Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Metastatic Left Colon and Rectal Cancer Treatment With Anti_EGFR Targeted Therapy

ABSTRACT: Colorectal cancer ranks the second lethal cancer and third prevalent malignant tumour worldwide, Despite of different odern modalities for diagnosis,large number of cases diagnosed at metastatic advanced stage . New treatment approach has been discovered habe been discovered making a huge revolution in metastatic colorectal cancer represented by targeted therapy including anti_EGFR ,anti_angiogenic and kinase inhibitors .

DISEASE(S): Metastatic Colorectal Adenocarcinoma,Adenocarcinoma,Rectal Neoplasms

PROVIDER: 109426 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

ACCESS DATA

Json Xml

Similar Datasets

Superenhancer-activation of KLHDC8A Drives Glioma Ciliation and Hedgehog signaling

Project description:Glioblastoma ranks among the most aggressive and lethal of all human cancers, with poor responses to all therapeutic modalities. Self-renewing, highly tumorigenic glioblastoma stem cells (GSCs) contribute to therapeutic resistance and maintain cellular heterogeneity. Identification of GSC vulnerabilities may provide novel therapeutic targets for treating glioblastoma. Here, we interrogated superenhancer landscapes of primary glioblastoma specimens and patient-derived GSCs, revealing a kelch domain-containing gene (KLHDC8A) with a previously unknown function as an epigenetically driven oncogene. Targeting KLHDC8A decreased GSC proliferation, reduced sphere formation, induced apoptosis, and impaired in vivo tumor growth. Transcription factor control circuitry analyses revealed that the master transcriptional regulator SOX2 contributes to KLHDC8A expression. Mechanistically, KLHDC8A functions in the assembly of primary cilia via interactions with Chaperonin-containing TCP1 (CCT) and establishes a platform for a critical stem-specific signaling node through the Hedgehog pathway. Furthermore, we identified that Hedgehog and Aurora B/C Kinase signaling are complementary in GSCs, and dual inhibition synergistically inhibits GSC proliferation. Collectively, superenhancers enrich for essential mediators of cellular identity and offer a novel regulatory mechanism whereby promotion of ciliogenesis establishes and maintains a core GSC signaling node via the Hedgehog pathway, potentially offering insights into therapeutic vulnerabilities for glioblastoma treatment.

2022-12-22 | GSE207760 | GEO

Genome-wide analysis of long noncoding RNA expression profile in gastric cancer

Project description:Gastric cancer (GC) remains one of the most prevalent tumor worldwide, and ranks third in cancer-related deaths globally. Long non-coding RNAs (lncRNAs) have been reported to play significant role in the progression and metastasis in gastric cancer (GC), however, the molecular mechanism are largely elusive. We aim to identify up-regulated lncRNA in GC and study their function in promoting tumor progression and metastasis.

2023-11-13 | GSE193109 | GEO

TERT Promoter Mutations Combined with TP53 Mutations as Potential Biomarkers for Hepatocellular Carcinoma Recurrence and Prognosis

Project description:Hepatocellular carcinoma (HCC) is the most prevalent form of liver cancer, and ranks among the most lethal malignancies globally, primarily due to its high rates of recurrence and metastasis. Despite the urgency, no reliable biomarkers currently exist for predicting tumor recurrence in HCC. Telomerase reverse transcriptase (TERT) promoter mutations (TERTpm) and cellular tumor antigen p53 mutations (TP53m) have been frequently documented in HCC, but their combined clinical significance remains undefined. In this study, we investigated the clinical implications of TERTpm, TP53m, and their co-occurrence in 50 HCC tissue samples using the next-generation sequencing (NGS) technology. We identified TERTpm (C228T) and TP53m in 16 (32%) and 24 (48%) samples, respectively. Our findings indicate that these mutations are more prevalent in male patients (100% for TERTpm, 83.33% for TP53m), in those with solitary tumors (87.5% for both), in individuals with G2-G3 hepatitis (100% / 83.3%), and in cases of moderately differentiated tumors (75.0% / 83.3%). Furthermore, patients with both TERTpm and TP53m exhibited a significantly higher risk of tumor relapse (P<0.05) and shorter progression-free survival (P<0.05). Collectively, our results suggest that presence of both TERTpm and TP53m may serve as a robust predictor of tumor recurrence and a marker of poor prognosis in HCC.

2024-08-01 | GSE273254 | GEO

Project description:CCNE1 amplification is synthetic lethal with PKMYT1 kinase inhibition

| PRJNA808613 | ENA

Effects of neobractatin and trametinib on gene expression in pancreatic cancer cells

Project description:Pancreatic ductal adenocarcinoma carcinoma (PDAC) is a highly lethal disease and ranks as the seventh leading cause of cancer-related deaths worldwide. Neobractatin (NBT), a natural compound derived from Garcinia bracteate, has shown great antitumor effects and has been identified as a regulator of pyroptosis in esophageal cancer cells. The effectiveness of combining NBT with the common targeted drug trametinib in inhibiting PDAC and its underlying mechanisms remain unclear. In this study, we aimed to explore the therapeutic potential of combining NBT with trametinib in PDAC.

2024-09-01 | GSE275621 | GEO

RNA-seq of mouse cell lines isolated from genetically engineered mouse models of extrahepatic cholangiocarcinoma and pancreatic cancer

Project description:Biliary tract cancer (BTC) ranks among the most lethal human malignancies, thereby representing an unmet clinical need. In this study, we find that the Pdx1-positive extrahepatic biliary epithelium is highly susceptible towards transformation by activated Pik3caH1047R, but completely refractory to oncogenic KrasG12D. Using genome-wide in vivo piggyBac transposon-based forward genetic screening and genetic loss-of-function experiments, we discover important extrahepatic cholangiocarcinoma (ECC) cancer genes and find that PI3K-signaling output strength and repression of the tumor suppressor p27Kip1 are critical context-specific determinants of tumor formation. This contrasts the pancreas, where oncogenic Kras in concert with Trp53 loss of function are key cancer drivers. Notably, inactivation of p27Kip1 permits KrasG12D-driven ECC development, and bypasses oncogene-induced senescence without triggering the Trp53 pathway. These studies provide a mechanistic link between PI3K-signaling, tissue-specific tumor suppressor barriers, and ECC pathogenesis, and present a novel genetic model of autochthonous ECC and genes driving this highly lethal tumor-subtype.

2021-07-05 | E-MTAB-10515 | biostudies-arrayexpress

Targeted MIP sequencing for healthy samples

Project description:We developed Del-Read, an algorithm targeting medium-sized deletions (6-100 BPs) in short-reads, which are challenging for current variant callers relying on alignment. Our focus was on Micro-Homology mediated End Joining deletions (MMEJ-dels), prevalent in myeloid malignancies. MMEJ-dels follow a distinct pattern, occurring between two homologies, allowing us to generate a comprehensive list of MMEJ-dels in the exome. Using Del-Read, we identified numerous novel germline and somatic MMEJ-dels in Beat AML and TCGA-breast datasets. Validation in 500 healthy individuals confirmed their presence.

2023-09-20 | E-MTAB-13306 | biostudies-arrayexpress

Project description:A highly prevalent and persistent densovirus discovered among sea stars from the Atlantic Coast of the United States

| PRJNA555067 | ENA

Comparative transcriptomic analysis of BA- or BL- associated murine colonic epithelium after O157 infection

Project description:A huge number of microorganisms are colonized in human gut and the balance of their composition is closely related to human health. Recently, many probiotics such as bifidobacteria or lactobacilli have been introduced in our life as effective agents. However, we have not well understood their beneficial mechanisms including host-bacterial crosstalk. Accordingly, we took advantage of the protective mechanisms of probiotics against lethal infection of enterohemorrhagic Escherichia coli O157:H7 in murine gnotobiote model system

2011-01-27 | GSE12998 | GEO

Acquired FGFR and FGF alterations confer resistance to estrogen receptor (ER) targeted therapy in ER+ metastatic breast cancer

Project description:Beyond acquired mutations in the estrogen receptor (ER), mechanisms of resistance to ER-directed therapies in ER+ breast cancer have not been clearly defined. We conducted a genome-scale functional screen spanning 10,135 genes to investigate genes whose overexpression confer resistance to selective estrogen receptor degraders. Pathway analysis of candidate resistance genes demonstrated that the FGFR, ERBB, insulin receptor, and MAPK pathways represented key modalities of resistance. In parallel, we performed whole exome sequencing in paired pre-treatment and post-resistance biopsies from 60 patients with ER+ metastatic breast cancer who had developed resistance to ER-targeted therapy. The FGFR pathway was altered via FGFR1, FGFR2, or FGF3/FGF4 amplifications or FGFR2 mutations in 24 (40%) of the post-resistance biopsies. In 12 of the 24 post-resistance tumors exhibiting FGFR/FGF alterations, these alterations were not detected in the corresponding pre-treatment tumors, suggesting that they were acquired or enriched under the selective pressure of ER-directed therapy. In vitro experiments in ER+ breast cancer cells confirmed that FGFR/FGF alterations led to fulvestrant resistance as well as cross-resistance to the CDK4/6 inhibitor palbociclib, through activation of the MAPK pathway. The resistance phenotypes were reversed by FGFR inhibitors and, to a lesser extent, MEK inhibitors, suggesting potential treatment strategies.

2020-06-30 | GSE153509 | GEO

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