air is not necessarily caused by a perforated viscus. The present study reviews the causes of pneumoperitoneum that do not necessitate laparotomy, and emphasizes the importance of obtaining a complete clinical history.
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http://dx.doi.org/10.1016/0002-9610(77)90418-4DOI Listing
September 1977

Surgery for gastric ulcer. Inivted commentary.

Authors:
G A Hallenbeck

World J Surg 1977 Jan;1(1):31-2

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http://dx.doi.org/10.1007/BF01654726DOI Listing
January 1977

The natural history of duodenal ulcer disease.

Authors:
G A Hallenbeck

Surg Clin North Am 1976 Dec;56(6):1235-42

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December 1976
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