2019
DOI: 10.1016/j.chest.2019.04.114
|View full text |Cite
|
Sign up to set email alerts
|

Common Pathogenic Mechanisms Between Idiopathic Pulmonary Fibrosis and Lung Cancer

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1

Citation Types

0
82
0
2

Year Published

2019
2019
2023
2023

Publication Types

Select...
9

Relationship

1
8

Authors

Journals

citations
Cited by 109 publications
(84 citation statements)
references
References 67 publications
0
82
0
2
Order By: Relevance
“…Previous studies have revealed a high incidence of lung cancer in IPF [31,[79][80][81] and a likely increase in the annual risk of lung cancer that appears to rise over the years following diagnosis [31]. Cell senescence, genetic and epigenetic alterations, abnormal expression of microRNAs, delayed apoptosis, and activation of specific transduction pathways have been observed in both IPF and cancer pathogenesis [3,82]. An even higher incidence has been reported in CPFE [83,84].…”
Section: Lung Cancermentioning
confidence: 99%
“…Previous studies have revealed a high incidence of lung cancer in IPF [31,[79][80][81] and a likely increase in the annual risk of lung cancer that appears to rise over the years following diagnosis [31]. Cell senescence, genetic and epigenetic alterations, abnormal expression of microRNAs, delayed apoptosis, and activation of specific transduction pathways have been observed in both IPF and cancer pathogenesis [3,82]. An even higher incidence has been reported in CPFE [83,84].…”
Section: Lung Cancermentioning
confidence: 99%
“…Previous studies have suggested that the core of the ILD and lung cancer copathogenesis is the irreversible loss of the capacity of the cell to grow and divide. ILD may lead to genetic and epigenetic alterations as well as the abnormal activation of common transduction pathways, including Wnt/b‐catenin and phosphoinositide 3‐kinase/protein kinase B . There are other scholars using microsatellite DNA analysis, whereby they have observed a loss of heterozygosity in MYCL1, FHIT, SPARC, p16Ink4, and TP53 genomic loci among ILD patients .…”
Section: Discussionmentioning
confidence: 99%
“…2 Both diseases present with major similarities in terms of pathogenetic pathways, as well as potential causative factors, such as smoking and viral infections. 3 Lung cancer patients with comorbid IPF have few treatment options because surgery, radiotherapy, and chemotherapy elevate the risk of exacerbation of IPF. [4][5][6] An optimal therapeutic strategy for patients with both diseases is sorely needed.…”
Section: Introductionmentioning
confidence: 99%