Lung Progression versus Regression Whole Genome Sequencing
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ABSTRACT:
PROVIDER: EGAS00001000837 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Around 50 samples of pre-invasive lung cancer lesions showing subsequent clinical and pathological progression or regression
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Project description:Background: Lung carcinoma-in-situ (CIS) lesions are the pre-invasive precursor to lung squamous cell carcinoma. However, only half progress to invasive cancer in three years, while a third spontaneously regress. Molecular profiling techniques have identified marked differences between progressive and regressive lesions. Here we present laser-captured stromal tissue, adjacent to previously profiled CIS lesions, to examine the role of the tumour microenvironment in spontaneous lesion regression. All samples in this dataset are paired with matched CIS lesions in dataset GSE108082.
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2018-12-22 | GSE124288 | GEO
Project description:Spontaneous regression is a well defined phenomenon commonly observed in human melanoma in its partial histopathological form but sporadically in its complete expression. Molecular mechanisms which might be involved in spontaneous regression are poorly understood so far. The Melanoblastoma bearing Libechov Minipig (MeLiM) model exhibits cutaneous melanomas which appear in utero or shortly after birth. These lesions are clinically and histologically highly comparable to their human counterparts. Nevertheless, in swine most of the highly invasive melanomas undergo complete spontaneous regression. Induction of regression is expressed by clinical features including changes in color, drying aspect and decrease in size; histologically we observed infiltration of histiocyte-like cells, fibrosis and lymphocytic infiltrate later. To characterize the regression phase on a transciptomic level, we performed time dependent gene expression profiling using the MeLiM model and porcine Affymetrix microarrays. We collected 5 different tumors of 5 siblings at 5 timepoints, from day 8 to day 91 after birth. After statistical analysis and reannotation of the 25 porcine microarrays we were able to identify 1411 genes regulated during regression. K-means clustering and subsequent functional clustering of these genes via Ingenuity Pathway analysis revealed significant pathways playing a role in melanoma regression. Genes involved in cell cycle, apoptosis, cellular movement, melanocyte-differentiation and pigmentation as well as genes of the immune reponse seem to be potential mediators of melanoma regression.
2008-09-10 | E-MEXP-1152 | biostudies-arrayexpress
Project description:In multiple sclerosis (MS), activated microglia and infiltrating macrophages phagocytose myelin focally in (chronic) active lesions. These demyelinating sites expand in time, but at some point turn inactive into a sclerotic scar. To identify molecular mechanisms underlying lesion activity and halt, we analyzed genome-wide gene expression in rim and peri-lesional regions of chronic active and inactive MS lesions, as well as in control tissue. Gene clustering revealed patterns of gene expression specifically associated with MS and with the presumed, subsequent stages of lesion development. Next to genes involved in immune functions, we found regulation of novel genes in and around the rim of chronic active lesions, such as NPY, KANK4, NCAN, TKTL1, and ANO4. Of note, the presence of many foamy macrophages in active rims was accompanied by a congruent upregulation of genes related to lipid binding, such as MSR1, CD68, CXCL16, and OLR1, and lipid uptake, such as CHIT1, GPNMB, and CCL18. Except CCL18, these genes were already upregulated in regions around active MS lesions, showing that such lesions are indeed expanding. In vitro downregulation of the scavenger receptors MSR1 and CXCL16 reduced myelin uptake. In conclusion, this study provides the gene expression profile of different aspects of MS pathology and indicates that early demyelination, mediated by scavenger receptors, is already present in regions around active MS lesions. Genes involved in early demyelination events in regions surrounding chronic active MS lesions might be promising therapeutic targets to stop lesion expansion.
2018-01-01 | GSE108000 | GEO
Project description:Background. Oral carcinogenesis is a complex process involving multiple genes. However, the genetic changes involved in this process are not demonstrated in the identical oral squamous carcinomas (OSCCs). Methods. According to the pathological characteristics, parts of normal tissues, oral dysplastic lesions (ODLs), and invasive cancers were procured from the identical OSCCs using laser microdissection (LMD), and large scale gene expression profiling was carried out on 33 samples derived from 11 OSCCs. Results. We analyzed genes differentially expressed in normal tissues vs. ODLs and ODLs vs. invasive tumors and identified the 15 candidate genes that continuously increasing or decreasing in its expression during oral carcinogenesis. One of these, ISG15 was chosen for further characterization. Real-time quantitative reverse transcriptase-polymerase chain reaction and immunohistochmistry analysis confirmed that ISG15 expression was consistently increasing during oral tumorigenesis. ISG15 high expression was significantly associated with poor prognosis (P=0.027). In addition, patients whose tumor had high ISG15 expression had worse 5-year survival rate than patients whose tumors had a low expression level (P=0.019). Conclusions. We identified the 15 genes that are continuously increasing or decreasing in its expression during oral carcinogenesis. One of these, ISG15 is likely to be associated with both dysgenesis and tumorigenesis, and may be a potential prognostic marker in these malignancies. Microarray samples of invasive tumor, adjacent dysplastic lesions and noncancerous normal tissues were collected from 11 patients with primary OSCCs. We analyzed genes differentially expressed in (i) normal vs. dysplastic tissues and (ii) dysplastic vs. tumor tissues.
2012-09-11 | E-GEOD-35261 | biostudies-arrayexpress
Project description:Background: Lung carcinoma-in-situ (CIS) lesions are the pre-invasive precursor to lung squamous cell carcinoma. However, only half progress to invasive cancer in three years, while a third spontaneously regress. Whether modern molecular profiling techniques can identify those pre-invasive lesions that will subsequently progress and distinguish them from those that will regress is unknown. Methods: Progressive and regressive CIS lesions were laser-captured and their genome, epigenome and transcriptome interrogated. We analysed 83 progressive lesions, 41 regressive and 33 normal epithelial control samples. DNA methylation and gene expression profiles were further validated using publicly available lung cancer data. Results: Somatic mutation burden was higher in progressive lesions than regressive CIS lesions, across base substitutions, rearrangements, insertions and deletions. Driver mutations were present in both progressive and regressive CIS lesions, but were more numerous in progressive cases. Progressive and regressive CIS lesions had distinct epigenomic and transcriptional profiles, with a strong chromosomal instability signature. Gene expression, methylation and copy number profiles can all predict accurately which CIS lesions will progress to lung cancer. Conclusion: Pre-invasive CIS lesions that will subsequently progress to invasive lung cancer can be distinguished from those that will regress using molecular profiling. Progression is associated with a strong chromosomal instability signature. These findings inform the development of novel therapeutic targets.
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Project description:The development of an HPV-associated cervical cancer usually takes a long time (years, decades) and comprises stepwise change of intraepithelial (preclinical) neoplastic forms, but after invasive carcinoma is established it demonstrates extremely aggressive behavior and heterogenic molecular profile. Women with pre-invasive neoplastic lesions or early-stage invasive cervical cancer who underwent treatment in the Republican Oncological Dispensary were enrolled in our study (all were HPV-positive). Tissue samples were excised during surgery before any other treatment. Comparative transcriptomic analysis of invasive cancers (with an emphasis to the earliest stages) versus non-invasive precursor lesions was performed by means of RNA sequencing.
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Project description:Breast cancer consists of at least five main molecular âintrinsicâ subtypes, which are reflected in both pre-invasive and invasive disease. Although previous studies have suggested that many of the molecular features of invasive breast cancer are established early, it is unclear what mechanisms drive progression, and whether the mechanisms of progression are dependent or independent of subtype. We have generated mRNA, miRNA and DNA copy number profiles from a total of 59 in situ lesions and 85 invasive tumors, in order to comprehensively identify those genes, signaling pathways, processes, and cell types that are involved in breast cancer progression. Our work provides evidence that there are molecular features associated with disease progression that are unique to the intrinsic subtypes. We additionally establish subtype-specific signatures that are able to identify a small proportion of pre-invasive tumors with expression profiles that resemble invasive carcinoma, indicating a higher likelihood of future disease progression. One-color design, totaling 48 arrays and 41 unique tissues. Arrays consist of 4 normal controls (1 unique), 28 DCIS lesions (26 unique), and 16 small invasive breast cancers (14 unique).
2016-07-07 | E-GEOD-59247 | biostudies-arrayexpress
Project description:Breast cancer consists of at least five main molecular âintrinsicâ subtypes, which are reflected in both pre-invasive and invasive disease. Although previous studies have suggested that many of the molecular features of invasive breast cancer are established early, it is unclear what mechanisms drive progression, and whether the mechanisms of progression are dependent or independent of subtype. We have generated mRNA, miRNA and DNA copy number profiles from a total of 59 in situ lesions and 85 invasive tumors, in order to comprehensively identify those genes, signaling pathways, processes, and cell types that are involved in breast cancer progression. Our work provides evidence that there are molecular features associated with disease progression that are unique to the intrinsic subtypes. We additionally establish subtype-specific signatures that are able to identify a small proportion of pre-invasive tumors with expression profiles that resemble invasive carcinoma, indicating a higher likelihood of future disease progression. One-color design, totaling 105 arrays and 103 unique tissues. Arrays consist of 3 normal controls (1 unique), 46 DCIS lesions (46 unique), and 56 small invasive breast cancers (56 unique).
2016-07-07 | E-GEOD-59246 | biostudies-arrayexpress