Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA172569 | ENA |
REPOSITORIES: ENA
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Project description:CGCI: HIV+ Tumor Molecular Characterization Project (HTMCP) – Lung Cancer (LC)
| PRJNA172566 | ENA
Project description:CGCI: HIV+ Tumor Molecular Characterization Project (HTMCP) – Diffuse Large B-cell Lymphoma (DLBCL)
| PRJNA172565 | ENA
Project description:Cervical cancer (CC) remains a significant public health issue in low- and middle-income countries (LMICs), especially in Western sub-Saharan Africa and Nigeria. While global CC incidence and mortality have declined, these regions continue to face high rates due to inadequate screening and the high prevalence of HIV, which increases CC risk by promoting persistent HPV infections. This study aimed to identify DNA methylation (DNAm) biomarkers for cervical intraepithelial neoplasia (CIN) and CC in HIV-positive Nigerian women and to assess their potential for clinical risk prediction. From 2018 to 2020, 538 participants were recruited from Nigerian tertiary hospitals. Cervical tissue samples were analyzed for DNAm using the Infinium MethylationEPIC BeadChip array, and HPV genotyping was conducted via next-generation sequencing. An epigenome-wide association study revealed 24 significant DNAm biomarkers associated with CIN and CC. These biomarkers showed hypermethylation in tumor suppressor genes (e.g., PRMD8), hypomethylation in oncogenes (e.g., MIR520H), and aberrant methylation in genes related to HIV/HPV infection and oncogenesis (e.g., GNB5, LMO4, FOXK2, NMT1). A machine learning-based DNAm classifier achieved 92.9% sensitivity and 88.6% specificity in predicting CC risk, with higher risk observed in adjacent normal cervical samples from CIN/CC patients and HIV/HPV co-infected women. DNAm biomarkers offer a promising approach to enhancing CC screening and early detection, particularly for HIV-positive women in LMICs. The DNAm-based model developed in this study shows potential for more accurate CC risk stratification, highlighting the need for further optimization, validation, and implementation in low-resource settings.
2024-11-01 | GSE279982 | GEO
Project description:Cervical cancer (CC) is the forth leading cause of deaths in gynecological tumor. Although the etiology of CC has been extensively investigated, the exact pathogenesis of CC remains incomplete. Therefore, we applied single-cell RNA sequencing on cancer tissue and normal adjacent tissue from a patient with CC. Together, we identified four tumor cell subpopulations in tumor cells, which had specific signature genes with different biological functions and presented different prognosis. Among them, we identified a subset of cancer stem cell (CSCs), which was related to the developmental hierarchy of tumor progression. These data facilitate the understanding of the CC landscape and provides deeper insights into the development of prognostic biomarkers and therapeutic targets in the CC.
2021-05-12 | GSE168652 | GEO
Project description:The effect of preventive vaccination against Human Papillomavirus (HPV) in reducing the burden of cervical cancer (CC) will not be seen before 30 years. It is still necessary to improve the procedures of screening and treatment against CC. Current methods for screening have low sensitivity (Pap test) or specificity (HPV tests) to detect high-grade cervical intraepithelial neoplasias (CIN) and CC (CIN2+). The objective of this study was the identification and characterization of cellular targets present in most CC and absent in normal cervical tissue that can be considered as potential markers for screening or therapeutic targets. Methods and Findings. A pyramidal strategy was used. Initially the expression of 8,638 genes was compared between 43 HPV16-positive CC and 12 healthy cervical epitheliums using the HG-Focus microarray. The expression intensity of 8,370 genes was validated in 24 samples with a second microarray (HG-ST1.0). A total of 997 genes were deregulated in CC and the 21 best ranked were validated and confirmed by qRT-PCR in 67 CC and 25 controls. According to the ROC analysis and the fold change (FC), the best (AUC M-bM-^IM-% 0.97 and FC M-bM-^IM-% 10) six genes (CCNB2, CDC20, PRC1, SYCP2, NUSAP1, CDKN3) belong to the mitosis pathway. They were further explored by qRT-PCR in 29 CIN1 and 21 CIN2/3 lesions to investigate whether they could differentiate CIN2+ from CIN1 and healthy cervical epitheliums (CIN1-). Three of these genes were associated exclusively with invasive tumors (CCNB2, PRC1, SYCP2) and three (CDC20, NUSAP1, CDKN3) also with CIN2/3. The sensitivity and specificity of CDKN3 and NUSAP1, along with CDKN2A, to detect CIN2+ was around 90%. The protein codified by these genes was confirmed by immunohistochemistry in CC. The effect of these markers on the survival was investigated in 40 CC patients followed by 42 months. Only high-expression level of CDKN3 was associated with a poor survival (20%; p = 2 x 10-4, Long-rank test) and it was independent from FIGO staging. Conclusions. CDKN3 and NUSAP1, together with CDKN2A, may be potential targets for development of screening methods. However, further studies are needed from a screening population to define the optimal trade-off between sensitivity and specificity for detection of CIN2+. CDKN3 may be also considered as a survival marker. Inhibition of mitosis is a well-known strategy to combat cancers. Therefore, CDKN3 may be a potential therapeutic target in CC. However, itM-BM-4s still necessary to demonstrate whether itM-BM-4s indispensable for tumor growth. cervical cancer vs. healthy cervix
2013-03-31 | E-GEOD-39001 | biostudies-arrayexpress
Project description:We performed a comprehensive proteogenomic profiling of cervical cancer (CC) tumors obtained from 139 Chinese women. This study provides a valuable public resource including proteomic, phosphoproteome, acetylproteome for researchers and clinicians to delve deeper into molecular causes of CC, and to identify potential treatments and advance clinical practice.
2024-10-09 | PXD055203 | Pride
Project description:Recurrent karyotypic abnormalities are a characteristic feature of cervical cancer (CC) cells, which may result in deregulated expression of important genes that contribute to tumor initiation and progression. To examine the role of genomic copy number alterations, we surveyed genetic lesions in CC utilizing single nucleotide polymorphism (SNP) array. We identified specific genetic alterations associated with CC. These data will be useful in identification of target altered genes, novel markers for predicting high risk precancerous lesions to invasive cancer, comparison of copy number alterations with gene expression changes can provide gene targets for pharmacologic intervention. We demonstrate specific regions of gene amplification (e.g., 11q22), copy number gains (e.g., 3q, 5p, and 20q), and deletions (e.g., 2q, 11q23) in the present study, which forma a framework for identification of critical genes in CC tumorigenesis. Keywords: Cervical cancer, copy number alterations, HPV type, gene amplification
2008-06-04 | GSE10092 | GEO
Project description:Although Human papillomavirus infection is the main causal factor for cervical cancer (CC), there is data suggesting genetic factors could modulate the risk and progression of CC. Sibling studies suggest that maternally inherited factors could be involved in CC. To assess whether mitochondrial DNA (mtDNA) polymorphisms are associated to cervical cancer, HPV infection and HPV types, a case-control study was performed in the Mexican mestizo population. The polymorphism of mtDNA D-Loop was investigated in 187 cervical cancer patients and 270 healthy controls. D-loop was amplified from a blood DNA sample and analyzed by sequencing. HPV was detected and typed in cervical scrapes from both groups. mtDNA polymorphisms were compared in the whole samples and stratified by HPV types. The expression of 29 mitochondrial genes was analyzed in a subset of 45 tumor biopsies using the expression microarray ST1.0. The Amerindian haplogroup B2 increased the risk for CC (OR=1.6, 95% CI: 1.05-2.58) and showed an additive effect of 36% over the risk conferred by the HPV (OR=153, 95% CI: 65.4-357.5). The frequency of HPV 16, 18, 31 and 45 in cancer samples was similar in all haplogroups but one (D1). It showed a very low frequency of HPV16, any HPV18 and high frequency of HPVs 31, 45 and other types. Two mtDNA genes (MT-TD, MTTK) could be involved in the increased risk conferred by the haplogroup B2, since they were up-regulated exclusively in B2 tumors (p<0.05, t-test). These findings will contribute to clarify the importance of genetic factors in CC.
2012-01-31 | GSE29570 | GEO
Project description:Cervical cancer (CC) is the fourth leading cause of deaths in gynecological malignancies. Although the etiology of CC has been extensively investigated, the exact pathogenesis of CC remains incomplete. Recently, single-cell technologies demonstrated advantages in exploring intra-tumoral diversification among various tumor cells. However, single-cell transcriptome (scRNA-seq) analysis of CC cells and microenvironment has not been conducted. In this study, a total of 6 samples (3 CC and 3 adjacent normal tissues) were examined by scRNA-seq. Here, we performed single-cell RNA sequencing (scRNA-seq) to survey the transcriptomes of 57,669 cells derived from three CC tumors with paired normal adjacent non-tumor (NAT) samples. Single-cell transcriptomics analysis revealed extensive heterogeneity in malignant cells of human CCs, wherein epithelial subpopulation exhibited different genomic and transcriptomic signatures. We also identified cancer-associated fibroblasts (CAF) that may promote tumor progression of CC, and further distinguished inflammatory CAF (iCAF) and myofibroblastic CAF (myCAF). CD8+ T cell diversity revealed both proliferative (MKI67+) and non-cycling exhausted (PDCD1+) subpopulations at the end of the trajectory path. We used the epithelial signature genes derived from scRNA-seq to deconvolute bulk RNA-seq data of CC, identifying four different CC subtypes, namely hypoxia (S-H subtype), proliferation (S-P subtype), differentiation (S-D subtype), and immunoactive (S-I subtype) subtype. Our results lay the foundation for precision prognostic and therapeutic stratification of CC.
2022-10-04 | E-MTAB-11948 | biostudies-arrayexpress
Project description:Dysregulation of glyco-gene expression in cancer can lead to aberrant glycans and glycoconjugates, which in turn can promote tumorigenesis. Cervical cancer display augmentation of aberrant sialylated glycans and increase of glyco-genes, which encoded enzymes participate in the sialylation pathways. Besides sialiltranferases, other glyco-genes, analyzed individually are reported as altered in cervical cancer. Here we show a comprehensive analysis of glyco-gene expression in cervical cancer to obtain a wide scenery of global changes in glycosylation pathways. First, we compared glyco-gene expression between normal tissue and cervical cancer. Second, we analyzed the glycogene expression in subtypes of cc to obtain hallmarks of glyco-gene expression in each case. Our results indicate that in cervical cancer the GPI-anchored biosynthesis is increased in cc while the synthesis of chondroitin and dermatan sulfate are decreased. Moreover, data show that adenocarcinoma displayed a homogenous glyco-gene expression pattern, where chondroitin /dermatan sulfate and heparan sulfate glycogenes are decreased, while keratan sulfate genes are increased. Dysregulation of glyco-gene expression in cancer can lead to aberrant glycans and glycoconjugates, which in turn can promote tumorigenesis. Cervical cancer display augmentation of aberrant sialylated glycans and increase of glyco-genes, which encoded enzymes participate in the sialylation pathways. Besides sialiltranferases, other glyco-genes, analyzed individually are reported as altered in cervical cancer. Here we show a comprehensive analysis of glyco-gene expression in cervical cancer to obtain a wide scenery of global changes in glycosylation pathways. First, we compared glyco-gene expression between normal tissue and cervical cancer. Second, we analyzed the glycogene expression in subtypes of cc to obtain hallmarks of glyco-gene expression in each case. Our results indicate that in cervical cancer the GPI-anchored biosynthesis is increased in cc while the synthesis of chondroitin and dermatan sulfate are decreased. Moreover, data show that adenocarcinoma displayed a homogenous glyco-gene expression pattern, where chondroitin /dermatan sulfate and heparan sulfate glycogenes are decreased, while keratan sulfate genes are increased.
2020-10-24 | GSE159976 | GEO