scholarly journals Biomarkers of risk to develop lung cancer in the new screening era

2016 ◽  
Vol 4 (8) ◽  
pp. 158-158 ◽  
Author(s):  
Thomas Atwater ◽  
Pierre P. Massion
2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Isaac Lamb ◽  
Huaxin Zhou ◽  
Patricia Smith ◽  
Catherine R. Sears, M.D.

Background and Hypothesis: Cigarette smoke (CS) exposure causes lung cancer, with both DNA damage and local inflammation playing a critical role in development. Our previous research links the DNA repair protein Xeroderma Pigmentosum Group C (XPC) with protection against lung cancer in CS- and carcinogen-exposed mouse models. In mice (XPC-deficient and wild-type [WT] littermates) exposed to continuous CS for 9 months, neither XPC-deficient nor WT mice develop lung cancer. XPC-deficient but not WT mice exposed to 5 months CS + 4 months air control (AC) (recovery model) develop lung cancer. In a direct carcinogen model, XPC-deficiency accelerates NTCU lung squamous cell development. Our hypothesis is that lung cancers in XPC-deficient mice are independent of treatment alterations in BAL inflammation. Experimental Design or Project Methods: Acellular bronchoalveolar lavage (BAL) samples from the three different mouse CS and carcinogen models were analyzed for the inflammatory cytokines IL-6, IL10, IL-12p70, IL-17A, IFN-γ, MCP-1, and TNF-α by a cytometric bead array (BD Biosciences) using a flow cytometer (FACScan) according to the manufacturer’s instructions. Raw data (mean fluorescence intensity) was analyzed by BD CBA Software. Statistical comparisons were by ANOVA, with p<0.05 considered significant. Results: All measured cytokine levels were low or undetectable in BAL from AC and CS mice, with no significant XPC genotype or treatment-related changes in the measured cytokines. Differences were observed in TNF-α and IL-6 between continuous and recovery CS models independent of treatment or genotype. NTCU caused a significant increase in BAL IL-6 independent of genotype. IL-17a was elevated in NTCU-treated mice that developed lung squamous cell carcinoma. Conclusion and Potential Impact: The XPC genotypic variation seen in lung carcinogenesis appears to be independent of BAL cytokines, suggesting that the variation is due to DNA damage rather than differences in local inflammation. Further mechanistic investigations will focus on DNA damage and repair as drivers of XPC-deficient lung cancers.  


Author(s):  
Yngvild Olsen ◽  
Joshua M. Sharfstein

What causes opioid addiction? Just like it is true that not everyone who smokes will develop lung cancer, it is true that not everyone who takes or even misuses an opioid will develop an opioid addiction. While the biology of opioid addiction is still...


Author(s):  
Miguel López-Lázaro

Tobacco use, most people would say. Smoking tobacco increases the risk of developing many typesof cancer and is responsible for approximately one-third of all cancer deaths. The associationbetween tobacco use and lung cancer is well known; lung cancer occurs about 20 times more oftenin heavy smokers than in nonsmokers [1]. However, many lung cancers are diagnosed in neversmokers [2], and most smokers do not develop lung cancer [3,4].


2014 ◽  
Vol 32 (15_suppl) ◽  
pp. e12515-e12515
Author(s):  
Lingling Du ◽  
Nathan A. Pennell ◽  
Paul Elson ◽  
Nooshin Hashemi

2017 ◽  
Vol 12 (1) ◽  
pp. S567
Author(s):  
Heidi Schmidt ◽  
John Kavanagh ◽  
Geoffrey Liu ◽  
Ming Tsao ◽  
Frances Shepherd

JAMA ◽  
1966 ◽  
Vol 195 (6) ◽  
pp. 471-475 ◽  
Author(s):  
M. J. Krant

2016 ◽  
Vol 1 (13) ◽  
pp. 162-168
Author(s):  
Pippa Hales ◽  
Corinne Mossey-Gaston

Lung cancer is one of the most commonly diagnosed cancers across Northern America and Europe. Treatment options offered are dependent on the type of cancer, the location of the tumor, the staging, and the overall health of the person. When surgery for lung cancer is offered, difficulty swallowing is a potential complication that can have several influencing factors. Surgical interaction with the recurrent laryngeal nerve (RLN) can lead to unilateral vocal cord palsy, altering swallow function and safety. Understanding whether the RLN has been preserved, damaged, or sacrificed is integral to understanding the effect on the swallow and the subsequent treatment options available. There is also the risk of post-surgical reduction of physiological reserve, which can reduce the strength and function of the swallow in addition to any surgery specific complications. As lung cancer has a limited prognosis, the clinician must also factor in the palliative phase, as this can further increase the burden of an already compromised swallow. By understanding the surgery and the implications this may have for the swallow, there is the potential to reduce the impact of post-surgical complications and so improve quality of life (QOL) for people with lung cancer.


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