ArticleCancer cell & microenvironment2016
Ascending the PEAK1 toward targeting TGFβ during cancer progression: Recent advances and future perspectives.
Article in Cancer cell & microenvironment, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- CRISPR/Cas13a-mediated interfacial cleaving of hairpin RNA reporter for PEAK1 nucleic acid sensing.RSC advances · 2025Article
- Colorectal carcinoma progression is not influenced by the pseudokinase PEAK1.Scientific reports · 2024Article
- Pseudopodium enriched atypical kinase 1(PEAK1) promotes invasion and of melanoma cells by activating JAK/STAT3 signals.Bioengineered · 2021Article
- DHPS-dependent hypusination of eIF5A1/2 is necessary for TGFβ/fibronectin-induced breast cancer metastasis and associates with prognostically unfavorable genomic alterations in TP53.Biochemical and biophysical research communications · 2019Article
- Multi-modality imaging features distinguish pancreatic carcinoma from mass-forming chronic pancreatitis of the pancreatic head.Oncology letters · 2018Article
- ITGA1 is a pre-malignant biomarker that promotes therapy resistance and metastatic potential in pancreatic cancer.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cancer is the second leading cause of death in the United States. Mortality in patients with solid, epithelial-derived tumors strongly correlates with disease stage and the systemic metastatic load. In such cancers, notable morphological and molecular changes have been attributed to cells as they pass through a continuum of epithelial-mesenchymal transition (EMT) states and many of these changes are essential for metastasis. While cancer metastasis is a complex cascade that is regulated by cell-autonomous and microenvironmental influences, it is well-accepted that understanding and controlling metastatic disease is a viable method for increasing patient survival. In the past 5 years, the novel non-receptor tyrosine kinase PEAK1 has surfaced as a central regulator of tumor progression and metastasis in the context of solid, epithelial cancers. Here, we review this literature with a special focus on our recent work demonstrating that PEAK1 mediates non-canonical pro-tumorigenic TGFβ signaling and is an intracellular control point between tumor cells and their extracellular microenvironment. We conclude with a brief discussion of potential applications derived from our current understanding of PEAK1 biology.
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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.