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Objective Studies are rarely reported on the factors influencing prognosis of surgically resected lung adenocarcinoma with a micropapillary pattern (LAC-MPP). This study aimed to explore the clinicopathological characteristics and risk factors of surgically resected LAC-MPP. Methods We retrospectively analyzed 384 cases of LAC treated in Henan Cancer Hospital between June 2015 and December 2017, which were classified into an MPP group (n = 82) and a non-MPP control group (n = 302) according to the results of postoperative pathology. We determined the expression of the fusion protein anaplastic lymphoma kinase (ALK), analyzed its association with the clinicopathological features of LAC-MPP, and explored the risk factors of postoperative MPP. Results Compared with the non-MPP group, the LAC-MPP patients showed a significantly higher expression of ALK (0.03% vs 12.20%, P < 0.05), rate of bronchial invasion (30.80% vs 48.78%, P < 0.05) and vascular tumor thrombus (0.99% vs 25.61%, P < 0.05), but a lower mutation rate of the epidermal growth factor receptor (EGFR) (64.24% vs 51.22%, P < 0.05). Multivariate logistic regression analysis revealed that the expression of ALK, vascular tumor thrombus, and age were significantly associated with the risk of postoperative MPP. Conclusion There is a high incidence rate of ALK expression in LAC-MPP patients after operation, which may provide some new ideas for the clinical treatment of the disease. Special attention should be paid to the expression of the ALK fusion protein and vascular tumor thrombus, and age in patients with LAC-MPP after operation.
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Objective To detect the mutation frequency of EML4-ALK fusion gene in lung cancer patients, and to inves-tigate the distribution of mutation character for EML4-ALK fusion gene in Ⅰ stage lung cancer patients and clinical features as well as provide a reference for the individual treatment of lung cancer .Methods 256 fresh tumor tissue specimens of lung cancer patients were screened from the specimen bank of our hospital and all the patients had accepted the surgical treatment from February 2013 to December 2014.Total RNA was extracted and then be transcribed into cDNA, the amplification-refrac-tory mutation system(ARMS) was used to detect mutation of EML4-ALK fusion gene.The results according to the positive con-trol, negative control and RNA quality control for EML4-ALK fusion type were analyzed.Results During the 256 patients ofⅠ stage lung cancer, there were 17 patients(6.64%) had mutations in EML4-ALK fusion gene.In lung adenocarcinoma mu-tation rate(16/207, 7.73%) was higher than that of lung squamous cell mutation rate(1/39, 2.56%), lung adeno-squamous mutation rate(0/4, 0) and large cell carcinoma(0/5, 0) of the mutation rate;young lung cancer patients( <63 years) of the mutation rate(14/139, 10.07%) was significantly higher than the high age of lung cancer patients(≥63 years old) mutation rate(3/117, 2.56%), P =0.009.EML4-ALK fusion with tumor invasion and visceral pleura group incidence (9/80, 11. 25%) was significantly higher than that of non-invasive and visceral pleura group incidence rate(8/176, 4.55%), P =0.045.Conclusion The occurence of EML4-ALK fusion correlates with patients’ age as well as whether visceral pleura is in-vaded, type 1 EML4-ALK fusion was detected more in phase I lung cancer patients.
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Crizotinib-associated severe hepatotoxicity has been rarely reported and experts recommended stopping crizotinib treatment in patients with grade 3/4 transaminase elevation. We experienced a case of anaplastic lymphoma kinase-positive non-small cell lung cancer occurring as a result of severe hepatotoxicity due to crizotinib-associated hepatitis, accompanied by the reactivation of chronic hepatitis B, which was reversed with dose reduction and anti-viral therapy. Our case highlights the possibility that crizotinib might induce hepatitis and this might be associated with the underlying presence of chronic hepatitis B. In addition, crizotinib could be continued with reduced unless there are any other therapeutic options.