ReviewPharmaceutical research2012
Novel anti-cancer compounds for developing combinatorial therapies to target anoikis-resistant tumors.
Review in Pharmaceutical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 21 citations in OpenAlex.
- Induction of immunogenic cell death by active components of natural products reshaping the tumor microenvironment for enhanced antitumor immunity.Frontiers in pharmacology · 2026Review
- Antitumor Properties of Matrikines of Different Origins: Prospects and Problems of Their Application.International journal of molecular sciences · 2023Review
- Haploinsufficiency Interactions between RALBP1 and p53 in ERBB2 and PyVT Models of Mouse Mammary Carcinogenesis.Cancers · 2021Article
- Spontaneous Cell Detachment and Reattachment in Cancer Cell Lines: An In Vitro Model of Metastasis and Malignancy.International journal of molecular sciences · 2021Article
- Article
- DNMT3b/OCT4 expression confers sorafenib resistance and poor prognosis of hepatocellular carcinoma through IL-6/STAT3 regulation.Journal of experimental & clinical cancer research : CR · 2019Article
- Rlip depletion prevents spontaneous neoplasia in TP53 null mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Mucin-1 aptamer-armed superparamagnetic iron oxide nanoparticles for targeted delivery of doxorubicin to breast cancer cells.BioImpacts : BI · 2018Article
- Can Some Marine-Derived Fungal Metabolites Become Actual Anticancer Agents?Marine drugs · 2015Review
- Andrographis paniculata elicits anti-invasion activities by suppressing TM4SF3 gene expression and by anoikis-sensitization in esophageal cancer cells.American journal of cancer research · 2015Article
- Combining histone deacetylase inhibitors with MDA-7/IL-24 enhances killing of renal carcinoma cells.Cancer biology & therapy · 2013Article
- Histone deacetylase inhibitors restore toxic BH3 domain protein expression in anoikis-resistant mammary and brain cancer stem cells, thereby enhancing the response to anti-ERBB1/ERBB2 therapy.Cancer biology & therapy · 2013Article
- "Just caring": can we afford the ethical and economic costs of circumventing cancer drug resistance?Journal of personalized medicine · 2013Article
- Cyclic versus hemi-bastadins. pleiotropic anti-cancer effects: from apoptosis to anti-angiogenic and anti-migratory effects.Molecules (Basel, Switzerland) · 2013Article
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
Abstract
Anoikis, a cell death pathway induced by loss of normal cell-matrix attachment or upon adhesion to a non-native matrix, ensures the balance between proliferative potential of normal cells and maintenance of tissue integrity. Thereby, anoikis serves as a potential molecular barrier against oncogenic transformation of normal cells. Cancer cells acquire anoikis resistance for survival and distant metastatic progression. During the acquisition of anoikis resistance, tumors modulate multiple cell signaling parameters through changes in the expression of up-stream receptors and by dynamically calibrating the dependency on down-stream signaling cascades. Many compounds that target the tumor-acquired switches in integrins, tumor antigens, growth factors, metabolic pathways, oxidative and osmotic-stress signaling are in various phases of pre-clinical and clinical development. Combinatorial approaches maximize the therapeutic efficacy and minimize the activation of alternate signaling pathways, which will otherwise contribute to drug resistance. In this regard, an integrated analysis of the mechanisms of action of potential drugs and lead compounds that can target significant nodes of anoikis signaling networks will provide a rational frame-work for further development and clinical use of respective agents, by formulating more effective combinatorial therapies, in patients with distinct drug-sensitivity profiles.
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.