Lung carcinoma-associated atypical adenomatoid hyperplasia, squamous cell dysplasia, and chromosome alterations in non-neoplastic bronchial mucosa

Kayser, Klaus; Kosjerina, Zdravko; Goldmann, Torsten; Kayser, Gian; Kazmierczak, Bernd; Vollmer, Ekkehard

doi:10.1016/j.lungcan.2004.07.042

Cited by 12 publications

(12 citation statements)

References 34 publications

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“…Furthermore, gene losses of chromosome 19 in adjacent bronchial mucosa were detected in SCC and LCC both in primary lung carcinomas. Chromosome 19 losses may be the early event in SCC oncogenesis [23]. Whole exon sequencing (n = 51) and copy number analysis (n =47) of resected SCLC tumors was compared with matched noncancer samples from Eastern SCLC patients.…”

Section: Bioinformatic Annotation Of Chromosome 19mentioning

confidence: 99%

Association of chromosome 19 to lung cancer genotypes and phenotypes

Wang

Zhang

Nilsson

et al. 2015

Cancer Metastasis Rev

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The Chromosome 19 Consortium, a part of the Chromosome-Centric Human Proteome Project (C-HPP, http://www.C-HPP.org ), is tasked with the understanding chromosome 19 functions at the gene and protein levels, as well as their roles in lung oncogenesis. Comparative genomic hybridization (CGH) studies revealed chromosome aberration in lung cancer subtypes, including ADC, SCC, LCC, and SCLC. The most common abnormality is 19p loss and 19q gain. Sixty-four aberrant genes identified in previous genomic studies and their encoded protein functions were further validated in the neXtProt database ( http://www.nextprot.org/ ). Among those, the loss of tumor suppressor genes STK11, MUM1, KISS1R (19p13.3), and BRG1 (19p13.13) is associated with lung oncogenesis or remote metastasis. Gene aberrations include translocation t(15, 19) (q13, p13.1) fusion oncogene BRD4-NUT, DNA repair genes (ERCC1, ERCC2, XRCC1), TGFβ1 pathway activation genes (TGFB1, LTBP4), Dyrk1B, and potential oncogenesis protector genes such as NFkB pathway inhibition genes (NFKBIB, PPP1R13L) and EGLN2. In conclusion, neXtProt is an effective resource for the validation of gene aberrations identified in genomic studies. It promises to enhance our understanding of lung cancer oncogenesis.

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Section: Bioinformatic Annotation Of Chromosome 19mentioning

confidence: 99%

Association of chromosome 19 to lung cancer genotypes and phenotypes

Wang

Zhang

Nilsson

et al. 2015

Cancer Metastasis Rev

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“…Shared genetic changes have been documented in tumors, precursor lesions and non-neoplastic lung parenchyma adjacent to tumors [30]. Chromosome alterations can occur in non-neoplastic bronchial mucosa at a distance of 4 cm from the tumor boundary [31]. Therefore it is not surprising that in the current study, low levels of PRMT5 expression were noted in reactive tissues adjacent to tumors in resection specimens and not in alveolar parenchyma distant from tumors or normal controls in TMA.…”

Section: Discussionmentioning

confidence: 99%

Cellular localization of protein arginine methyltransferase-5 correlates with grade of lung tumors

Shilo

Sharma

et al. 2013

Diagn Pathol

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BackgroundProtein arginine methyltransferase-5 (PRMT5) is a chromatin-modifying enzyme capable of methylating histone and non-histone proteins, and is involved in a wide range of cellular processes that range from transcriptional regulation to organelle biosynthesis. As such, its overexpression has been linked to tumor suppressor gene silencing, enhanced tumor cell growth and survival.Material and methodsQuantitative real-time polymerase chain reaction, Western immunoblot and immunohistochemistry were used to characterize PRMT5 expression in lung cancer cell lines and human tumors. Clinicopathological findings of tissue microarray based samples from 229 patients with non-small cell lung carcinomas (NSCLC) and 133 cases with pulmonary neuroendocrine tumors (NET) were analyzed with regard to nuclear and cytoplasmic PRMT5 expression.ResultsThere was statistically significant difference in PRMT5 messenger RNA expression between tumors and nonneoplastic lung tissues. Immunoblot experiments showed abundant expression of PRMT5 and its symmetric methylation mark H4R3 in lung carcinoma but not in non-neoplastic human pulmonary alveolar and bronchial epithelial cell lines. More than two thirds of lung tumors expressed PRMT5. High levels of cytoplasmic PRMT5 were detected in 20.5% of NSCLC and in 16.5% of NET; high levels of nuclear PRMT5 were detected in 38.0% of NSCLC and 24.0% of NET. Cytoplasmic PRMT5 was associated with high grade in both NSCLC and pulmonary NET while nuclear PRMT5 was more frequent in carcinoid tumors (p < 0.05).ConclusionThe observed findings support the role of PRMT5 in lung tumorigenesis and reflect its functional dichotomy in cellular compartments.Virtual slideThe virtual slides for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1611895162102528

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“…Lesions in AAH are usually small, asymptomatic and radiologically invisible, helical (Spiral) CT combined with surgical biopsy is the most commonly reported method for diagnosis of AAH. At an almost indistinguishable point, AAH lesions can become bronchoalveolar cell carcinoma (BAC) [8]. Clinically it has been suggested using size of the lesion to distinguish between AAH (size ≤ 5 mm) and BAC/Adenocarcinoma (> 5 mm) [8].…”

Section: Introductionmentioning

confidence: 99%

A novel autoantibody test for the detection of pre-neoplastic lung lesions

Lowe

Shen

et al. 2014

Mol Cancer

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BackgroundAtypical adenomatous hyperplasia (AAH) and squamous cell dysplasia (SCD) are associated with the development of malignant lesions in the lung. Accurate diagnosis of AAH and SCD could facilitate earlier clinical intervention and provide useful information for assessing lung cancer risk in human populations. Detection of AAH and SCD has been achieved by imaging and bronchoscopy clinically, but sensitivity and specificity remain less than satisfactory. We utilized the ability of the immune system to identify lesion specific proteins for detection of AAH and SCD.MethodsAAH and SCD tissue was surgically removed from six patients of Chinese descent (3 AAH and 3 SCD) with corresponding serum samples. Total RNA was extracted from the tissues and a cDNA library was generated and incorporated into a T7 bacteriophage vector. Following enrichment to remove "normal" reactive phages, a total of 200 AAH related and 200 SCD related phage clones were chosen for statistical classifier development and incorporation into a microarray. Microarray slides were tested with an independent double-blinded population consisting of 100 AAH subjects, 100 SCD subjects and 200 healthy control subjects.ResultsSensitivity of 82% and specificity of 70% were achieved in the detection of AAH using a combination of 9 autoantibody biomarkers. Likewise, 86% sensitivity and 78% specificity were achieved in the detection of SCD using a combination of 13 SCD-associated markers. Sequencing analysis identified that most of these 22 autoantibody biomarkers had known malignant associations.ConclusionsBoth diagnostic values showed promising sensitivity and specificity in detection of pre-neoplastic lung lesions. Hence, this technology could be a useful non-invasive tool to assess lung cancer risk in human populations.

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Lung carcinoma-associated atypical adenomatoid hyperplasia, squamous cell dysplasia, and chromosome alterations in non-neoplastic bronchial mucosa

Cited by 12 publications

References 34 publications

Association of chromosome 19 to lung cancer genotypes and phenotypes

Association of chromosome 19 to lung cancer genotypes and phenotypes

Cellular localization of protein arginine methyltransferase-5 correlates with grade of lung tumors

A novel autoantibody test for the detection of pre-neoplastic lung lesions

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