- 作者列表："Xiong YY","Xu Y","Zhao Y","Sun H","Bai XY","Wu D","Qian JM
:Objective: To analyze the clinical features and prognosis of lung cancer patients with metastasis-induced acute pancreatitis (MIAP), and to provide clues for early diagnosis. Methods: The characteristics and prognosis of 8 patients with MIAP in lung cancer admitted to Peking Union Medical College Hospital from January 2002 to September 2019 were retrospectively analyzed and were compared with non-tumor-induced AP. Results: Sevencases(7/8) were Mild AP, one (1/8) was Severe AP. Four patients (4/8) presented with AP as the reporting sign and lung cancer was not diagnosed until (112±36) days after the onset of AP. Clinical manifestations included abdominal pain (8/8), weight loss (4/8), nausea and vomiting (2/8), and jaundice (1/8). Stages of lung cancer were all Ⅳ.Histopathology proved that seven cases (7/8) were small cell lung cancer, and one case (1/8) was poorly differentiated adenocarcinoma. The median survival time was 11 months. Compared with non-tumor-induced AP, lung cancer patients with MIAP were older[(62±9) vs (48±15), P=0.018], the incidence of primary pancreatic duct dilatation (37.5% vs 3.1%, P=0.004) and abdominal lymphadenopathy (37.5% vs 6.3%, P=0.017) were higher; the level of hemoglobin [105.3±15.6) g/L vs (147.9±24.8) g/L, P<0.001] and hematocrit [(31.4±5.3) vs (42.5±6.1), P<0.001] were lower. Conclusions: Patientswith MIAP in lung cancer had poor outcome and unspecific symptoms. Old age, anemia, main pancreatic duct dilatation and abdominal lymphadenopathy are diagnostic clues that merit clinical attention. :目的： 分析肺癌转移相关性急性胰腺炎（MIAP）患者的临床特征及预后，为临床早期诊断提供线索。 方法： 回顾性分析2002年1月至2019年9月北京协和医院收治的8例肺癌MIAP患者病例特点及转归，并与非肿瘤所致急性胰腺炎（AP）进行比较。 结果： 7例（7/8）为轻症AP，1例（1/8）为重症AP。4例（4/8）以AP为首发表现，自AP起病至肺癌确诊平均时间为（112±36）d。临床表现以腹痛（8/8）为主，其次为消瘦（4/8）、恶心呕吐（2/8）、梗阻性黄疸（1/8）等。肺癌分期均为Ⅳ期，7例（7/8）为小细胞肺癌，1例（1/8）为低分化腺癌。中位生存期11个月。与非肿瘤所致AP对比，肺癌MIAP患者年龄更大[（62±9）岁比（48±15）岁，P=0.018）]，主胰管扩张（37.5%比3.1%，P=0.004）和腹腔淋巴结肿大（37.5%比6.3%，P=0.017）发生率更高；血红蛋白[（105.3±15.6）g/L比（147.9±24.8）g/L，P<0.001）]和红细胞压积（31.4±5.3比42.5±6.1，P<0.001）更低。 结论： 肺癌MIAP预后较差，症状不特异。老年、贫血、主胰管扩张和腹腔淋巴结肿大是其诊断线索，诊疗中应予以重视。.
目的: 分析肺癌转移所致急性胰腺炎 (MIAP) 患者的临床特点及预后，为早期诊断提供线索。方法: 回顾性分析 2002 年 1 月至 2019 年 9 月北京协和医院收治的 8 例肺癌MIAP患者的特点及预后，并与非肿瘤诱发AP进行比较。结果: Sevencases(7/8) 为轻度AP，1 例 (1/8) 为重度AP。4 例 (4/8) 患者以AP为报告征象，直到AP发病后 (112 ± 36) d才确诊为肺癌。临床表现包括腹痛 (8/8) 、体重减轻 (4/8) 、恶心呕吐 (2/8) 和黄疸 (1/8)。肺癌分期均为 Ⅳ 期，病理证实小细胞肺癌 7 例 (7/8)，低分化腺癌 1 例 (1/8)。中位生存时间为 11 个月。与非肿瘤诱导的AP相比，发生MIAP的肺癌患者年龄较大 [(62 ± 9) vs (48 ± 15)，P = 0.018]，原发性胰管扩张 (37.5% vs 3.1%，P = 0.004) 和腹腔淋巴结肿大 (37.5% vs 6.3%，P = 0.017) 的发生率较高; 血红蛋白水平 [105.3 ± 15.6] g/L vs (147.9 ± 24.8) g/L，P<0.001] 和红细胞压积 [(31.4 ± 5.3) vs (42.5 ± 6.1)，P<0.001] 较低。结论: MIAP肺癌患者预后差，症状不明确。高龄、贫血、主胰管扩张和腹部淋巴结肿大是值得临床重视的诊断线索。 : 目的: 分析肺癌转移相关性急性胰腺炎(MIAP)患者的临床特征及预后，为临床早期诊断提供线索。方法: 回顾分析 2002 年 1 月至 2019 年 9 月北京协商和医院治疗的 8 例肺癌患者病情点滴及转归，并与非肿瘤所致急性肠炎进行比较。结果: 7 例(7/8)为轻度症状，1 例(1/8)为重度症状。4 例(4/8)以首次表现为主，自起病至肺癌诊断平均时间为(112 ± 36)d。临床表现腹泻 (8/8)为主，其次为消瘦(4/8)、恶心呕吐(2/8)、 (1/8)等。肺癌分期均为 ⅳ 期，7 例(7/8)为小细胞肺癌，1 例(1/8)为小细胞肺癌。中期生存期 11 个月。与非肿瘤患者相比，肺癌患者年龄更大[(62 ± 9) 比(48 ± 15)岁，P = 0.018)]，主要扩张(37.5% 比 3.1%，P = 0.004)和腹腔淋巴瘤大(37.5% 比 6.3%，P = 0.017) 生产率更高;血红蛋白[(105.3 ± 15.6)g/L比(147.9 ± 24.8)g/L，P<0.001)]和红细胞压积(31.4 ± 5.3 比 42.5 ± 6.1，P<0.001)更低。结论: 肺癌预后较差，症状不特殊。老年、贫困，诊疗应当重视。
METHODS::Pulmonary artery sling is a rare congenital anomaly of the origin and course of the left pulmonary artery. Patients with this condition typically present with respiratory failure in young infancy, and asymptomatic cases are uncommon. We describe the case of an adult patient with a lung adenocarcinoma of the right upper lobe, extending into the hilum and superior mediastinum, and with a previously unknown pulmonary artery sling anomaly. The local invasiveness of the tumor and the peculiar vascular anatomy contributed to a unique surgical scenario, wherein multiple reconstructive procedures were required.
METHODS::Patients with idiopathic pulmonary fibrosis (IPF) have higher risk of developing lung cancer, for example, squamous cell carcinoma (SCC), and show poor prognosis, while the molecular basis has not been fully investigated. Here we conducted DNA methylome analysis of lung SCC using 20 SCC samples with/without IPF, and noncancerous lung tissue samples from smokers/nonsmokers, using Infinium HumanMethylation 450K array. SCC was clustered into low- and high-methylation epigenotypes by hierarchical clustering analysis. Genes hypermethylated in SCC significantly included genes targeted by polycomb repressive complex in embryonic stem cells, and genes associated with Gene Ontology terms, for example, "transcription" and "cell adhesion," while genes hypermethylated specifically in high-methylation subgroup significantly included genes associated with "negative regulation of growth." Low-methylation subgroup significantly correlated with IPF (78%, vs. 17% in high-methylation subgroup, p = 0.04), and the correlation was validated by additional Infinium analysis of SCC samples (n = 44 in total), and data from The Cancer Genome Atlas (n = 390). The correlation between low-methylation subgroup and IPF was further validated by quantitative methylation analysis of marker genes commonly hypermethylated in SCC (HOXA2, HOXA9 and PCDHGB6), and markers specifically hypermethylated in high-methylation subgroup (DLEC1, CFTR, MT1M, CRIP3 and ALDH7A1) in 77 SCC cases using pyrosequencing (p = 0.003). Furthermore, low-methylation epigenotype significantly correlated with poorer prognosis among all SCC patients, or among patients without IPF. Multivariate analysis showed that low-methylation epigenotype is an independent predictor of poor prognosis. These may suggest that lung SCC could be stratified into molecular subtypes with distinct prognosis, and low-methylation lung SCC that significantly correlates with IPF shows unfavorable outcome.
METHODS::The role of Fyn-related kinase (FRK) in malignant tumors remains controversial. Our study investigated the function of FRK in lung cancer. Immunohistochemistry staining and generating a knockout of FRK by CRISPR/Cas9 in H1299 (FRK-KO-H1299) cells were strategies used to explore the role of FRK. Immunohistochemistry staining indicated that FRK expression was elevated in 223 lung cancer tissues compared to 26 distant normal lung tissues. FRK contributed to poor survival status in lung cancer patients and acted as a predictor for poor prognosis of lung cancer. Knockout of FRK by CRISPR/Cas9 markedly inhibited proliferation, invasion, colony formation and epithelial-mesenchymal transition (EMT) process in the lung cancer cell line H1299. Further exploration indicated that FRK-KO damaged the stemness phenotype of H1299 by inhibiting CD44 and CD133 expression. Seahorse detection and a U-13 C flux assay revealed that FRK-KO induced metabolism reprogramming by inhibiting the Warburg effect and changing the energy type in H1299 cells. Epidermal growth factor stimulation recovered the expression of FRK and biological functions, metabolic reprogramming and stemness phenotype of H1299 cells. FRK plays an oncogenic role in lung cancer cells via a novel regulation mechanism of enhancing the stemness of H1299 cells by inducing metabolism reprogramming, which finally promotes EMT and metastasis. Our study also indicates that FRK could be used as a potential therapeutic target for drug development.