Bronchoalveolar Cell Carcinoma of the Lung

groups of men non-employed through illness are likely to be heterogeneous with regard to type and severity of illness. Thus for some men, but not all, illness will be directly responsible for their weight loss and reduction in smoking and drinking.This study indicates the need to take account of the long term effects of higher levels of smoking and alcohol consumption and less exercise before unemployment when comparing mortality and morbidity among groups of unemployed and employed people, such as in the Office of Population Censuses and Surveys longitudinal study.Y3The British Regional Heart Study is a British Heart

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“…X' for trend (df= 1) [3][4][5][6][7] (1-6 to 8 8) 2-3 (10 to 52) [3][4][5][6][7][8][9] (1 8 to 8 7) 1-9…”

Section: Discussionmentioning

confidence: 99%

Relation of bronchioloalveolar carcinoma to tobacco.

Morabia

Wynder

1992

BMJ

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“…We therefore reasoned that the VR3 might be important for viral transformation. To this end we generated a series of chimeric envelopes between the exogenous JSRV 21 and the related endogenous enJS56A1 in the context of the pCMV2JS21⌬GP envelope expression plasmid (Fig. 1).…”

Section: Tm Region Of Jsrv Envelope Is a Determinant Of Cell Transformentioning

confidence: 99%

“…OPC is a naturally occurring disease in most countries of the world and is characterized by the transformation of the differentiated epithelial cells of the lungs, type II pneumocytes and Clara cells (17,33). OPC is being extensively studied for its similarities with a particular type of human lung cancer known as bronchioloalveolar carcinoma (BAC) (17,21,23,33). The causes of BAC are unknown.…”

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confidence: 99%

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A Phosphatidylinositol 3-Kinase Docking Site in the Cytoplasmic Tail of the Jaagsiekte Sheep Retrovirus Transmembrane Protein Is Essential for Envelope-Induced Transformation of NIH 3T3 Cells

Palmarini

Maeda

Murgia

et al. 2001

J Virol

106

163

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Jaagsiekte sheep retrovirus (JSRV) is the causative agent of a transmissible lung cancer of sheep known as ovine pulmonary carcinoma. Recently, we have found that the expression of the JSRV envelope (Env) is sufficient to transform mouse NIH 3T3 cells in classical transformation assays. To further investigate the mechanisms of JSRV oncogenesis, we generated a series of envelope chimeras between JSRV and the JSRVrelated endogenous retroviruses of sheep (enJSRVs) and assessed them in transformation assays. Chimeras containing the exogenous JSRV SU region and the enJSRV TM region were unable to transform NIH 3T3 cells. Additional chimeras containing only the carboxy-terminal portion of TM (a region that we previously identified as VR3) of the endogenous envelope with SU and the remaining portion of TM from the exogenous JSRV were also unable to transform NIH 3T3 cells. The VR3 region includes the putative membrane-spanning region and cytoplasmic tail of the JSRV TM glycoprotein; this suggested that the cytoplasmic tail of the JSRV Env mediates transformation, possibly via a cell signaling mechanism. Mutations Y590 and M593 in the cytoplasmic tail of the JSRV envelope were sufficient to inhibit the transforming abilities of these constructs. Y590 and Jaagsiekte sheep retrovirus (JSRV) is the etiological agent of a contagious lung cancer of sheep known as ovine pulmonary carcinoma (OPC) or sheep pulmonary adenomatosis (4,16,30,36). OPC is a naturally occurring disease in most countries of the world and is characterized by the transformation of the differentiated epithelial cells of the lungs, type II pneumocytes and Clara cells (17,33). OPC is being extensively studied for its similarities with a particular type of human lung cancer known as bronchioloalveolar carcinoma (BAC) (17,21,23,33). The causes of BAC are unknown. BAC is not strongly associated with cigarette smoking, and its incidence appears to be increasing in the United States (1,5,6,51). Thus, the JSRV/ OPC model can offer a foundation for understanding the molecular mechanisms of type II pneumocytes and Clara cell transformation, especially considering the role played by retroviruses in the discovery of cellular oncogenes (46). M593 are part of a Y-X-X-M motif that is recognized by the phosphatidylinositol 3-kinase (PI-3K). PI-3K initiates a cell signaling pathway that inhibits apoptosis and is required for a number of mitogens during the G 1 -to-S-phase transition of the cell cycle. PI-3K activatesCell transformation by JSRV is offering a new paradigm for retroviral oncogenesis (45). The JSRV genome does not contain a cell-derived oncogene, which would suggest that JSRV induces cell transformation by insertional activation of protooncogenes (46). However, the incubation period in experimentally inoculated lambs can be as short as 2 to 3 weeks (47, 52), which appears too short for insertional activation to occur. Our recent study showed that the expression of the envelope (Env) protein of JSRV is able to transform rodent fibroblasts in vitro (27). Thus, ...

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“…65 Adenocarcinoma of the bronchioloalveolar type with uncertain etiology was identified as the most common lung carcinoma among individuals aged <45 years, particularly women, 66 and smoking was not considered an important etiologic factor. 67 Needless to say, the development of lung carcinoma in never-smokers is of great concern, particularly in Asia, where up to 70% of lung carcinomas in women may be unrelated to smoking. 68 All in all, it has been proven that viruses, endogenous and exogenous chemicals, incidental and therapeutic radiation, long-standing chronic inflammation, and a wide variety of genetic mutations can cause cancer.…”

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confidence: 99%

A note from history: Landmarks in history of cancer, part 7

Hajdu

Vadmal

Tang

2015

Cancer

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In the 2 and half decades reviewed , research established that chromosomal translocation, deletion, and DNA amplification are prerequisites to cancerogenesis and that oncogenes, tumor-suppressor genes, growth factors, and cytokines play crucial roles in the pathomechanism of cancer. Human papillomavirus, human immunodeficiency virus, herpes virus, and hepatitis B virus were identified as cancer-causing viruses. Several laboratory tests were developed for the detection of primary and recurrent cancers, and cancer prevention by screening methods was popularized. Sonography, computerized tomography, magnetic resonance imaging, positron emission tomography, excision of sentinel lymph nodes, and immunohistochemical techniques became routine procedures. Clinicopathologic staging and classification of tumors were standardized. Limited surgery, adjuvant and neoadjuvant chemoradiation, and the therapeutic use of monoclonal antibodies, tumor vaccines, and targeted chemotherapy became routine practice. The decline in cancer incidence and mortality demonstrated that cancer prevention and advancement in oncology are pivotal to success in the crusade against cancer. Above all, it was clearly established that the care of patients with cancer can be accomplished best in a multidisciplinary setting involving surgical oncologists, radiologists, radiation therapists, medical oncologists, surgical pathologists, and laboratory scientists. In conclusion, the 25 years from 1970 and 1995 are the high-water mark in clinical oncology, and this is the period when oncology turned from art to science. Cancer 2015;121:2480-513.

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Bronchoalveolar Cell Carcinoma of the Lung

Cited by 76 publications

References 10 publications

Relation of bronchioloalveolar carcinoma to tobacco.

Relation of bronchioloalveolar carcinoma to tobacco.

A Phosphatidylinositol 3-Kinase Docking Site in the Cytoplasmic Tail of the Jaagsiekte Sheep Retrovirus Transmembrane Protein Is Essential for Envelope-Induced Transformation of NIH 3T3 Cells

A note from history: Landmarks in history of cancer, part 7

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