Browse
Submit Data
Databases
API
Help

Dataset Information

20 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Eyelid metastasis from lung adenocarcinoma.

ABSTRACT:

Purpose

To report an unusual case of lung metastasis presenting as an eyelid lesion.

Observations

An 82-year-old man presented with a right upper lid lesion of 2 weeks' duration proven to be adenocarcinoma of the lung.

Conclusions and importance

Metastasis to the eyelid is a rare occurrence. We present a review of the literature emphasizing factors contributing to its low incidence.

SUBMITTER: Dhannawat SS

PROVIDER: S-EPMC7724377 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Eyelid metastasis from lung adenocarcinoma.

Dhannawat Sneh S SS Sherwood Charles C Bahadur Rosanna R

American journal of ophthalmology case reports 20201120

<h4>Purpose</h4>To report an unusual case of lung metastasis presenting as an eyelid lesion.<h4>Observations</h4>An 82-year-old man presented with a right upper lid lesion of 2 weeks' duration proven to be adenocarcinoma of the lung.<h4>Conclusions and importance</h4>Metastasis to the eyelid is a rare occurrence. We present a review of the literature emphasizing factors contributing to its low incidence. ...[more]

PMID: 33319121

Similar Datasets

Brain metastasis from lung adenocarcinoma patients

Project description:Microarray analysis of 28 brain metastasis samples from lung adenocarcinoma patients. 28 brain metastasis samples: 19 from Marc Ladanyi 9 from William L. Gerald

| S-ECPF-GEOD-14108 | biostudies-other

Thyroid metastasis revealing a lung adenocarcinoma.

Project description:Thyroid metastasis revealing a primary lung cancer is an extremely rare condition. Only few cases have been reported in the literature. A multidisciplinary approach is essential for the diagnosis. The prognosis is generally poor. We report a case of a 50-year-old man presented with cervical nodules corresponding to a thyroid nodule and lymph nodes. The ultrasonography-guided fine-needle aspiration cytology of the thyroid nodule and a cervical lymphadenopathy concluded to a poorly differentiated adenocarcinoma. Cervical lymphadenopathy biopsy with immunohistochemistry and additional imaging explorations contributed to the diagnosis of a lung adenocarcinoma stage IVB. He died few days after the diagnosis.

| S-EPMC7256324 | biostudies-literature

Neurotrophin receptor TrkB promotes lung adenocarcinoma metastasis.

Project description:Lung cancer is notorious for its ability to metastasize, but the pathways regulating lung cancer metastasis are largely unknown. An in vitro system designed to discover factors critical for lung cancer cell migration identified brain-derived neurotrophic factor, which stimulates cell migration through activation of tropomyosin-related kinase B (TrkB; also called NTRK2). Knockdown of TrkB in human lung cancer cell lines significantly decreased their migratory and metastatic ability in vitro and in vivo. In an autochthonous lung adenocarcinoma model driven by activated oncogenic Kras and p53 loss, TrkB deficiency significantly reduced metastasis. Hypoxia-inducible factor-1 directly regulated TrkB expression, and, in turn, TrkB activated Akt signaling in metastatic lung cancer cells. Finally, TrkB expression was correlated with metastasis in patient samples, and TrkB was detected more often in tumors that did not have Kras or epidermal growth factor receptor mutations. These studies demonstrate that TrkB is an important therapeutic target in metastatic lung adenocarcinoma.

| S-EPMC4104911 | biostudies-literature

First presentation of lung adenocarcinoma as a subungual metastasis.

Project description:Subungual metastasis as a presenting feature of lung adenocarcinoma is rare and may be confused with a benign inflammatory disorder of the nail unit with subsequent diagnostic and management delay. We discuss the case of a 46-year-old man with a subungual metastasis as a presenting feature of lung adenocarcinoma.

| S-EPMC2528977 | biostudies-other

Brain metastasis from lung adenocarcinoma patients

Project description:Microarray analysis of 28 brain metastasis samples from lung adenocarcinoma patients. 28 brain metastasis samples: 19 from Marc Ladanyi 9 from William L. Gerald

2010-06-17 | E-GEOD-14108 | biostudies-arrayexpress

A case report of eyelid Merkel cell carcinoma occurring under treatment with nivolumab for a lung adenocarcinoma.

Project description:BACKGROUND:Merkel cell carcinoma (MCC) is a rare neuroendocrine malignancy of the skin characterized by high aggressiveness. Four main factors are implicated in its development: immunosuppression, ultraviolet radiation, age and the Merkel cell polyomavirus (MCPyV). In recent years, immune checkpoint inhibitors have shown clinical activity in MCC treatment. CASE PRESENTATION:We report the case of an 82-year-old man with a lung adenocarcinoma diagnosis, who underwent immunotherapy with nivolumab as second-line treatment. Seven months after the diagnosis of lung cancer during the nivolumab treatment, the patient developed an eyelid MCC, initially misdiagnosed as a chalazion. A palliative radiotherapy was performed with clinical benefit. After a total of seven cycles of nivolumab, computed tomography showed a lung and cerebral disease progression. In addition, clinical conditions worsened leading to the patient's death 13 months after the initial lung cancer diagnosis. CONCLUSIONS:Cases of co-occurrence of MCC and non-small cell lung cancer (NSCLC) have rarely been reported. Interestingly, common risk factors may be postulated for both cancers. Considering the rarity of this adverse event, its short-term temporal relation with the administration of the drug, which makes a relation improbable, and the coexistence of other risk factors, which may provide plausible explanations, it is possible to conclude according to the WHO Adverse Reaction Terminology that a causal relation between the occurrence of this serious adverse event and the exposure to the drug is unlikely. However, the case deserves to be reported in the literature.

| S-EPMC6198491 | biostudies-literature

TGF-?/Smad signaling through DOCK4 facilitates lung adenocarcinoma metastasis.

Project description:The mechanisms by which TGF-? promotes lung adenocarcinoma (ADC) metastasis are largely unknown. Here, we report that in lung ADC cells, TGF-? potently induces expression of DOCK4, but not other DOCK family members, via the Smad pathway and that DOCK4 induction mediates TGF-?'s prometastatic effects by enhancing tumor cell extravasation. TGF-?-induced DOCK4 stimulates lung ADC cell protrusion, motility, and invasion without affecting epithelial-to-mesenchymal transition. These processes, which are fundamental to tumor cell extravasation, are driven by DOCK4-mediated Rac1 activation, unveiling a novel link between TGF-? and Rac1. Thus, our findings uncover the atypical Rac1 activator DOCK4 as a key component of the TGF-?/Smad pathway that promotes lung ADC cell extravasation and metastasis.

| S-EPMC4318142 | biostudies-literature

LINC00852 Promotes Lung Adenocarcinoma Spinal Metastasis by Targeting S100A9.

Project description:Background: Lung adenocarcinoma has a strong tendency to develop into bone metastases, especially spinal metastases (SM). Long noncoding RNAs (lncRNAs) play critical roles in regulating several biological processes in cancer cells. However, the mechanisms underlying the roles of lncRNAs in the development of SM have not been elucidated to date. Methods: Clinical specimens were collected for analysis of differentially expressed lncRNAs. The Kyoto Encyclopedia of Genes and Genomes (KEGG) was used to examine the effects of these genes on pathways. RNA pull-down was utilized to identify the targeting protein of lncRNAs. The effects of lncRNA on its target were detected in A549 and SPCA-1 cells via perturbation of the lncRNA expression. Oncological behavioral changes in transfected cells and phosphorylation of kinases in the relevant pathways, with or without inhibitors, were observed. Further, tumorigenicity was found to occur in experimental nude mice. Results: LINC00852 and the mitogen-activated protein kinase (MAPK) pathway were found to be associated with SM. Moreover, the LINC00852 target S100A9 had a positive regulatory role in the progression, migration, invasion, and metastasis of lung adenocarcinoma cells, both in vitro and in vivo. Furthermore, S100A9 strongly activated the P38 and REK1/2 kinases, and slightly activated the phosphorylation of the JNK kinase in the MAPK pathway in A549 and SPCA-1 cells. Conclusion: LINC00852 targets S100A9 to promote progression and oncogenic ability in lung adenocarcinoma SM through activation of the MAPK pathway. These findings suggest a potential novel target for early intervention against SM in lung cancer.

| S-EPMC6277606 | biostudies-literature

VPS33B suppresses lung adenocarcinoma metastasis and chemoresistance to cisplatin.

Project description:The presence of VPS33B in tumors has rarely been reported. Downregulated VPS33B protein expression is an unfavorable factor that promotes the pathogenesis of lung adenocarcinoma (LUAD). Overexpressed VPS33B was shown to reduce the migration, invasion, metastasis, and chemoresistance of LUAD cells to cisplatin (DDP) in vivo and in vitro. Mechanistic analyses have indicated that VPS33B first suppresses epidermal growth factor receptor (EGFR) Ras/ERK signaling, which further reduces the expression of the oncogenic factor c-Myc. Downregulated c-Myc expression reduces the rate at which it binds the p53 promoter and weakens its transcription inhibition; therefore, decreased c-Myc stimulates p53 expression, leading to decreased epithelial-to-mesenchymal transition (EMT) signal. NESG1 has been shown to be an unfavorable indicator of non-small-cell lung cancer (NSCLC). Here, NESG1 was identified as an interactive protein of VPS33B. In addition, NESG1 was found to exhibit mutual stimulation with VPS33B via reduced RAS/ERK/c-Jun-mediated transcription repression. Knockdown of NESG1 activated EGFR/Ras/ERK/c-Myc signaling and further downregulated p53 expression, which thus activated EMT signaling and promoted LUAD migration and invasion. Finally, we observed that nicotine suppressed VPS33B expression by inducing PI3K/AKT/c-Jun-mediated transcription suppression. Our study demonstrates that VPS33B as a tumor suppressor is significantly involved in the pathogenesis of LUAD.

| S-EPMC8093570 | biostudies-literature

DDX17 promotes the growth and metastasis of lung adenocarcinoma.

Project description:DEAD box RNA helicase 17 (DDX17) has been shown to be an RNA binding protein involved in RNA metabolism and associated with cancer progression. However, the biological role of DDX17 in the pathogenesis of lung adenocarcinoma (LUAD) has not been well characterized. Here, we demonstrated that DDX17 promoted the proliferation, migration and invasion of H1299 and A549 lung adenocarcinoma cells. Analyses of public datasets showed that DDX17 is upregulated in LUAD specimens. Our tumor xenograft models confirmed the in vivo promoting role of DDX17 in the growth and metastasis of LUAD. Mechanistic analyses further revealed that DDX17 protein interacts with the mRNA of MYL9 and MAGEA6 and upregulates their levels. MYL9 could mediate the function of DDX17 to regulate the actin cytoskeleton rearrangement and cell adhesion, particularly by modulating the stress fiber and focal adhesion formation, whereas DDX17 might inhibit the autophagy process through MAGEA6/AMPKα1 axis in LUAD cells. Collectively, our study revealed the oncogenic role and pathways of DDX17 in LUAD.

| S-EPMC9588018 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data