Clinicopathological characteristics of surgically resected lung cancer associated with idiopathic pulmonary fibrosis

Kawasaki, Hidenori; Nagai, Kanji; Yokose, Tomoyuki; Nishimura, Mitsuyo; Takahashi, Kenro; Suzuki, Kenji; Kakinuma, R.; Nishiwaki, Yutaka

doi:10.1002/1096-9098(200101)76:1<53::aid-jso1009>3.0.co;2-t

Cited by 73 publications

(48 citation statements)

References 12 publications

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“…In normal bronchial and bronchiolar basal cells, the hidden basal position could represent a means to avoid contact with potentially noxious agents, including tobacco smoke, transported by respiratory gases. Accordingly, the incidence of peripheral carcinoma is significantly increased in IPF/UIP (Hironaka and Fukayama, 1999), including squamous carcinoma (Kawasaki et al, 2001), a cancer type that can be considered as typically derived from the basal cell transformation and characterized by p63 gene amplification (Hibi et al, 2000). …”

Section: Discussionmentioning

confidence: 98%

“…A final issue that needs to be taken into account is the possible role of ⌬N-p63 in the development of lung cancer in IPF/UIP (Kawasaki et al, 2001;Matsushita et al, 1995;Turner-Warwick et al, 1980). Inactivation of the p53 function because of point mutations has been considered central to this transformation (Hojo et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, recent experimental evidence has been provided suggesting that the combined function of p63 and p73 is required for p53-dependent apoptosis in response to DNA damage (Flores et al, 2002). Having considered all these facts, we hypothesized that the p63 gene products, through interference with the p53 pathway, may exert a relevant role in the abnormal process of tissue repair and remodeling occurring in IPF/UIP and also in the increased rate of malignant transformation observed in this disease (Kawasaki et al, 2001;Matsushita et al, 1995;Mizushima and Kobayashi, 1995;Turner-Warwick et al, 1980). Using antibodies that specifically recognize either the transactivating TA-p63 or the truncated ⌬N-p63 isoforms (Hibi et al, 2000;Yang et al, 1998) …”

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confidence: 99%

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Abnormal Re-epithelialization and Lung Remodeling in Idiopathic Pulmonary Fibrosis: The Role of ΔN-p63

Chilosi

Poletti

Murer³

et al. 2002

Laboratory Investigation

201

163

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SUMMARY:Products of the p63 gene, a recently described member of the p53 family, are constitutively expressed in the basal cells of human bronchi and bronchioli. The truncated isoforms of the p63 gene (⌬N-p63 proteins) counteract the apoptotic and cell cycle inhibitory functions of p53 after DNA damage, and this property is likely to be central in the cell renewal strategy of stratified epithelial tissues. To investigate the dysfunctional repair processes that characterize idiopathic pulmonary fibrosis/usual interstitial pneumonia (IPF/UIP), we immunohistochemically analyzed the expression of the transactivating and dominantnegative isoforms of the p63 gene on 16 tissue samples obtained from patients suffering from this disorder. In most IPF cases herein investigated, epithelial cells expressing ⌬N-p63 were observed at sites of abnormal proliferation at the bronchiolo-alveolar junctions, characterized by epithelial hyperplasia, squamous metaplasia, bronchiolization, and abnormal p53 nuclear accumulation. Similar features were not observed in normal lung and in samples taken from other pulmonary diseases used as controls, including acute interstitial pneumonia, idiopathic bronchiolitis obliterans organizing pneumonia, nonspecific interstitial pneumonia, and desquamative interstitial pneumonia. On the basis of these findings, we can hypothesize a new model for UIP pathogenesis, involving a deregulated development of mesenchymal-epithelial interactions and abnormal proliferation of epithelial cells at the bronchiolo-alveolar junction after cell injury. In our view, the progressive loss of alveolar tissue and lung remodeling after injury in IPF/UIP is concomitantly produced by pneumocyte loss and alveolar collapse on one hand and by progressive bronchiolar proliferation and architectural distortion on the other. (Lab Invest 2002, 82:1335-1345.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Abnormal Re-epithelialization and Lung Remodeling in Idiopathic Pulmonary Fibrosis: The Role of ΔN-p63

Chilosi

Poletti

Murer³

et al. 2002

Laboratory Investigation

201

163

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“…For example, Kawasaki et al reported that IIP was observed in 7.5% of surgically resected cases of LC (5). Although IIP patients show a higher incidence of LC, with a relative risk of 7-14 (2-4,6,7), no standard therapy for LC complicated by IIP (NSCLC-IIP) has yet been established.…”

Section: Introductionmentioning

confidence: 99%

Chemotherapy for non-small cell lung cancer complicated by idiopathic interstitial pneumonia

et al. 2012

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Abstract. Idiopathic interstitial pneumonia (IIP) is considered to be one of the risk factors for lung cancer (LC). However, therapeutic options for patients with LC complicated by IIP are not well established. In this study, we investigated the feasibility and efficacy of chemotherapy for patients with non-small cell lung cancer (NSCLC) complicated by IIP (NSCLC-IIP). We retrospectively analyzed 22 NSCLC-IIP patients who received chemotherapy. To determine how IIP affected the clinical outcomes in NSCLC, they were compared with 276 NSCLC patients without IIP, who were treated with chemotherapy alone. The response rate (partial response + stable disease) was 72.3% (17/22), whereas the incidence of acute exacerbation (AE) was 13.6% (3/22) in NSCLC-IIP patients treated with chemotherapy. NSCLC-IIP patients had significantly shorter survival compared with NSCLC patients without IIP (P<0.001) following chemotherapy, although the response rates to chemotherapy were not significantly different between the two groups. Multivariate analysis demonstrated that, in NSCLC patients receiving chemotherapy, IIP was a significantly unfavorable factor for progression-free and overall survival. Despite similar response rates to chemotherapy, NSCLC-IIP patients showed poorer prognosis than NSCLC patients without IIP, possibly due to the natural course of IIP. Chemotherapy may be a feasible option for NSCLC-IIP, if the risks of adverse effects are acceptable.

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“…1,2 Postoperative acute exacerbation (AE) of UIP is a serious complication in the surgical treatment for primary lung cancer combined with UIP. 3,4 Careful preoperative evaluation and perioperative management are required to achieve an optimal outcome in lung cancer patients combined with UIP.…”

Section: Introductionmentioning

confidence: 99%

Predictive factors for postoperative acute exacerbation of interstitial pneumonia combined with lung cancer

Shintani

Ohta

Iwasaki

et al. 2010

Gen Thorac Cardiovasc Surg

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Clinicopathological characteristics of surgically resected lung cancer associated with idiopathic pulmonary fibrosis

Abstract: These results suggest that IPF has the potential to develop into lung cancer, especially peripheral squamous cell carcinoma. Further molecular analyses are necessary to clarify the relationship between IPF and lung cancer.

Cited by 73 publications

References 12 publications

Abnormal Re-epithelialization and Lung Remodeling in Idiopathic Pulmonary Fibrosis: The Role of ΔN-p63

Abnormal Re-epithelialization and Lung Remodeling in Idiopathic Pulmonary Fibrosis: The Role of ΔN-p63

Chemotherapy for non-small cell lung cancer complicated by idiopathic interstitial pneumonia

Predictive factors for postoperative acute exacerbation of interstitial pneumonia combined with lung cancer

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