ReviewNature reviews. Clinical oncology2009
Molecular targets for treatment of inflammatory breast cancer.
Review in Nature reviews. Clinical oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 52 citations in OpenAlex.
- The interplay of inflammation and remodeling in the pathogenesis of chronic rhinosinusitis: current understanding and future directions.Frontiers in immunology · 2023Review
- ZKSCAN5 ActivatesFrontiers in oncology · 2022Article
- New Treatment Strategies for the Inflammatory Breast Cancer.Current treatment options in oncology · 2021Review
- Hemoglobin overexpression and splice signature as new features of inflammatory breast cancer?Journal of advanced research · 2021Article
- Microchannel network hydrogel induced ischemic blood perfusion connection.Nature communications · 2020Article
- Article
- Long non-coding RNAs: Functional regulatory players in breast cancer.Non-coding RNA research · 2019Review
- CSF-1/CSF-1R axis is associated with epithelial/mesenchymal hybrid phenotype in epithelial-like inflammatory breast cancer.Scientific reports · 2018Article
- Hyperactivated mTOR and JAK2/STAT3 Pathways: Molecular Drivers and Potential Therapeutic Targets of Inflammatory and Invasive Ductal Breast Cancers After Neoadjuvant Chemotherapy.Clinical breast cancer · 2016Article
- Interferon-induced transmembrane protein 1 (IFITM1) overexpression enhances the aggressive phenotype of SUM149 inflammatory breast cancer cells in a signal transducer and activator of transcription 2 (STAT2)-dependent manner.Breast cancer research : BCR · 2016Article
- Article
- Bevacizumab in HER2-negative inflammatory breast cancer.Oncoscience · 2016Article
- Inflammatory Breast Cancer: A Distinct Clinicopathological Entity Transcending Histological Distinction.PloS one · 2016Article
- Obesity and cancer, a case for insulin signaling.Cell death & disease · 2015Review
- Circulating tumor cells in newly diagnosed inflammatory breast cancer.Breast cancer research : BCR · 2015Article
- Article
- AZD8931, an equipotent, reversible inhibitor of signaling by epidermal growth factor receptor (EGFR), HER2, and HER3: preclinical activity in HER2 non-amplified inflammatory breast cancer models.Journal of experimental & clinical cancer research : CR · 2014Article
- EZH2 knockdown suppresses the growth and invasion of human inflammatory breast cancer cells.Journal of experimental & clinical cancer research : CR · 2013Article
- Inflammatory breast cancer: what we know and what we need to learn.The oncologist · 2012Review
- Interaction of low molecular weight hyaluronan with CD44 and toll-like receptors promotes the actin filament-associated protein 110-actin binding and MyD88-NFκB signaling leading to proinflammatory cytokine/chemokine production and breast tumor invasion.Cytoskeleton (Hoboken, N.J.) · 2011Article
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 3 institutions in 3 countries.
Funding
Abstract
Despite progress in combined-modality treatment with chemotherapy, surgery, and radiation therapy, the long-term outcome for patients with inflammatory breast cancer (IBC) remains poor. Therapies that target vasculolymphatic processes--angiogenesis, lymphangiogenesis, and vasculogenesis--have shown potential in the treatment for IBC, as represented by bevacizumab. Although the therapeutic effect of targeting lymphangiogenesis and vasculogenesis requires further investigation, targeting of angiogenesis has potential, not only through true antiangiogenic effects, but also through antitumor effects in concert with other pathways. Therapies that target cell proliferation pathways are the most promising targeted therapies for IBC. In particular, therapies that target human epidermal growth factor receptor 2 (for example, trastuzumab and lapatinib) have performed well in the clinical setting, leading to improved outcomes for patients with IBC. Metastatic pathways could have a unique, key role in the aggressiveness of the IBC phenotype. Further extensive work on the unique molecular characteristics of IBC is essential to ensure improved outcomes for patients with this disease. In this Review we discuss three pathways--vasculolymphatic, cell proliferation and metastatic--that could represent important targets in the treatment of IBC.
Indexed as
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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.