Expression of IGF-I, TGF-alpha and p53 protein in imprint smears of bronchial biopsy specimens of lung cancer

Abstract Context.—The diagnosis of lung cancer is often confirmed by cytology and biopsy specimens obtained during a bronchoscopic procedure. At our institution, these specimens are read by different pathologists, and the rate of concordance was not known. Objectives.—To evaluate the concordance rate in the diagnosis of lung cancer types between cytology and biopsy specimens and to correlate discordance with patient outcome. Design.—Specimens obtained during the same procedure, between January 1, 2000, and December 31, 2005, were identified. Cases with cytology and biopsy specimens positive for cancer were evaluated for concordance of histologic type, small cell versus non–small cell lung carcinoma. Cases with different types were considered discordant, and slides were reviewed. Results.—Of 231 cases, 225 (97.4%) had concordant diagnoses. Discordance was the result of misinterpretation of undifferentiated carcinoma, overinterpretation of squamous dysplasia, interpretation of suboptimal specimens with necrosis and crush artifact, and sampling error. Conclusions.—Even though the cytology and biopsy specimens were reviewed by different pathologists, the concordance rate for histologic type at our institution was high, emphasizing that this is a safe practice. The few discordant cases did not affect the patient's outcome.

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P53 protein overexpression in transbronchial biopsy specimens from small cell lung cancer (SCLC) patients

Lung Cancer ◽

10.1016/0169-5002(94)93837-7 ◽

1994 ◽

Vol 11 ◽

pp. 17

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Cell Lung Cancer ◽

P53 Protein ◽

Transbronchial Biopsy ◽

Small Cell ◽

Protein Overexpression ◽

Small Cell Lung ◽

Biopsy Specimens

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Cell Type Accuracy of Bronchial Biopsy Specimens in Primary Lung Cancer

CHEST Journal ◽

10.1378/chest.109.5.1199 ◽

1996 ◽

Vol 109 (5) ◽

pp. 1199-1203 ◽

Cited By ~ 46

Author(s):

Juan J. Soler Cataluña ◽

Miguel Perpiñá ◽

José V. Greses ◽

Victor Calvo ◽

José D. Padilla ◽

...

Keyword(s):

Lung Cancer ◽

Primary Lung Cancer ◽

Bronchial Biopsy ◽

Cell Type ◽

Biopsy Specimens

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Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer

Scientific Reports ◽

10.1038/s41598-021-91454-2 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Shao-Yuan Chen ◽

Koichi Tsuneyama ◽

Mao-Hsiung Yen ◽

Jiunn-Tay Lee ◽

Jiun-Liang Chen ◽

...

Keyword(s):

Lung Cancer ◽

Solid Tumors ◽

Tumor Cells ◽

Hyperbaric Oxygen ◽

A549 Cell ◽

P53 Protein ◽

Tumor Hypoxia ◽

A549 Cells ◽

Xenograft Tumor ◽

Tumor Models

AbstractTumor cells have long been recognized as a relative contraindication to hyperbaric oxygen treatment (HBOT) since HBOT might enhance progressive cancer growth. However, in an oxygen deficit condition, tumor cells are more progressive and can be metastatic. HBOT increasing in oxygen partial pressure may benefit tumor suppression. In this study, we investigated the effects of HBOT on solid tumors, such as lung cancer. Non-small cell human lung carcinoma A549-cell-transferred severe combined immunodeficiency mice (SCID) mice were selected as an in vivo model to detect the potential mechanism of HBOT in lung tumors. HBOT not only improved tumor hypoxia but also suppressed tumor growth in murine xenograft tumor models. Platelet endothelial cell adhesion molecule (PECAM-1/CD31) was significantly increased after HBOT. Immunostaining of cleaved caspase-3 was demonstrated and apoptotic tumor cells with nuclear debris were aggregated starting on the 14th-day after HBOT. In vitro, HBOT suppressed the growth of A549 cells in a time-dependent manner and immediately downregulated the expression of p53 protein after HBOT in A549 cells. Furthermore, HBOT-reduced p53 protein could be rescued by a proteasome degradation inhibitor, but not an autophagy inhibitor in A549 cells. Our results demonstrated that HBOT improved tissue angiogenesis, tumor hypoxia and increased tumor apoptosis to lung cancer cells in murine xenograft tumor models, through modifying the tumor hypoxic microenvironment. HBOT will merit further cancer therapy as an adjuvant treatment for solid tumors, such as lung cancer.

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744 p53 protein accumulation, tobacco smoking, clinico-pathologic features and prognosis in non-small cell lung cancer (NSCLC)

Lung Cancer ◽

10.1016/s0169-5002(97)80124-9 ◽

1997 ◽

Vol 18 ◽

pp. 191

Author(s):

M. Tammemagi ◽

B. Mullen ◽

M. Johnston ◽

J. McLaughlin ◽

A.G. Casson

Keyword(s):

Lung Cancer ◽

Small Cell Lung Cancer ◽

Cell Lung Cancer ◽

Tobacco Smoking ◽

P53 Protein ◽

Small Cell ◽

Protein Accumulation ◽

Small Cell Lung ◽

Pathologic Features

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The Histopathology of Lung Cancer in Liverpool: A Survey of Bronchial Biopsy Histology

British Journal of Cancer ◽

10.1038/bjc.1961.53 ◽

1961 ◽

Vol 15 (3) ◽

pp. 429-439 ◽

Cited By ~ 9

Author(s):

F Whitwell

Keyword(s):

Lung Cancer ◽

Bronchial Biopsy

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Differential Impacts of Insulin-Like Growth Factor-Binding Protein-3 (IGFBP-3) in Epithelial IGF-Induced Lung Cancer Development

Endocrinology ◽

10.1210/en.2010-0693 ◽

2011 ◽

Vol 152 (6) ◽

pp. 2164-2173 ◽

Cited By ~ 13

Author(s):

Woo-Young Kim ◽

Mi-Jung Kim ◽

Hojin Moon ◽

Ping Yuan ◽

Jin-Soo Kim ◽

...

Keyword(s):

Lung Cancer ◽

Lung Tumor ◽

Binding Protein ◽

Cancer Development ◽

Lung Carcinogenesis ◽

Tobacco Carcinogen ◽

Igf I ◽

The Impact ◽

Igfbp 3

The IGF axis has been implicated in the risk of various cancers. We previously reported a potential role of tissue-derived IGF in lung tumor formation and progression. However, the role of IGF-binding protein (IGFBP)-3, a major IGFBP, on the activity of tissue-driven IGF in lung cancer development is largely unknown. Here, we show that IGF-I, but not IGF-II, protein levels in non-small-cell lung cancer (NSCLC) were significantly higher than those in normal and hyperplastic bronchial epithelium. We found that IGF-I and IGFBP-3 levels in NSCLC tissue specimens were significantly correlated with phosphorylated IGF-IR (pIGF-IR) expression. We investigated the impact of IGFBP-3 expression on the activity of tissue-driven IGF-I in lung cancer development using mice carrying lung-specific human IGF-I transgene (Tg), a germline-null mutation of IGFBP-3, or both. Compared with wild-type (BP3+/+) mice, mice carrying heterozygous (BP3+/−) or homozygous (BP3−/−) deletion of IGFBP-3 alleles exhibited decreases in circulating IGFBP-3 and IGF-I. Unexpectedly, IGFTg mice with 50% of physiological IGFBP-3 (BP3+/−; IGFTg) showed higher levels of pIGF-IR/IR and a greater degree of spontaneous or tobacco carcinogen [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone]-induced lung tumor development and progression than did the IGFTg mice with normal (BP3+/+;IGFTg) or homozygous deletion of IGFBP-3 (BP3−/−; IGFTg). These data show that IGF-I is overexpressed in NSCLC, leading to activation of IGF-IR, and that IGFBP-3, depending on its expression level, either inhibits or potentiates IGF-I actions in lung carcinogenesis.

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