Trial reportThe oncologist2010
Cyclophosphamide dose intensification may circumvent anthracycline resistance of p53 mutant breast cancers.
Trial report in The oncologist, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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
24 citing papers in PubMed, 53 citations in OpenAlex.
- TP53 status for prediction of sensitivity to taxane versus non-taxane neoadjuvant chemotherapy in breast cancer (EORTC 10994/BIG 1-00): a randomised phase 3 trial.The Lancet. Oncology · 2011Trial
- Determinants of response to neoadjuvant chemotherapy in breast cancer: Integrated roles of immune pathways, DNA damage response, and cell cycle regulators.Molecular biology reports · 2026Review
- Predictive Factors of Response to Neoadjuvant Chemotherapy (NACT) and Immune Checkpoint Inhibitors in Early-Stage Triple-Negative Breast Cancer Patients (TNBC).Current oncology (Toronto, Ont.) · 2025Review
- Comprehensive Analysis of Transcriptomics and Genetic Alterations Identifies Potential Mechanisms Underlying Anthracycline Therapy Resistance in Breast Cancer.Biomolecules · 2022Article
- Impact of TP53 mutations in Triple Negative Breast Cancer.NPJ precision oncology · 2022Article
- Clonal evolution in primary breast cancers under sequential epirubicin and docetaxel monotherapy.Genome medicine · 2022Article
- Article
- TP53 Mutations and Outcomes in Breast Cancer: Reading beyond the Headlines.Trends in cancer · 2020Review
- Article
- Lymphovascular invasion as a negative prognostic factor for triple-negative breast cancer after surgery.Radiation oncology journal · 2017Article
- Constitutively activated ERK sensitizes cancer cells to doxorubicin: Involvement of p53-EGFR-ERK pathway.Journal of biosciences · 2017Article
- TP53 Mutations in Breast and Ovarian Cancer.Cold Spring Harbor perspectives in medicine · 2017Review
- Role of TP53 mutations in triple negative and HER2-positive breast cancer treated with neoadjuvant anthracycline/taxane-based chemotherapy.Oncotarget · 2016Article
- p53 as an Effector or Inhibitor of Therapy Response.Cold Spring Harbor perspectives in medicine · 2015Review
- Targeting MCM2 function as a novel strategy for the treatment of highly malignant breast tumors.Oncotarget · 2015Article
- Concomitant inactivation of the p53- and pRB- functional pathways predicts resistance to DNA damaging drugs in breast cancer in vivo.Molecular oncology · 2015Article
- TP53 status predicts long-term survival in locally advanced breast cancer after primary chemotherapy.Acta oncologica (Stockholm, Sweden) · 2014Article
- Genomic patterns resembling BRCA1- and BRCA2-mutated breast cancers predict benefit of intensified carboplatin-based chemotherapy.Breast cancer research : BCR · 2014Article
- Long-term survival of advanced triple-negative breast cancers with a dose-intense cyclophosphamide/anthracycline neoadjuvant regimen.British journal of cancer · 2014Article
- Chemosensitivity and p53; new tricks by an old dog.Breast cancer research : BCR · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The predictive value of p53 for the efficacy of front-line anthracycline-based chemotherapy regimens has been a matter of significant controversy. Anthracyclines are usually combined with widely different doses of alkylating agents, which may significantly modulate tumor response to these combinations. We analyzed three series of de novo stage II-III breast cancer patients treated front line with anthracycline-based regimens of various cyclophosphamide dose intensities: 65 patients with estrogen receptor (ER)(-) tumors treated with anthracyclines alone (Institut Jules Bordet, Brussels), 51 unselected breast cancer patients treated with intermediate doses of cyclophosphamide (MD Anderson Cancer Center, Houston, TX), and 128 others treated with a dose-dense anthracycline-cyclophosphamide combination (St. Louis, Paris). After chemotherapy and surgery, pathologic complete response (pCR) was evaluated. p53 status was determined by a yeast functional assay on the pretreatment tumor sample. In a multivariate analysis of the pooled results, a lack of ER expression and high-dose cyclophosphamide administration were associated with a higher likelihood of pCR. A sharp statistical interaction was detected between p53 status and cyclophosphamide dose intensity. Indeed, when restricting our analysis to patients with ER(-) tumors, we confirmed that a mutant p53 status was associated with anthracycline resistance, but found that p53 inactivation was required for response to the dose-intense alkylating regimen. The latter allowed very high levels of pCR in triple-negative tumors. Thus, our data strongly suggest that cyclophosphamide dose intensification in ER(-) p53-mutated breast cancer patients could significantly improve their response.
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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.