triple negative breast neoplasms


Summary: Breast neoplasms that do not express ESTROGEN RECEPTORS; PROGESTERONE RECEPTORS; and do not overexpress the NEU RECEPTOR/HER-2 PROTO-ONCOGENE PROTEIN.

Top Publications

  1. McCormack V, Joffe M, van den Berg E, Broeze N, Silva I, Romieu I, et al. Breast cancer receptor status and stage at diagnosis in over 1,200 consecutive public hospital patients in Soweto, South Africa: a case series. Breast Cancer Res. 2013;15:R84 pubmed
    ..These observations provide initial indications that late-stage aggressive breast cancers may not be an inherent feature of the breast cancer burden across Africa. ..
  2. Zeng Z, Chen X, Zhu D, Luo Z, Yang M. Low Expression of Circulating MicroRNA-34c is Associated with Poor Prognosis in Triple-Negative Breast Cancer. Yonsei Med J. 2017;58:697-702 pubmed publisher
    ..021). In conclusion, this study demonstrated reduced miR-34a/c expression is highly associated with tumor progression and indicated worse prognosis. Also, miR-34c was an independent risk factor for OS in TNBC patients. ..
  3. Chen L, Zhang Z, Yi Z, Li J. MicroRNA-211-5p suppresses tumour cell proliferation, invasion, migration and metastasis in triple-negative breast cancer by directly targeting SETBP1. Br J Cancer. 2017;117:78-88 pubmed publisher
    ..These findings collectively demonstrate a tumour suppressor role of miR-211-5p in TNBC progression by targeting SETBP1, suggesting that miR-211-5p could serve as a potential prognostic biomarker and therapeutic target for TNBC. ..
  4. Sobande F, Dusek L, Matějková A, Rozkoš T, Laco J, Ryska A. EGFR in triple negative breast carcinoma: significance of protein expression and high gene copy number. Cesk Patol. 2015;51:80-6 pubmed
    ..Further studies with much larger sample sizes are essential in understanding the role EGFR plays in TNBC biology in order to identify the patients that could benefit from EGFR targeted therapy. ..
  5. Choi Y, Kim S, Youn I, Kang B, Park W, Lee A. Rim sign and histogram analysis of apparent diffusion coefficient values on diffusion-weighted MRI in triple-negative breast cancer: Comparison with ER-positive subtype. PLoS ONE. 2017;12:e0177903 pubmed publisher
    ..7% (7/72) vs. 2.7% (4/149), P = 0.035). Poorer clinicopathologic outcomes were found in TNBC. Whole-lesion ADC histogram analysis revealed ADC kurtosis to be higher in TNBC than ER-positive subtype BC. ..
  6. Gámez Pozo A, Trilla Fuertes L, Prado Vazquez G, Chiva C, Lopez Vacas R, Nanni P, et al. Prediction of adjuvant chemotherapy response in triple negative breast cancer with discovery and targeted proteomics. PLoS ONE. 2017;12:e0178296 pubmed publisher
  7. Saleh S, Bertos N, Gruosso T, Gigoux M, Souleimanova M, Zhao H, et al. Identification of Interacting Stromal Axes in Triple-Negative Breast Cancer. Cancer Res. 2017;77:4673-4683 pubmed publisher
    ..This approach produces a simple ontology that captures TNBC heterogeneity and informs how tumor-associated properties interact to affect prognosis. Cancer Res; 77(17); 4673-83. ©2017 AACR. ..
  8. Li X, Oprea Ilies G, Krishnamurti U. New Developments in Breast Cancer and Their Impact on Daily Practice in Pathology. Arch Pathol Lab Med. 2017;141:490-498 pubmed publisher
    ..In this brief review, we highlight the developments that are most relevant to pathology and are changing or could potentially impact our daily practice. ..
  9. Yu Z, Li A, Wang M. CLImAT-HET: detecting subclonal copy number alterations and loss of heterozygosity in heterogeneous tumor samples from whole-genome sequencing data. BMC Med Genomics. 2017;10:15 pubmed publisher
    ..CLImAT-HET, a novel algorithm is introduced to infer CNA/LOH segments from heterogeneous tumor samples. We demonstrate CLImAT-HET's ability to accurately recover clonal compositions using tumor WGS data without a match normal sample. ..

More Information


  1. Woodward W, Fang P, Arriaga L, Gao H, Cohen E, Reuben J, et al. A Phase 2 Study of Preoperative Capecitabine and Concomitant Radiation in Women With Advanced Breast Cancer. Int J Radiat Oncol Biol Phys. 2017;99:777-783 pubmed publisher
    ..However, patients with TN breast cancer had poor outcomes even when response was achieved. Further study in non-TN patients may be warranted. ..
  2. Masuda N, Lee S, Ohtani S, Im Y, Lee E, Yokota I, et al. Adjuvant Capecitabine for Breast Cancer after Preoperative Chemotherapy. N Engl J Med. 2017;376:2147-2159 pubmed publisher
    ..Funded by the Advanced Clinical Research Organization and the Japan Breast Cancer Research Group; CREATE-X UMIN Clinical Trials Registry number, UMIN000000843 .). ..
  3. Zagouri F, Kotoula V, Kouvatseas G, Sotiropoulou M, Koletsa T, Gavressea T, et al. Protein expression patterns of cell cycle regulators in operable breast cancer. PLoS ONE. 2017;12:e0180489 pubmed publisher
    ..0%, 79.1%, 67.4% and OS 88.4%, 90.4%, 78.9%, respectively. It seems that the expression of cell cycle regulators in the absence of p53 protein is associated with favorable prognosis in operable breast cancer. ..
  4. Kummel S, Paepke S, Huober J, Schem C, Untch M, Blohmer J, et al. Randomised, open-label, phase II study comparing the efficacy and the safety of cabazitaxel versus weekly paclitaxel given as neoadjuvant treatment in patients with operable triple-negative or luminal B/HER2-negative breast cancer (GENEVIEVE). Eur J Cancer. 2017;84:1-8 pubmed publisher NCT01779479. ..
  5. Pitner M, Taliaferro J, Dalby K, Bartholomeusz C. MELK: a potential novel therapeutic target for TNBC and other aggressive malignancies. Expert Opin Ther Targets. 2017;21:849-859 pubmed publisher
    ..Addressing these issues is the first step toward identifying a patient population that could benefit from MELK inhibition in combination with other therapies. ..
  6. Geyer F, Pareja F, Weigelt B, Rakha E, Ellis I, Schnitt S, et al. The Spectrum of Triple-Negative Breast Disease: High- and Low-Grade Lesions. Am J Pathol. 2017;187:2139-2151 pubmed publisher
  7. Tanabe Y, Tsuda H, Yoshida M, Yunokawa M, Yonemori K, Shimizu C, et al. Pathological features of triple-negative breast cancers that showed progressive disease during neoadjuvant chemotherapy. Cancer Sci. 2017;108:1520-1529 pubmed publisher
    ..The combinations of high proliferation, metaplastic features, and immunohistochemical statuses of some EMT and basal-like markers and androgen receptor appeared to be able to characterize the TNBCs that showed cPD after NAC. ..
  8. Li W, Zhang H, Nie M, Tian Y, Chen X, Chen C, et al. Ursolic acid derivative FZU-03,010 inhibits STAT3 and induces cell cycle arrest and apoptosis in renal and breast cancer cells. Acta Biochim Biophys Sin (Shanghai). 2017;49:367-373 pubmed publisher
    ..In conclusion, our results suggest that the UA derivative FZU-03,010 is more potent in inhibiting cancer cell survival, and FZU-03,010 has the potential to be developed as a therapeutic for renal cell cancers and TNBCs. ..
  9. Sledge G, Mamounas E, Hortobagyi G, Burstein H, Goodwin P, Wolff A. Past, present, and future challenges in breast cancer treatment. J Clin Oncol. 2014;32:1979-86 pubmed publisher
  10. Goode G, Gunda V, Chaika N, Purohit V, Yu F, Singh P. MUC1 facilitates metabolomic reprogramming in triple-negative breast cancer. PLoS ONE. 2017;12:e0176820 pubmed publisher
    ..Collectively, these results suggest that MUC1 serves as a metabolic regulator in TNBC, facilitating the metabolic reprogramming of glutamine utilization that influences TNBC tumor growth. ..
  11. Darvishi B, Farahmand L, Eslami S Z, Majidzadeh A K. NF-?B as the main node of resistance to receptor tyrosine kinase inhibitors in triple-negative breast cancer. Tumour Biol. 2017;39:1010428317706919 pubmed publisher
  12. Spurdle A, Couch F, Parsons M, McGuffog L, Barrowdale D, Bolla M, et al. Refined histopathological predictors of BRCA1 and BRCA2 mutation status: a large-scale analysis of breast cancer characteristics from the BCAC, CIMBA, and ENIGMA consortia. Breast Cancer Res. 2014;16:3419 pubmed publisher
    ..The estimates will improve BRCA1 and BRCA2 variant classification and inform patient mutation testing and clinical management. ..
  13. Bajikar S, Wang C, Borten M, Pereira E, Atkins K, Janes K. Tumor-Suppressor Inactivation of GDF11 Occurs by Precursor Sequestration in Triple-Negative Breast Cancer. Dev Cell. 2017;43:418-435.e13 pubmed publisher
    ..Intracellular GDF11 retention adds to the concept of tumor-suppressor inactivation and reveals a cell-biological vulnerability for TNBCs lacking therapeutically actionable mutations. ..
  14. Yao D, Zhou Y, Zhu L, Ouyang L, Zhang J, Jiang Y, et al. Design, synthesis and structure-activity relationship studies of a focused library of pyrimidine moiety with anti-proliferative and anti-metastasis activities in triple negative breast cancer. Eur J Med Chem. 2017;140:155-171 pubmed publisher
    ..In vitro experiments revealed that Y29 attenuated metastasis by PDGFR-? inhibition-induced autophagy and could enhance autophagy-related cell death through AKT-MAPK feedback loop in MDA-MB-231 cells. ..
  15. Tsai Y, Tseng L, Hsu C, Yang M, Chiu J, Shyr Y. Brain-derived neurotrophic factor (BDNF) -TrKB signaling modulates cancer-endothelial cells interaction and affects the outcomes of triple negative breast cancer. PLoS ONE. 2017;12:e0178173 pubmed publisher
    ..Finally, overexpression of TrkB, but not of BDNF, is significantly associated with a poor survival outcome for TNBC patients. ..
  16. Anderson W, Rosenberg P, Katki H. Tracking and evaluating molecular tumor markers with cancer registry data: HER2 and breast cancer. J Natl Cancer Inst. 2014;106: pubmed publisher
  17. Zhang J, Song W, Wang Y, Liu M, Sun M, Liu H. Study on correlation between PKIB and pAkt expression in breast cancer tissues. Eur Rev Med Pharmacol Sci. 2017;21:1264-1269 pubmed
    ..PKIB will be a potential therapeutic target for breast cancer, especially in the diagnosis and treatment of triple negative breast cancer. ..
  18. Ma F, Li H, Li Y, Ding X, Wang H, Fan Y, et al. Aldehyde dehydrogenase 1 (ALDH1) expression is an independent prognostic factor in triple negative breast cancer (TNBC). Medicine (Baltimore). 2017;96:e6561 pubmed publisher
    ..04; P?=?0.04).Immunohistochemistry staining of ALDH1 in tumor cells is an independent prognostic indicator of RFS and OS in TNBC patients. ..
  19. Schouten P, Linn S. Challenges in the Use of DNA Repair Deficiency As a Biomarker in Breast Cancer. J Clin Oncol. 2015;33:1867-9 pubmed publisher
  20. Tung N, Winer E. Tumor-infiltrating lymphocytes and response to platinum in triple-negative breast cancer. J Clin Oncol. 2015;33:969-71 pubmed publisher
  21. Hall S, Toulany J, Bennett L, Martinez Farina C, Robertson A, Jakeman D, et al. Jadomycins Inhibit Type II Topoisomerases and Promote DNA Damage and Apoptosis in Multidrug-Resistant Triple-Negative Breast Cancer Cells. J Pharmacol Exp Ther. 2017;363:196-210 pubmed publisher
  22. Li X, Wei B, Sonmez C, Li Z, Peng L. High tumor budding count is associated with adverse clinicopathologic features and poor prognosis in breast carcinoma. Hum Pathol. 2017;66:222-229 pubmed publisher
    ..05). TB is associated with poor prognosis in ER+/HER2- and TNBC cancer. Evaluation of H-TB may be sufficient in breast carcinoma. ..
  23. Moriya C, Taniguchi H, Nagatoishi S, Igarashi H, Tsumoto K, Imai K. PRDM14 directly interacts with heat shock proteins HSP90α and glucose-regulated protein 78. Cancer Sci. 2018;109:373-383 pubmed publisher
    ..These results suggest that HSP90α and GRP78 interact with PRDM14 and participate in cancer regulation. ..
  24. Zhang W, Grivennikov S. Top Notch cancer stem cells by paracrine NF-?B signaling in breast cancer. Breast Cancer Res. 2013;15:316 pubmed
    ..A recent study, however, suggests that paracrine NF-?B activation promotes the expansion of cancer stem cells through the activation of Notch in basal-type breast cancer cells. ..
  25. Li B, Ní Chonghaile T, Fan Y, Madden S, Klinger R, O Connor A, et al. Therapeutic Rationale to Target Highly Expressed CDK7 Conferring Poor Outcomes in Triple-Negative Breast Cancer. Cancer Res. 2017;77:3834-3845 pubmed publisher
    ..i>Cancer Res; 77(14); 3834-45. ©2017 AACR. ..
  26. Chen Y, Yeh M, Yu M, Wei Y, Chen W, Chen J, et al. Lapatinib-induced NF-kappaB activation sensitizes triple-negative breast cancer cells to proteasome inhibitors. Breast Cancer Res. 2013;15:R108 pubmed publisher
    ..These findings suggest that combination therapy of a proteasome inhibitor with lapatinib may benefit TNBC patients. ..
  27. Loi S. Host antitumor immunity plays a role in the survival of patients with newly diagnosed triple-negative breast cancer. J Clin Oncol. 2014;32:2935-7 pubmed
  28. Sparano J. Defining a role and predicting benefit from platinum-based therapy in breast cancer: an evolving story. J Clin Oncol. 2015;33:1-3 pubmed publisher
  29. Zhong Q, Wang Z, Rong Q, Wang S, Jin J, Wang W, et al. [Prognostic value of sequencing of radiotherapy and chemotherapy following breast-conserving surgery for patients with breast cancer]. Zhonghua Zhong Liu Za Zhi. 2017;39:308-314 pubmed publisher
    ..Further research is warranted to investigate the benefit of different molecular types in different sequencing of radiotherapy and chemotherapy after breast-conserving surgery. ..
  30. Min L, Zhang C, Qu L, Huang J, Jiang L, Liu J, et al. Gene regulatory pattern analysis reveals essential role of core transcriptional factors' activation in triple-negative breast cancer. Oncotarget. 2017;8:21938-21953 pubmed publisher
    ..We identified a core co-regulatory module specifically existing in TNBC, which enabled subtype re-classification and provided a biologically feasible view of breast cancer. ..
  31. Martignetti L, Tesson B, Almeida A, Zinovyev A, Tucker G, Dubois T, et al. Detection of miRNA regulatory effect on triple negative breast cancer transcriptome. BMC Genomics. 2015;16:S4 pubmed publisher
    ..The R script implementing our method together with the datasets used in the study can be downloaded here ( ..
  32. Kashiwagi S, Asano Y, Goto W, Takada K, Takahashi K, Noda S, et al. Use of Tumor-infiltrating lymphocytes (TILs) to predict the treatment response to eribulin chemotherapy in breast cancer. PLoS ONE. 2017;12:e0170634 pubmed publisher
    ..031, HR = 0.063). The results of this study suggest that TILs may be useful as a predictive marker of the therapeutic effect of eribulin chemotherapy in TNBC. ..
  33. Hedrick E, Safe S. Transforming Growth Factor β/NR4A1-Inducible Breast Cancer Cell Migration and Epithelial-to-Mesenchymal Transition Is p38α (Mitogen-Activated Protein Kinase 14) Dependent. Mol Cell Biol. 2017;37: pubmed publisher
  34. Valencia O, Samuel S, Viscusi R, Riall T, Neumayer L, Aziz H. The Role of Genetic Testing in Patients With Breast Cancer: A Review. JAMA Surg. 2017;152:589-594 pubmed publisher
    ..Cost is an especially important part of the genetic testing process and point of discussion with patients. ..
  35. Song W, Hwang Y, Youngblood V, Cook R, Balko J, Chen J, et al. Targeting EphA2 impairs cell cycle progression and growth of basal-like/triple-negative breast cancers. Oncogene. 2017;36:5620-5630 pubmed publisher
    ..A small molecule kinase inhibitor of EphA2 effectively suppressed tumor cell growth in vivo, including TNBC patient-derived xenografts. Thus, our data identify EphA2 as a novel molecular target for TNBC. ..
  36. Zhou W, Song F, Wu Q, Liu R, Wang L, Liu C, et al. miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5. PLoS ONE. 2017;12:e0176395 pubmed publisher
    ..MiR-217 suppresses TNBC, at least partially, through down-regulating the KLF5 expression. These results suggest that the miR-217-KLF5 axis might serve as a potential target for treatment of TNBC. ..
  37. Dihge L, Bendahl P, Ryden L. Nomograms for preoperative prediction of axillary nodal status in breast cancer. Br J Surg. 2017;104:1494-1505 pubmed publisher
  38. Lim Y, Lee S, Choi N, Kwon J, Eom K, Kang E, et al. Failure patterns according to molecular subtype in patients with invasive breast cancer following postoperative adjuvant radiotherapy: long-term outcomes in contemporary clinical practice. Breast Cancer Res Treat. 2017;163:555-563 pubmed publisher
    ..The preferential and long-term risk of brain metastasis in the HER2 subtype underlines the importance of alternative anti-HER2 therapies. ..
  39. Pomp V, Leo C, Mauracher A, Korol D, Guo W, Varga Z. Differential expression of epithelial–mesenchymal transition and stem cell markers in intrinsic subtypes of breast cancer. Breast Cancer Res Treat. 2015;154:45-55 pubmed
    ..This information is important in understanding the biology of triple negative breast cancer, also in terms of future studies dealing with targeted therapies based on the alterations of EMT and stem cell markers. ..
  40. Egger S, Willson M, Morgan J, Walker H, Carrick S, Ghersi D, et al. Platinum-containing regimens for metastatic breast cancer. Cochrane Database Syst Rev. 2017;6:CD003374 pubmed publisher
    ..Further randomised trials of platinum-based regimens in this subpopulation of women with metastatic breast cancer are required. ..
  41. Shuptrine C, Ajina R, Fertig E, Jablonski S, Kim Lyerly H, Hartman Z, et al. An unbiased in vivo functional genomics screening approach in mice identifies novel tumor cell-based regulators of immune rejection. Cancer Immunol Immunother. 2017;66:1529-1544 pubmed publisher
    ..Thus, this innovative approach has utility in identifying unknown tumor-specific regulators of immune recognition in multiple settings to reveal novel targets for future immunotherapies. ..
  42. de Nonneville A, Goncalves A, Zemmour C, Cohen M, Classe J, Reyal F, et al. Adjuvant chemotherapy in pT1ab node-negative triple-negative breast carcinomas: Results of a national multi-institutional retrospective study. Eur J Cancer. 2017;84:34-43 pubmed publisher
    ..Although current consensus guidelines recommend consideration of CT in all TNBC larger than 5 mm, clinicians should carefully discuss benefit/risk ratio with patients, given the unproven benefits. ..
  43. Chen T, Liu C, Lu H, Yin M, Shao C, Hu X, et al. The expression of APE1 in triple-negative breast cancer and its effect on drug sensitivity of olaparib. Tumour Biol. 2017;39:1010428317713390 pubmed publisher
    ..These results suggested that the expression of APE1 was an important basis for the maintenance of poly (ADP-ribose) polymerase 1, and the deletion of APE1 may be related to the resistance of olaparib...
  44. Hanigan T, Aboukhatwa S, Taha T, Frasor J, Petukhov P. Divergent JNK Phosphorylation of HDAC3 in Triple-Negative Breast Cancer Cells Determines HDAC Inhibitor Binding and Selectivity. Cell Chem Biol. 2017;24:1356-1367.e8 pubmed publisher
  45. Qin H, Liu X, Li F, Miao L, Li T, Xu B, et al. PAD1 promotes epithelial-mesenchymal transition and metastasis in triple-negative breast cancer cells by regulating MEK1-ERK1/2-MMP2 signaling. Cancer Lett. 2017;409:30-41 pubmed publisher
    ..These results also raise the possibility that PAD1 may function as an important new biomarker for TNBC tumors and suggest that PAD1-specific inhibitors could potentially be utilized to treat metastatic breast cancer. ..
  46. Yamada M, Kubo M, Kai M, Yamamoto H, Nakamura M. [Efficacy of GC Therapy for the Patient of iTNBC with Resistance to TAC Therapy]. Gan To Kagaku Ryoho. 2017;44:703-705 pubmed
    ..Thus, a combination regimen of gemcitabine and carboplatin(GC)was administered. The treatment was successful, and the patient underwent a curative operation after 6 courses of the GC therapy. ..
  47. Du Y, Song L, Zhang L, Ling H, Zhang Y, Chen H, et al. The discovery of novel, potent ERR-alpha inverse agonists for the treatment of triple negative breast cancer. Eur J Med Chem. 2017;136:457-467 pubmed publisher
    ..All these results suggest that compound 11 represents a novel potent ERR? inverse agonist and is promising in the discovery of antitumor compounds for the treatment of triple negative breast cancer. ..
  48. Masuda H, Baggerly K, Wang Y, Iwamoto T, Brewer T, Pusztai L, et al. Comparison of molecular subtype distribution in triple-negative inflammatory and non-inflammatory breast cancers. Breast Cancer Res. 2013;15:R112 pubmed publisher
    ..Studies are needed to identify the subtle molecular or microenvironmental differences that contribute to the differing clinical behaviors between TN-IBC and TN-non-IBC. ..
  49. Sinha G. Downfall of iniparib: a PARP inhibitor that doesn't inhibit PARP after all. J Natl Cancer Inst. 2014;106:djt447 pubmed publisher
  50. Chang C, Wang Y, Li R, Rossi D, Liu D, Rossi E, et al. Combination Therapy with Bispecific Antibodies and PD-1 Blockade Enhances the Antitumor Potency of T Cells. Cancer Res. 2017;77:5384-5394 pubmed publisher
    ..They also support the use of 3D spheroids as a predictive alternative to in vivo models for evaluating T-cell functions. Cancer Res; 77(19); 5384-94. ©2017 AACR. ..
  51. Park I, Hwang S, Song I, Heo S, Kim Y, Bang W, et al. Expression of the MHC class II in triple-negative breast cancer is associated with tumor-infiltrating lymphocytes and interferon signaling. PLoS ONE. 2017;12:e0182786 pubmed publisher
    ..Further studies are warranted to improve our understanding regarding TIL influx, as well as patients' responses to immunotherapy. ..
  52. Yamashita N, Kondo M, Zhao S, Li W, Koike K, Nemoto K, et al. Picrasidine G decreases viability of MDA-MB 468 EGFR-overexpressing triple-negative breast cancer cells through inhibition of EGFR/STAT3 signaling pathway. Bioorg Med Chem Lett. 2017;27:2608-2612 pubmed publisher
    ..These results suggest that PG may contribute to the development of targeted therapy of patients with EGFR-overexpressing TNBC. ..
  53. Marotti J, de Abreu F, Wells W, Tsongalis G. Triple-Negative Breast Cancer: Next-Generation Sequencing for Target Identification. Am J Pathol. 2017;187:2133-2138 pubmed publisher
    ..Herein, we review the genomic findings of TNBC and discuss current efforts in precision medicine as they relate to TNBC. ..