Immune profiles of early onset vs late onset colorectal cancer
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ABSTRACT:
PROVIDER: PRJNA732397 | ENA |
REPOSITORIES: ENA
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Project description:Despite a decrease in the incidence of colorectal cancer (CRC) over the last 40 years, the incidence of CRC in people under 50 years old is increasing around the globe. Early onset (50 years old) and late onset (65 years old) CRC appear to have differences in their clinicopathological and genetic features, but it is unclear if there are differences in the tumor microenvironment. We hypothesized that the immune microenvironment of early onset CRC is distinct from late onset CRC and promotes tumor progression. We used Nanostring immune profiling to analyze mRNA expression of immune genes in FFPE surgical specimens from patients with early (N=40) and late onset (N=39) CRC. We found three genes, SAA1, C7, and CFD, have increased expression in early onset colorectal cancer and distinct immune signatures based on the tumor location. After adjusting for clinicopathological features, increased expression of CFD and SAA1 were associated with worse progression free survival and increased expression of C7 was associated with worse overall survival. We also performed gain of function experiments with CFD and SAA1 in subcutaneous tumor murine models and found that CFD is associated with higher tumor volumes, impacted several immune genes and impacted three genes in mice that were also found to be differentially expressed in early onset CRC (EGR1, PSMB9, CXCL9). Our data demonstrate that the immune microenvironment, characterized by a distinct innate immune response signature in early onset CRC, is unique, location dependent, and might contribute to worse outcomes.
2021-05-25 | GSE175433 | GEO
Project description:To identify the gene expression of early-onset colorectal cancer, we sampled early-onset colorectal cancer patients (age < 50) and late-onset colorectal cancer paitients (age > 70) We then performed gene expression profiling analysis using data obtained from RNA-seq of early-onset colorectal cancer tissues and late-onset colorectal cancer tissues.
2023-02-08 | GSE213092 | GEO
Project description:Preeclampsia is a severe placenta-related pregnancy disorder that is generally divided into two subtypes named early-onset preeclampsia (onset <34 weeks of gestation), and lateonset preeclampsia (onset ≥34 weeks of gestation), with distinct pathophysiological origins. Both forms of preeclampsia have been associated with maternal systemic inflammation. However, alterations in the placental immune system have been less well characterized. Here, we studied immunological alterations in early- and late-onset preeclampsia placentas using a targeted expression profile approach. RNA was extracted from snap-frozen placenta samples (healthy n=13, early-onset preeclampsia n=13, and late-onset preeclampsia n=6). The expression of 730 immune-related genes from the Pan Cancer Immune Profiling Panel was measured, and the data were analyzed Q10 in the advanced analysis module of nSolver software (NanoString Technology). The results showed that early-onset preeclampsia placentas displayed reduced expression of complement, and toll-like receptor (TLR) associated genes, specifically TLR1 and TLR4. Mast cells and M2 macrophages were also decreased in early-onset preeclampsia compared to healthy pl acentas. The findings were confirmed by an immunohistochemistry approach using 20 healthy, 19 early-onset preeclampsia, and 10 late-onset preeclampsia placentas. We conclude that the placental innate immune system is altered in early-onset preeclampsia compared to uncomplicated pregnancies. The absence of these alterations in late-onset preeclampsia placentas indicates dissimilar immunological profiles. The study revealed distinct pathophysiological processes in earlyonset and late-onset preeclampsia placentas and imply that a tailored treatment to each subtype is desirable.
2021-12-13 | GSE190639 | GEO
Project description:Placental Immune alterations in early-onset preeclampsia and late-onset preeclampsia
| PRJNA787896 | ENA
Project description:The clinical and pathological features of early-onset colorectal cancer (EOCRC) differ from those of late-onset colorectal cancer (LOCRC). Our research aims to thoroughly elucidate the distinctions between them by analyzing clinical prognosis, metastatic patterns, gene expression, and genomic mutation profiles. Our deliberation will uncover latent strategies for personalized therapeutic of both EOCRC and LOCRC.
| 92169 | ecrin-mdr-crc
Project description:Early-Onset Colorectal Carcinoma (EOCRC) is a growing concern as reports indicate a worldwide increase in the incidence of CRC among young adults (<50 years old). In an effort to understand the different mode of pathogenesis in young-onset CRC, we performed a pilot study wherein we looked at colorectal tumors from both young (< 50 years old) and old patients (>55 years old) and screened them to eliminate tumors positive for Microsatellite Instability (MSI) and showing activation of the Wnt pathway, known canonical factors in CRC pathogenesis. RNA isolated from 3 EOCRC and 2 Late-Onset (LOCRC) tumors and paired normal tissues without MSI, nuclear β-catenin and APC mutations were sent for small RNA seq to identify miRNA alterations between the two subsets. Comparative analysis revealed differential expression of 23 miRNAs specific to EOCRC and 11 miRNAs specific to LOCRC.
2023-07-26 | GSE236991 | GEO
Project description:The early-onset mechanisms of idiopathic chronic pancreatitis, after the exclusion of known genetic risk factors, are rather unclear. Therefore, we attempt to pursue other potential pathology in our study and screened the differentially microRNAs from plasma samples of early-onset and late-onset ICP by microarray.
2011-09-25 | E-MEXP-3383 | biostudies-arrayexpress
Project description:Background: Causative genes for autosomal dominantly inherited familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC) have been well characterized. There is, however, another 10-15 % early onset colorectal cancer (CRC) whose genetic components are currently unknown. In this study, we used DNA chip technology to systematically search for genes differentially expressed in early onset CRC. Keywords: disease state analysis
2007-03-20 | GSE4107 | GEO
Project description:Analysis of breast cancer gene expression profiles. The hypothesis tested in the present study was that if differential profiles exsist between early and late onset breast cancer. Results provide important information regarding up- or down-regulated genes playing a mechanistic role in cancer.
2016-11-21 | GSE89116 | GEO
Project description:Early-onset colorectal cancer (EOCRC; age younger than 50 years) incidence has been steadily increasing over the last decades worldwide with causes unexplained. A unique molecular feature of EOCRC is that these cases harbor a greater incidence of Nodal Modulator 1 (NOMO1) somatic deletions compared with late-onset CRC. Yet the mechanisms of NOMO1 in early-onset colorectal carcinogenesis are currently unknown. Here we show that 50% of heterozygous NOMO1 deleted–EOCRCs presented pathogenic mutations in this gene, suggesting that NOMO1 can be inactivated by deletion or mutation in EOCRC. To study its role in EOCRC, CRISPR/cas9 technology was used to generate NOMO1 knockout HCT-116 (EOCRC) and HS-5 (bone marrow) cell lines. Loss of NOMO1 in these cell lines did not perturb Nodal pathway signaling. Results from expression microarray, RNA sequencing and protein expression analysis by LC-IMS/MS revealed that NOMO1 inactivation deregulates other signaling pathways independent of the Nodal pathway such as epithelial-mesenchymal transition. Importantly, NOMO1 inactivation increased the migration capacity of CRC cells. Additionally, a gut-specific conditional KO mouse model of NOMO1 revealed no subsequent tumor development in mice. Overall, these findings suggest that NOMO1 could not be a driver of early-onset colorectal carcinogenesis, but its loss promotes an increased migration capacity of CRC cells. Further study is warranted to explore other signaling pathways deregulated by the loss of NOMO1 that may play a relevant role in the pathogenesis of the disease.
2022-10-15 | PXD033636 | Pride