Breast cancer metastasis to gynecological organs – a clinico-pathological and molecular profiling study.
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE115080 | GEO | 2018/11/19
REPOSITORIES: GEO
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Project description:Breast cancer metastasis to gynecological organs – a clinico-pathological and molecular profiling study.
| PRJNA473678 | ENA
Project description:Initial screening for potential metastases suppressors down regulated by methylation was performed using breast cancer cell line models specific for site-specific metastasation. Gene expression profiling and qRT-PCR validations were conducted on tumor tissues from primary breast cancer (BC) and BCBM. CADM1 and RECK were further characterized for their methylation patterns and finally the protein expression of CADM1 was validated in a large number of BC and BCBM samples and correlated with clinico-pathologic parameters.
2014-03-04 | GSE44354 | GEO
Project description:Bone is the most frequent site of metastases from breast cancer (BC), although no biomarkers are yet available to predict the risk of skeletal dissemination. Here, we attempted to identify a gene signature correlated with bone metastasis (BM) onset in circulating tumor cells (CTCs) isolated from 40 metastatic BC patients, grouped according to their metastasis sites at the time of enrollment, namely “BM” (bone-only), “ES” (extra-skeletal) or “BM+ES” (bone and extra-skeletal). A 134-gene panel, derived from an extensive literature review, was validated on sub-clones of the MDA-MB-231 BC cell line with variable organotropism and then applied to CTC groups for targeted RNA sequencing. No correlation was found between CTC number and clinico-pathologic variables, whereas 31 differentially expressed genes emerged from “BM” and “ES” CTC comparison. The putative prognostic meaning of the “top-10” most deregulated genes was finally explored and pointed out by employing an external BC dataset.
2020-10-29 | GSE160314 | GEO
Project description:We performed cancer-immune gene expression analysis on a case series of glioblastoma second surgery samples due to novel enhancement following chemoradiation that were confirmed based on clinico-pathologic outcome as disease progression (PD) or pseudoprogression (psPD). This was accomplished using an nCounter Pancancer 360 IO panel. Our goals were to (1) determine if psPD events could be distinguished from PD events using differences in immune cell activation versus cancer cell proliferation and (2) examine whether samples stratified based on their molecular profile in the same way as documented clinico-pathologic diagnosis.
2023-12-04 | GSE231994 | GEO
Project description:The aim of the present study was to investigate LCN2 in endometrial cancer in relation to clinico-pathologic phenotype, angiogenesis, markers of epithelial-mesenchymal transition (EMT), and patient survival.
2012-04-01 | E-MTAB-1007 | biostudies-arrayexpress
Project description:Following the removal of implanted mammary tumors, nude mice develop multiple-organ metastases at late stage. The metastases may originate from the primary tumors before the resection surgery, or alternatively, from some established metastases. By multiple approaches, we have proved that bone environment could invigorate cancer cells for further dissemination. this study aims to examine if metastatic dissemination from bone to other sites occurs in natural setting of metastatic spread. We herein apply the rapidly evolving barcode system using homing guide RNA/Cas9 to trace the metastases formation in mouse. hgRNA/Cas9 is a self-targeting Crispr system which allows the mutation occurs in the DNA sequence of guide RNA. Tumor cells wer labelled with doxycycline inducible evolving barcoding system. Upon doxycycline treatment the DNA sequence of hgRNA accumulate mutations with time. The diversity of barcodes in each lesion can infer the timeing of seeding while the mutation patterns of barcodes suggest the phylogenetic correlation of metastases. Several findings were made on this study. First, at the terminal stage, multi-organ metastases are not genetically grouped according to sites of metastases. Nonnegative Matrix Factorization (NMF) analysis of mutant barcodes suggested the early disseminated metastases, which have highest level of Shannon entropy, were featured with a common cluster of mutant barcodes irrespective of their locations. Second, most metastases are potentially multiclonal as indicated by multiple clusters of independent mutant barcodes. Third, when we use Shannon entropy as an index of metastasis age , putative parent-child relationship between metastases with unique mutant barcodes clearly exemplified secondary metastatic seeding from bone to other organs. Finally, we did not observe a clear correlation between tumor burden and Shannon entropy across different metastases, suggesting that putative parental metastases might remain small after seeding further metastases.
2021-04-29 | GSE161145 | GEO
Project description:Genomic profiling of primary colorectal carcinomas was performed in relation to the spread of CTCs in peripheral and hepatic venous blood, liver metastases, and distant metastases beyond the liver, with the intent to identify specific patterns for the different stages of metastatic spread.
2018-08-21 | GSE82228 | GEO
Project description:In patients with metastatic melanoma, the identification and validation of accurate prognostic biomarkers will assist rational treatment planning. Studies based on "-omics" technologies have focussed on a single high-throughput data type such as gene or microRNA transcripts. Occasionally, these features were evaluated in conjunction with limited clinico-pathologic data. With the increased availability of multiple data types, there is a pressing need to tease apart which of these sources contain the most valuable prognostic information. We evaluated and integrated several data types derived from the same tumor specimens in AJCC stage III melanoma patients - gene, protein, and microRNA expression as well as clinical, pathologic and mutation information - to determine their relative impact on prognosis. We used classification frameworks based on pre-validation and bootstrap multiple imputation classification to compare the prognostic power of each data source, both individually as well as integratively. We found that the prognostic utility of clinico-pathologic information was not out-performed by various "-omics" platforms. Rather, a combination of clinico-pathologic variables and mRNA expression data performed best. Furthermore, a patient-based classification analysis revealed that the prognostic accuracy of various data types was not the same for different patients, providing useful insights for ongoing developments in the individualized treatment of melanomas patients. SPECIAL NOTE: In this study, survival data were re-extracted from the MIA research database for all patients and brought up to date, revealing discrepancies affecting survival class in the case of four patients compared with the previous dataset (GSE53118: http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53118). The current survival data are considered to be more accurate although the expression information has not changed. In addition, there were 5 samples (122, 144, 195, 264, and 358) for which gene expression information were not available at the time of analysis. However, the associated clinical information for these samples is provided since it was analysed elsewhere in the accompanying publication. Samples eligible for this study (n=84) were obtained from lymph node specimens (Melanoma Institute Australia (MIA) Biospecimen Bank) in which macroscopic tumor was observed, obtained from patients believed to be without distant metastases at the time of tumor banking based on clinical examination and computerised axial tomographic scanning of the brain, chest, abdomen and pelvis. Specimens were macro-dissected at time of banking and subsequently reviewed to meet minimum criteria for tumor cell content (>80%) and amount of necrosis (<30%). Linked clinical and pathologic data were obtained from the MIA research database. We previously analyzed the distribution of survival times in these samples and identified more favorable and less favorable groups as patients having time from surgery to death from melanoma greater than 4 years with no sign of relapse (n=25) or less than 1 year (n=22), respectively (Mann et al. 2013, PMID: 22931913). Since that publication, survival data have been re-extracted from the MIA research database for all patients and brought up to date, revealing discrepancies affecting survival class in the case of four patients compared with the previous dataset. The current survival data are considered to be more accurate. MRNA expression profiling and somatic mutation profiling, were performed as previously described in Mann et al. 2013 (PMID: 22931913).
2014-08-18 | E-GEOD-54467 | biostudies-arrayexpress
Project description:1. To determine the association between LVD and clinico-pathologic variables in archived colorectal cancer and Nasopharyngeal carcinoma specimens
2. To determine the association between VEGF-C,-D expression with COX-2 expression and clinico-pathologic variables in colorectal cancer and Nasopharyngeal carcinoma
3. To determine the effect of celecoxib on lymphangiogenesis in Nasopharyngeal carcinoma Lymphangiogenesis and factors modulating lymphangiogenesis are associated with clinico-pathological outcome in Nasopharyngeal carcinoma and colorectal cancer. Celecoxib down-regulates lymphangiogenesis Archival colorectal cancer and Nasopharyngeal carcinoma tumor specimens will be obtained from the Department of Pathology. To determine the effect of celecoxib on lymphangiogenesis in Nasopharyngeal carcinoma, the investigators intend to analyze archived specimens collected in a previously conducted study. Colorectal tumor and nodal specimens and Nasopharyngeal carcinoma primary will be examined for MVD, LVD and growth factor expression using established haematoxylin and eosin and immunohistochemical techniques. Quantification of LVD and MVD shall be performed by two pathologists blinded to clinico-pathological variables using standardised methods.
| 2075499 | ecrin-mdr-crc
Project description:The lymphatic system is a common avenue for the spread of breast cancer cells and dissemination through it occurs at least as frequently as hematogenous metastasis. Approximately 75% of primary breast cancers are estrogen receptor (ER) positive and the majority of these maintain receptor expression as lymph node (LN) metastases. However, it is unknown if ER function is equivalent in cancer cells growing in the breast and in the LNs. We have developed a model to assess estrogen responsiveness in ER(+) breast tumors and LN metastases. Fluorescent ER(+) MCF-7 tumors were grown in ovariectomized nude mice supplemented with estradiol. Once axillary LN metastasis arose, estradiol was withdrawn (EWD), for 1 or 4 weeks, or continued, to assess estradiol responsiveness. On EWD, proliferation rates fell similarly in tumors and LN metastases. However, estradiol-dependent ER down-regulation and progesterone receptor induction were deficient in LN metastases, indicating that ER-dependent transcriptional function was altered in the LN. Cancer cells from estradiol-treated and EWD primary tumors and matched LN metastases were isolated by laser capture microdissection. Global gene expression profiling identified transcripts that were regulated by the tissue microenvironment, by hormones, or by both. Interestingly, numerous genes that were estradiol regulated in tumors lost estradiol sensitivity or were regulated in the opposite direction by estradiol in LN metastases. We propose that the LN microenvironment alters estradiol signaling and may contribute to local antiestrogen resistance. Experiment Overall Design: 10 samples, including 3 each of estrogen and estrogen withdrawn axillary lymph nodes and 2 each of estrogen and estrogen withdrawn primary mammary gland tumors.
2008-06-11 | E-GEOD-11317 | biostudies-arrayexpress