ArticleStem cell investigation2016
Epigenetic regulation of human
Article in Stem cell investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- miR-136-5p Preferentially Suppresses Cancer Stem-like Cells in Pancreatic Cancer.International journal of molecular sciences · 2026Article
- Hypoxic stimulation of DCLK1 transcription and alternative-promoter switching fuels tumor malignancy in clear cell renal cell carcinoma.Cell death & disease · 2025Article
- Targeting the PI3K/AKT/mTOR pathway offer a promising therapeutic strategy for cholangiocarcinoma patients with high doublecortin-like kinase 1 expression.Journal of cancer research and clinical oncology · 2024Article
- Structure-Guided Prediction of the Functional Impact of DCLK1 Mutations on Tumorigenesis.Biomedicines · 2023Review
- Oncogenic functions and clinical significances of DCLK1 isoforms in colorectal cancer: a systematic review and meta-analysis.Cancer cell international · 2022Review
- Cytoplasmic expression of DCLK1-S, a novel DCLK1 isoform, is associated with tumor aggressiveness and worse disease-specific survival in colorectal cancer.Cancer biomarkers : section A of Disease markers · 2022Article
- Pleiotropic effects of DCLK1 in cancer and cancer stem cells.Frontiers in molecular biosciences · 2022Review
- DCLK1 promotes colorectal cancer stemness and aggressiveness via the XRCC5/COX2 axis.Theranostics · 2022Article
- DCLK1 and its interaction partners: An effective therapeutic target for colorectal cancer.Oncology letters · 2021Review
- Structural basis for small molecule targeting of Doublecortin Like Kinase 1 with DCLK1-IN-1.Communications biology · 2021Article
- DCLK1 isoforms and aberrant Notch signaling in the regulation of human and murine colitis.Cell death discovery · 2021Article
- DCLK1, a promising colorectal cancer stem cell marker, regulates tumor progression and invasion through miR-137 and miR-15a dependent manner.Clinical and experimental medicine · 2021Article
- Genome-wide DNA methylation analysis by MethylRad and the transcriptome profiles reveal the potential cancer-related lncRNAs in colon cancer.Cancer medicine · 2020Article
- Suppressing STAT5 signaling affects osteosarcoma growth and stemness.Cell death & disease · 2020Article
- Danhong Injection Alleviates Cardiac Fibrosis via Preventing the Hypermethylation of Rasal1 and Rassf1 in TAC Mice.Oxidative medicine and cellular longevity · 2020Article
- Disparate cell proliferation and p53 overexpression in colonic crypts with normal epithelial lining found below the neoplastic canopy of conventional adenomas.The journal of pathology. Clinical research · 2019Article
- Cancer stem cells in progression of colorectal cancer.Oncotarget · 2018Review
- Epigenetic signatures in cardiac fibrosis, special emphasis on DNA methylation and histone modification.Heart failure reviews · 2018Review
- FOXD3 Regulates CSC Marker, DCLK1-S, and Invasive Potential: Prognostic Implications in Colon Cancer.Molecular cancer research : MCR · 2017Article
- Identification of regulatory role of DNA methylation in colon cancer gene expression via systematic bioinformatics analysis.Medicine · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Colorectal carcinogenesis is a multi-step process. While ~25% of colorectal cancers (CRCs) arise in patients with a family history (genetic predisposition), ~75% of CRCs are due to age-associated accumulation of epigenetic alterations which can result in the suppression of key tumor suppressor genes leading to mutations and activation of oncogenic pathways. Sporadic colon-carcinogenesis is facilitated by many molecular pathways of genomic instability which include chromosomal instability (CIN), micro-satellite instability (MSI) and CpG island methylator phenotype (CIMP), leading towards loss of homeostasis and onset of neoplastic transformation. The unopposed activation of Wnt/β-catenin pathways, either due to loss of APC function or up-regulation of related stimulatory pathways, results in unopposed hyperproliferation of colonic crypts, considered the single most important risk factor for colon carcinogenesis. Hypermethylation of CpG islands within the promoters of specific genes can potentially inactivate DNA repair genes and/or critical tumor suppressor genes. Recently, CpG methylation of the 5' promoter of human (h)
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.