Lung carcinomas are the leading cause of cancer-related deaths in the\u00a0United States and worldwide.\u00a0Lung squamous cell carcinomas\u00a0(non-small cell lung\u00a0cancers that arise in the bronchi of the lungs and make up approximately 30 percent of all lung cancers) are poorly\u00a0 understood, particularly with respect to the cell type and signals that contribute\u00a0to disease onset.<\/p>\n
According to the researchers, treatments for lung squamous cell carcinomas\u00a0are limited\u00a0and research into the etiology of the disease is\u00a0required to create new ways to treat it.<\/p>\n
\u201cOur study offers insight into how damage to the airways of the lung develops into lesions that can transition to cancer. Identifying and treating pre-cancer lesions would offer an opportunity for intercepting lung cancer development,\u201d said corresponding author Bob Varelas, PhD, associate professor of biochemistry.<\/p>\n
The study shows that disruption of proteins that control the shape of the lung epithelium drives signals that promote precancerous cellular growth in the airways of the lung. Using a combination of new experimental models, human tissues and bio-computational approaches, the researchers were able to show that damage to the architecture (polarity) of the lung epithelium drives signals that promote the formation of lesions that resemble human pre-cancer lesions that are known to progress to lung squamous cell carcinoma. The polarity damage can be caused in part by factors known to contribute to lung cancer, such as cigarette smoke exposure.<\/p>\n
The researchers further identified factors that control a gene expression program associated with pre-cancer development and progression in human patients. From these genes they identified one factor, the growth factor Neuregulin-1, that is associated with pre-cancer cell growth that can be therapeutically targeted for treatment of pre-cancer lesions in experimental models. \u201cTargeting these signals may allow us to prevent and treat the formation of pre-cancer lesions,\u201d explained Dr. Varelas.<\/p>\n
Funding for this study was provided by the Boston University Flow Cytometry core and support by the National Center for Advancing Translational Sciences, NIH, through BU-CTSI Grant Number 1UL1TR001430. X.V. was funded by a grant from the NIH NHLBI (R01HL124392) and an American Cancer Society\u2013Ellison New England Research Scholar Grant (RSG-17-138-01- CSM); N.M.K. was funded by NIH NHLBI Grant F31HL146163; J.H.B. was funded by NIH NHLBI Grant F31HL132506; J.G.K. was funded by NIH NCI Grant F31CA232683; J.B. was supported by a Janssen Pharmaceuticals Sponsored Research Agreement; and S.M. was supported by T32HL125232.<\/p>\n","protected":false},"excerpt":{"rendered":"
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