Efficacy of neoadjuvant Cisplatin in triple-negative breast cancer.

By D. Silver, A. Richardson, A. Eklund, Z. Wang, Zoltan Szallasi, Qiyuan Li, N. Juul, C. Leong, Diana Calogrias, Ayodele Buraimoh and 12 more. Journal of Clinical Oncology, 2010

947 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics

View Paper: https://www.semanticscholar.org/paper/1d99c86bb948c23eeb2d639a010fc77f4d7f0493

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. R. Huang
2. Tetsuo Noda
3. J. P. Thiery
4. J. Bartek
5. A. Richardson
6. Yoshio Miki
7. T. Tan
8. X. Chen

In Genetics

1. William T. Barry
2. J. P. Thiery
3. X. Chen
4. Paul Geeleher
5. Nancy J. Cox
6. S. West
7. L. Gianni
8. R. Huang

Citations in the corpus

• 53BP1 loss rescues BRCA1 deficiency and is associated with triple-negative and BRCA-mutated breast cancers (2010, background): “Consistent with this, BRCA1-deficient tumors show excellent responses to therapies exploiting a HR defect, such as platinum drug”
• Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies. (2011, background): “Because of GE similarities between basal-like TNBC and BRCA1-mutation carriers, PARP inhibitors are currently being tested in clinical trials for TNBC (46).”
• Strategies for subtypes—dealing with the diversity of breast cancer: highlights of the St Gallen International Expert Consensus on the Primary Therapy of Early Breast Cancer 2011 (2011, background): “Neoadjuvant studies including cisplatin have produced pCR rates between 22% and 40% among unselected triple-negative cases [66, 67], while 10 of 12 cases with BRCA1 mutations achieved pCR with single agent cisplatin [68].”
• NEW STRATEGIES FOR TRIPLE NEGATIVE BREAST CANCER – DECIPHERING THE HETEROGENEITY (2014, background): “The observed pCR was 22%, 50% of patients had a partial response, and 14%had a complete response (14).”
• Clinical drug response can be predicted using baseline gene expression levels and in vitro drug sensitivity in cell lines (2014, methodology): “tients, as cisplatin is not routinely used to treat breast cancer [20].”
• DNA interstrand crosslink repair and cancer (2011, positive): “The role of HR in ICL repair Extremely positive results have been obtained with the ICL-inducing agent carboplatin in early phase clinical trials for the treatment of triple-negative breast cancers — those that do not express HER2 (also known as ERBB2) or oestrogen and progesterone recepto”
• Triple-negative breast cancer: disease entity or title of convenience? (2010, background): “One small prospective study showed a 64% (18 out of 28 patients) overall response rate and a modest 21% (6 of 28) pCR rate in TNBC patients treated with neoadjuvant cisplatin monotherapy”
• Refinement of Triple-Negative Breast Cancer Molecular Subtypes: Implications for Neoadjuvant Chemotherapy Selection (2016, background): “Combined analysis of TNBC patients demonstrated that TNBC subtypes significantly differ in response to similar neoadjuvant chemotherapy with 41% of BL1 patients achieving a pathological complete response compared to 18% for BL2 and 29% for LAR with 95% confidence intervals (CIs; [33, 51], [9, 28], [”
• Epithelial-mesenchymal transition spectrum quantification and its efficacy in deciphering survival and drug responses of cancer patients (2014, positive): “Overall, the EMT status is unlikely to be the sole prognostic factor for survival where the composition of histotype or molecular subtype may play a role; this suggests the requirement for stratification of cancers in addition to deciphering the EMT status.”
• Homologous Recombination Deficiency (HRD) Score Predicts Response to Platinum-Containing Neoadjuvant Chemotherapy in Patients with Triple-Negative Breast Cancer (2016, methodology): “Confirming this concept, two neoadjuvant clinical trials have demonstrated that a subset of sporadic, non-BRCA1/2– mutated TNBC are sensitive to single-agent platinum chemotherapy (12, 13).”
• Ploidy and large-scale genomic instability consistently identify basal-like breast carcinomas with BRCA1/2 inactivation. (2012, neutral): “status (12) strongly support the need to more accurately stratify sporadic BLC/TNBC according to actual BRCAness, which could easily be obtained using our genomic-based”