BackgroundMyelolipoma is a rare neoplasm composed of yellowish adipose tissue and reddish-brown tissue corresponding to hematopoietic or hemorrhages. It typically occurs in adrenal glands as a solitary, well-circumscribed mass, and the thoracic location is extremely unusual.Case presentationWe present a rare case who is a 54 years old male with bilateral Myelolipoma of the posterior mediastinum. He underwent the surgery via video-assisted thoracic surgery both sides interval 3 months. Histological examination showed both tumors consisted of mature fat tissue and hematopoietic tissue, including myeloid, erythroid, and megakaryocytic elements surrounded. We discussed the etiology, histopathology, differential diagnosis and recommended management of extra-adrenal myelolipoma and analyzed the features of the thoracic myelolipoma including mediastinal and pulmonary location.ConclusionsLiterature review showed 16 similar cases, with a 2/1 male/female ratio and a mean age of 58 years. Eight of sixteen cases were observed in the mediastinum and six of sixteen cases were displayed in the pulmonary and one showed on the chest wall. CT and MRI scans are able to indicate the presence of extra-adrenal myelolipoma. Pathological analysis is an effective method to clarify the diagnosis. Observation and surgery are two regular treatment methods. Small, asymptomatic tumors should be monitored, while large tumors that cause unendurable symptoms may be removed by surgery.
BackgroundThe “seed and soil” hypothesis emphasizes the importance of interactions between tumor cells and their microenvironment. CAFs (Cancer associated fibroblasts) are important components of the tumor microenvironment. They were widely involved in cancer cells growth and metastasis. Fibroblasts may also play a role in inflammatory disease. The phenotype conversion of fibroblasts in lung diseases has not been investigated previously. We hypothesized that fibroblasts phenotypes may vary among different types of lung disease.MethodsThe study included six types of lung tissues, ranging from normal lung to lung adenocarcinoma with lymphatic metastasis. Para-carcinoma tissues which were 2-cm-away from the tumor focus were also included in the analysis. The expression of target proteins including alpha-SMA (smooth muscle actin), FAP (fibroblast activation protein), vimentin, E-cadherin, and CK-19 (cytokeratin-19) were examined by immunohistochemistry. TGF-beta(transforming growth factor) and Twist were detected simultaneously in all samples.ResultsA progressive increase in the levels of alpha-SMA, vimentin and CK-19 was observed in correlation to the degree of malignancy from normal lung tissue to lung adenocarcinoma with lymphatic metastasis, whereas E-cadherin expression showed the opposite trend. TGF-beta and Twist were detected in cancer tissues and inflammatory pseudotumors. None of the proteins were detected in para-carcinoma tissues.ConclusionsFibroblast phenotypes varied according to the type and degree of lung malignancy and fibroblasts phenotypic conversion occurs as a gradual process with specific spatiotemporal characteristics. Similar fibroblast phenotypes in inflammatory diseases and cancer tissues suggested a correlation between inflammation and cancer and implied a common mechanism underlying the formation of fibroblasts in inflammatory diseases and lung cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s13019-014-0147-z) contains supplementary material, which is available to authorized users.
BackgroundDistinguishing between multiple primary lung cancers and metastatic tumors is often difficult when the tumor histology is same. Since genomic instability is a common feature of cancer, we hypothesized that independently arising neoplasms in an individual patient would exhibit measurable genomic variation, enabling discrimination of tumor lineage and relatedness. The feasibility of analyzing genomic instability expression profiles to distinguish multiple primary lung cancers from metastatic tumors was evaluated.MethodsThis study enrolled 13 patients, with multiple primary lung cancers demonstrating with the histology, who underwent surgery between April 2003 and December 2012 at the Department of the Thoracic Surgery at West China Hospital in Sichuan province of China and 10 patients who were diagnosed as metastasis disease during the same period for comparison purposes. Genomic DNA from lung cancers from individual patients was analyzed by six microsatellites (D2S1363, D6S1056, D7S1824, D10S1239, D15S822, and D22S689) with PCR to identify discordant allelic variation. The experiments were approved by the West China Hospital Ethics committee (No.2013 (33)) and all patients agreed to participate in the study and signed an informed consent form.ResultsAll of the 10 patients with distant metastasis showed a consistent consequence that we called “unique trend” between primary tumor and distant metastasis. The “trend” is representive in this study, which means that all alleles corresponding to six microsatellite markers were detected in DNA from primary tumors but were reduced or not observed in DNA from metastatic tumors. In the group of synchronous lung tumor with different histological types, the result showed a “contradictory trend”. Some alleles were detected in DNA from primary tumors but were reduced or not observed in DNA from metastatic tumors and other alleles corresponding to six microsatellite markers were detected in DNA from metastatic tumors but were reduced or not observed in DNA from primary tumors. In the third group (synchronous lung tumor with same histological types), 2 of 8 patients showed “unique trend” and the others showed “contradictory trend”.ConclusionsWith polymorphic microsatellite markers, the “unique trend” that represents metastasis cancers and the “contradictory trend” that represents primary multiple tumors are useful in the diagnosis between tumors found at the same time in the pulmonary even diagnosed with the histopathological evaluation from a single patient.
Although tyrosine kinase inhibitors (TKIs) targeting epidermal growth factor receptor (EGFR) have a favorable and durable treatment response, almost all patients will eventually acquire resistance and develop disease progression. Re-administration of first and second-generation EGFR TKIs has been successfully executed in advanced non-small cell lung cancer (NSCLC) subsequent to EGFR-TKI resistance.However, osimertinib rechallenge following osimertinib resistance in EGFR T790M-negative patient is less explored. Herein, we describe a metastatic adenocarcinoma NSCLC patient with exon 19 deletion in EGFR (19del) who acquired resistance to initial gefitinib and second-line osimertinib but was successfully rechallenged with osimertinib following treatment failure with chemotherapy. The osimertinib rechallenge, despite the absence of EGFR T790M, was considered after the development of multiple small pulmonary lesions and an increase in EGFR exon 19 deletion. After a month of osimertinib rechallenge, pulmonary and brain lesions significantly reduced achieving partial response. The success of osimertinib rechallenge following previous osimertinib resistance in a metastatic NSCLC patient with EGFR 19del in the absence of T790M suggests that re-administration of osimertinib can be a treatment option in similar situations.In addition, this case also highlights the importance of mutational profiling for treatment monitoring to understand the mutational landscape of the patient and guide subsequent treatment including treatment rechallenge.
Background: Lung squamous cell carcinoma (LUSC) approximately accounts for a third of lung cancers.However, the role of N6-methyladenosine (m6A) in LUSC remains largely unknown according to previous studies. Methods:In this study, we investigated the mutations, copy number variants (CNVs), expression of 20 m6A RNA methylation regulators, and clinical data from The Cancer Genome Atlas-LUSC (TCGA-LUSC). These data were used for the training cohort of screening potential biomarkers. The prognostic model of m6A RNA methylation regulators was constructed. A receiver operating characteristic (ROC) analysis was undertaken to determine the area under the curves (AUCs) (for 3-and 5-year survival) for the model. Additionally, the accuracy of the two-gene model was confirmed with external data verifications.Combined two-gene model and clinincal information were performed to construct a nomogram to predict patient's prognostic risk assessment.Results: Fat mass-and obesity-associated protein (FTO) and methyltransferase-like 3 (METTL3) were identified as potential prognostic biomarkers to evaluate benign and malignant tumors and prognosticate.The following prognostic model of m6A RNA methylation regulators was constructed: risk score = 0.162 × FTO − 0.069 × METTL3. Patients in low-risk group [median overall survival (mOS), 43.4 months] had longer survival than those with high-risk (mOS, 67.3 months) with P=0.0023. The smoking grade and risk score could be independent prognostic factors (P=0.00098 and P=0.0014, respectively). Ultimately, a nomogram was developed to assist clinicians to predict clinical outcomes.Conclusions: FTO and METTL3 are potential prognostic biomarkers of LUSC. The two-gene model's use of prognostic risk scores may provide guidance in the selection of therapeutic strategies.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.