ReviewInternational journal of gastrointestinal cancer2003
NF-kappaB in pancreatic cancer.
Review in International journal of gastrointestinal cancer, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 52 citations in OpenAlex.
- Phase II trial of nafamostat mesilate/gemcitabin/S-1 for unresectable pancreatic cancer.PloS one · 2022Trial
- Circadian transcriptome of pancreatic adenocarcinoma unravels chronotherapeutic targets.JCI insight · 2024Article
- Innate and adaptive immune-directed tumour microenvironment in pancreatic ductal adenocarcinoma.Frontiers in immunology · 2024Review
- The NF-κB/miR-488/ERBB2 axis modulates pancreatic cancer cell malignancy and tumor growth through cell cycle signaling.Cancer biology & therapy · 2022Article
- MIF inhibitor, ISO-1, attenuates human pancreatic cancer cell proliferation, migration and invasion in vitro, and suppresses xenograft tumour growth in vivo.Scientific reports · 2020Article
- Advances in Tumor-Stroma Interactions: Emerging Role of Cytokine Network in Colorectal and Pancreatic Cancer.Journal of oncology · 2019Review
- Oncogenic TRIM31 confers gemcitabine resistance in pancreatic cancer via activating the NF-κB signaling pathway.Theranostics · 2018Article
- Inhibition of Neddylation Modification Sensitizes Pancreatic Cancer Cells to Gemcitabine.Neoplasia (New York, N.Y.) · 2017Article
- Article
- Effect of NF-κB inhibition on chemoresistance in biliary-pancreatic cancer.Surgery today · 2015Review
- Article
- A novel NF-κB/MMP-3 signal pathway involves in the aggressivity of glioma promoted by Bmi-1.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Insulin-like growth factor 1 receptor promotes the growth and chemoresistance of pancreatic cancer.Digestive diseases and sciences · 2013Article
- Genetically engineered mouse models of pancreatic adenocarcinoma.Molecular oncology · 2013Review
- Article
- Targeting mitochondrial STAT3 with the novel phospho-valproic acid (MDC-1112) inhibits pancreatic cancer growth in mice.PloS one · 2013Article
- Mucin (Muc) expression during pancreatic cancer progression in spontaneous mouse model: potential implications for diagnosis and therapy.Journal of hematology & oncology · 2012Article
- Anti-neoplastic activity of two flavone isomers derived from Gnaphalium elegans and Achyrocline bogotensis.PloS one · 2012Article
- Molecular predictors of gemcitabine response in pancreatic cancer.World journal of gastrointestinal oncology · 2011Article
- Up-regulation of miR-146a contributes to the inhibition of invasion of pancreatic cancer cells.Cancer research · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the genetic profile of pancreatic cancer is emerging as a result of much research, the role of specific genetic alterations that initiate tumorigenesis and produce its cardinal clinical features of locally aggressive growth, metastasis, and chemotherapy resistance remains unresolved. Recently, a number of studies have shown that the inhibition of constitutive NF-kappaB activation, one of the frequent molecular alterations in pancreatic cancer, inhibits tumorigenesis and metastasis. It also sensitizes pancreatic cancer cell lines to anticancer agent-induced apoptosis. Therefore because of the crucial role of NF-kappaB in pancreatic cancer, it is a potential target for developing novel therapeutic strategies for the disease. In vivo and in vitro models that mimic the tumorigenic phenotypes in the appropriate histological and molecular concert would be very useful for confirming the suspected role of the pancreatic cancer signature genetic lesions and better understanding the molecular basis of this disease.
Indexed as
Identifiers
What OpenQuestion holds
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.