High-grade lung adenocarcinomas with micropapillary and/or solid patterns: a review.
OBJECTIVE
The purpose of review is to discuss the most recent research findings on lung adenocarcinomas with solid and micropapillary patterns.


RESULTS
Multiple recent studies have confirmed that both patterns are associated with adverse clinicopathologic features such as lymphovascular and pleural invasion, as well as lymph node metastasis, and consequently with poor disease-free survival, overall survival, or both. Radiologic characteristics such as high F-fluorodeoxyglucose (FDG) uptake, a solid nodule, and size ≥2 cm have been found to be useful to detect solid and micropapillary patterns. A seminal study has shown that the presence of a micropapillary component (≥5%) is a risk factor for early locoregional recurrence in patients undergoing limited resection for small (<2 cm) adenocarcinomas, but not for patients undergoing lobectomy. Several studies have demonstrated that micropapillary-predominant tumors are associated with EGFR mutations, whereas solid-predominant tumors are negatively associated with mutations of this gene and positively associated with KRAS mutations, indicative of the lack of response to EGFR tyrosine kinase inhibitors. The possible role of molecular events such as loss of BRG1/BRM and activation of c-Met has been identified in solid pattern and micropapillary pattern, respectively.


CONCLUSIONS
Micropapillary and solid patterns are markers for early recurrence and poor survival in lung adenocarcinomas. In order to overcome the unfavorable outcomes, the preoperative detection of these patterns, development of targeted therapy for KRAS mutants, and discovery of biomarkers that play a significant role in development or progression or both of these patterns are warranted to help in treating lung adenocarcinoma patients with micropapillary or solid patterns or both effectively.
aClinic of Thoracic Oncology, Instituto Nacional de Cancerologia, México City, Mexico bDepartment of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Vicente
V
Morales-Oyarvide
Mari
M
Mino-Kenudson
D000230:Adenocarcinoma / Q000401:mortality / Q000473:pathology*; D000077192:Adenocarcinoma of Lung; D014408:Biomarkers, Tumor / Q000378:metabolism; D004265:DNA Helicases / Q000378:metabolism; D018450:Disease Progression; D018572:Disease-Free Survival; D066246:ErbB Receptors / Q000378:metabolism; D006801:Humans; D008175:Lung Neoplasms / Q000401:mortality / Q000473:pathology*; D009154:Mutation / Q000235:genetics*; D009364:Neoplasm Recurrence, Local / Q000473:pathology*; D009367:Neoplasm Staging; D009687:Nuclear Proteins / Q000378:metabolism; D011379:Prognosis; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D019859:Proto-Oncogene Proteins c-met / Q000378:metabolism; D016283:Proto-Oncogene Proteins p21(ras); D012307:Risk Factors; D014157:Transcription Factors / Q000378:metabolism; D018631:ras Proteins / Q000378:metabolism
D014408:Biomarkers, Tumor; C117307:KRAS protein, human; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; C084011:SMARCA2 protein, human; D014157:Transcription Factors; C512478:EGFR protein, human; D066246:ErbB Receptors; D019859:Proto-Oncogene Proteins c-met; C084108:SMARCA4 protein, human; D004265:DNA Helicases; D016283:Proto-Oncogene Proteins p21(ras); D018631:ras Proteins