ArticleOncogene2009
Reversibility and recurrence of IGF-IR-induced mammary tumors.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 57 citations in OpenAlex.
- Costs and Causes of Oncology Drug Attrition With the Example of Insulin-Like Growth Factor-1 Receptor Inhibitors.JAMA network open · 2023Article
- Emerging Role of IGF-1 in Prostate Cancer: A Promising Biomarker and Therapeutic Target.Cancers · 2023Review
- Mini Review: Molecular Interpretation of the IGF/IGF-1R Axis in Cancer Treatment and Stem Cells-Based Therapy in Regenerative Medicine.International journal of molecular sciences · 2022Review
- Quercetin blocks the aggressive phenotype of triple-negative breast cancer by inhibiting IGF1/IGF1R-mediated EMT program.Journal of food and drug analysis · 2021Article
- Role of the IGF-1 Axis in Overcoming Resistance in Breast Cancer.Frontiers in cell and developmental biology · 2021Review
- Knockdown of IGF-1R Triggers Viral RNA Sensor MDA5- and RIG-I-Mediated Mitochondrial Apoptosis in Colonic Cancer Cells.Molecular therapy. Nucleic acids · 2019Article
- β-catenin/TCF activity regulates IGF-1R tyrosine kinase inhibitor sensitivity in colon cancer.Oncogene · 2018Article
- LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells.Oncotarget · 2017Article
- Re-expression of miR-200c suppresses proliferation, colony formation and in vivo tumor growth of murine claudin-low mammary tumor cells.Oncotarget · 2017Article
- Loss of insulin-like growth factor II imprinting is a hallmark associated with enhanced chemo/radiotherapy resistance in cancer stem cells.Oncotarget · 2016Article
- Osteopontin regulates proliferation, apoptosis, and migration of murine claudin-low mammary tumor cells.BMC cancer · 2016Article
- Minireview: Were the IGF Signaling Inhibitors All Bad?Molecular endocrinology (Baltimore, Md.) · 2015Review
- The role of the insulin-like growth factor-1 system in breast cancer.Molecular cancer · 2015Review
- High levels of dietary soy decrease mammary tumor latency and increase incidence in MTB-IGFIR transgenic mice.BMC cancer · 2015Article
- Purification of Bone Marrow Clonal Cells from Patients with Myelodysplastic Syndrome via IGF-IR.PloS one · 2015Article
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- Loss of Akt1 or Akt2 delays mammary tumor onset and suppresses tumor growth rate in MTB-IGFIR transgenic mice.BMC cancer · 2013Article
- The expression and significance of insulin-like growth factor-1 receptor and its pathway on breast cancer stem/progenitors.Breast cancer research : BCR · 2013Article
- Targeting insulin and insulin-like growth factor signaling in breast cancer.Journal of mammary gland biology and neoplasia · 2012Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The type-I insulin-like growth factor receptor (IGF-IR) is frequently overexpressed in breast cancer and therapeutic agents targeting IGF-IR are currently in development. The ultimate success of anti-IGF-IR therapies will depend on the extent to which established tumors remain dependent upon IGF-IR signaling for sustained growth. To investigate the potential benefits and pitfalls of targeting IGF-IR, we used a doxycycline inducible mouse model of IGF-IR initiated breast cancer. We found that downregulation of IGF-IR results in tumor-size-dependent regression to an undetectable state. Partially regressed tumors almost always resumed growth in the absence of doxycycline and a proportion of tumors that regressed to an undetectable state ultimately recurred. This re-emergence of tumor growth in the absence of doxycycline was facilitated by IGF-IR-dependent and IGF-IR-independent mechanisms. Tumor escape from IGF-IR dependence was associated with an epithelial to mesenchymal transition and upregulation of transcriptional repressors of E-cadherin. These results suggest that tumors initiated by IGF-IR have the ability to become independent of this initiating oncogene, and IGF-IR independence is associated with characteristics consistent with an epithelial to mesenchymal transition.
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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.