| 图片： | |
|---|---|
| 名称： | |
| 描述： | |
- 求教有关细支气管肺泡癌的新进展
-
emilypeaker 离线
- 帖子：654
- 粉蓝豆：1570
- 经验：2182
- 注册时间：2011-01-03
- 加关注 | 发消息
Semin Respir Crit Care Med. 2011 Feb;32(1):52-61. Epub 2011 Apr 15.
Bronchioloalveolar carcinoma.
Source
Division of Pulmonary Critical Care Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA. darenber@umich.edu
Abstract
This review focuses on aspects of bronchioloalveolar carcinoma (BAC) in which it differs importantly from other forms of non-small-cell lung cancer. BAC is a form of adenocarcinoma with unique clinical, radiological, and epidemiological features. With the notable exception of a lower likelihood of a positive positron-emission tomographic (PET) scan in BAC, staging, diagnosis, and treatment are largely the same as for other histological subtypes of lung cancer. However, additional treatment options exist that are equivalent, if not more effective, for many patients with BAC. The diagnosis of BAC should be reserved for those tumors meeting the 1999/2004 criteria set forth by the World Health Organization. Revised nomenclature proposed by an expert consensus panel may change how this disease is viewed. Additional clinical trials are needed on patients with BAC, employing strict definitions and enrollment criteria to allow the results to be applied to appropriate patient populations.
- Suffered from papillary thyroid carcinoma, then major in Endocrine tumor.
-
emilypeaker 离线
- 帖子：654
- 粉蓝豆：1570
- 经验：2182
- 注册时间：2011-01-03
- 加关注 | 发消息
Cancer Res. 2011 Nov 1;71(21):6665-75. Epub 2011 Sep 12.
Progression of human bronchioloalveolar carcinoma to invasive adenocarcinoma is modeled in a transgenic mouse model of K-ras-induced lung cancer by loss of the TGF-β type II receptor.
Source
Department of Pathology, Columbia University College of Physicians and Surgeons, New York, New York, USA.
Abstract
Clinical investigations have suggested that repression of the TGF-β type II receptor (TβRII) may be an important step in progression of lung adenocarcinoma from an indolent in situ state to a frank invasive carcinoma. To test this hypothesis, we compared the effects of deleting the murine homolog of this receptor (Tgfbr2) in a mouse model of mutant K-ras-induced lung carcinoma, which normally induces the formation of multifocal tumors of low invasive potential. In this model, loss of Tgfbr2 induced a highly invasive phenotype associated with lymph node metastasis and reduced survival. Tumor-associated stromal cells displayed an immunosuppressive profile marked by increased numbers of B and T cells. Moreover, tumor stromal cell profiling revealed a developmental TGF-β response profile that associated with a collagenized extracellular matrix and increased invasion of TGF-β nonresponsive tumor cells. Together, these results suggest that our KrasTgfbr2(-/-) mouse model of invasive lung carcinoma mirrors the genomic response and clinical progression of human lung adenocarcinoma, recapitulating changes in lung stromal pathways that occur in the tumor microenvironment during malignant progression in this disease.
- Suffered from papillary thyroid carcinoma, then major in Endocrine tumor.
