Previous studies have investigated the association between HOXA13 and non-small cell lung cancer. However, the role of HOXA13 expression in the occurrence and progression of lung adenocarcinoma (LUAD) has not yet been investigated. In the present study, HOXA13-related data mining of The Cancer Genome Atlas (TCGA), polymerase chain reaction (PCR) data from our cases and the case information in Oncomine was conducted for validation. The expression data of HOXA13 in lung cancer cell lines were also collected from the Cancer Cell Line Encyclopedia (CCLE) database for further verification. A comprehensive meta-analysis of the expression of HOXA13 was also performed, integrating the data of TCGA, in-house PCR and Oncomine. Genes that were co-expressed with HOXA13 were subsequently identified through cBioPortal and Multi Experiment Matrix (MEM), and the potential role and mechanism of HOXA13 in LUAD was investigated. The expression value of HOXA13 in the LUAD group, which comprised 237 cases, was 3.74±2.694, significantly higher than its expression value in the non-cancerous group (0.92±0.608, P<0.001). The pooled SMD for HOXA13 was 0.346 (95% CI, 0.052–0.640; P=0.068; I2=51.3%; P=0.021), The meta-analysis of diagnostic tests revealed that the area under the summary receiver operating characteristic curve (SROC) was 0.78 (95% CI, 0.75–0.82). The results demonstrated that HOXA13 is highly expressed in LUAD. In addition to the studies on HOXA13 expression in tissues, the expression data of HOXA13 in lung cancer cell lines were also collected from the CCLE database for further verification of these conclusions. Genes that were co-expressed with HOXA13 were identified for pathway analysis. The most enriched Gene Ontology terms in the genes co-expressed with HOXA13 were positive regulation of transcription from RNA polymerase II promoter, signal transduction and positive regulation of GTPase activity in biological process; cytoplasm, integral component of membrane and plasma membrane in cellular component; and significantly involved in protein binding, transcription factor activity, sequence-specific DNA binding and sequence-specific DNA binding in molecular function. Kyoto Encyclopedia of Genes and Genomes analysis revealed that these target genes were clearly involved in Pathways in cancer, Proteoglycans in cancer and cAMP signaling pathway. The hub genes obtained from the four protein-protein interaction networks were associated with HOXA13. The results of the bioinformatics research in the present study revealed that HOXA13 may influence the expression of these hub genes in such a way as to promote the occurrence and development of LUAD. In conclusion, the expression of HOXA13 in patients with LUAD and its potential clinical value were analyzed comprehensively in the present study using data from a variety of sources. Through bioinformatics analysis, evidence that HOXA13 may promote the occurrence and development of LUAD was obtained.
Background: The current study was to investigate the volume doubling time (VDT) of lung adenocarcinomas considering epidermal growth factor receptor (EGFR) mutation status of exon 19 and 21, when compared with EGFR wide type.Methods: Eighty-eight patients with pathologically proven adenocarcinomas, which underwent two or more computed tomography (CT) scans spared by 25 or more days, were included. EGFR mutations at exons 19 and 21 were determined using amplification refractory mutation system and all patients were divided into three groups-EGFR wide type group, EGFR mutation in exon 19 and 21 groups. Threedimensional manual segmentations for all tumors were performed on first and latest follow-up CT scans; subsequently, VDTs were calculated and compared among three groups. Clinicopathoradiologic characters were also collected for subgroup analysis.Results: EGFR mutations occurred in 49 (55.7%) patients, 19 in exon 19 and 30 in exon 21, respectively.The median VDT of all patients (33 men, 55 women; median age, 62 years) was 214 days (range, −4,092 to 10,920 days). Highly differentiated adenocarcinomas (median, 408 days) demonstrated longer VDT than those moderately (median, 172 days) or poorly (median, 144 days) differentiated (P=0.04). The VDT distribution was similar among EGFR wide type group (median, 207 days), EGFR mutation in exon 19 group (median, 288 days) and exon 21 group (median, 144 days) (P=0.21). In subgroup analysis, the median VDT of adenocarcinomas with EGFR mutation in exon 19 was longer than that of EGFR wide type for males (P=0.03) or patients without spiculation sign in chest CT (P=0.04). Totally 24 adenocarcinomas presented negative VDTs, most of which tended to be stable. Positive VDT values were used for all median description.Conclusions: Overall VDT of lung adenocarcinomas seems not affected by EGFR mutation status.Researches with large population are warranted for further study.
Lung adenocarcinoma is one of the most common solid tumors, and diffuse large B-cell lymphoma (DLBCL) is the most common histological subtype of adult non-Hodgkin’s lymphoma. Although extra-nodular lesions are frequently observed in patients with DLBCL, urinary bladder involvement is rare. We report the case of a 77-year-old woman with lung adenocarcinoma who was diagnosed with a second primary bladder DLBCL, 9 months after treatment with molecular targeted drugs. Simultaneous therapies for her lymphoma with lenalidomide and rituximab and a tyrosine kinase inhibitor therapy for her lung cancer were both effective. This result was consistent with previous reports suggesting that patients unable to tolerate intensive chemotherapy could benefit from targeted therapies. Current research into the use of lenalidomide for the treatment of lymphomas and solid tumors is promising in terms of exploring immunotherapy as an alternative option for patients with concurrent solid tumors and lymphomas who have poor tolerance to radiotherapy and chemotherapy.
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