Journal articles: 'Triple negative breast cancers'

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Ray, Mandira, and Blase N. Polite. "Triple-Negative Breast Cancers." Cancer Journal 16, no. 1 (January 2010): 17–22. http://dx.doi.org/10.1097/ppo.0b013e3181d3eef5.

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Gonzalez, Lorena, Joanne Mortimer, and Laura Kruper. "De-escalation of Systemic Therapy for Early-Stage, Node-Negative Her2+ and Triple-Negative Breast Cancer." Current Breast Cancer Reports 13, no. 3 (June 14, 2021): 151–56. http://dx.doi.org/10.1007/s12609-021-00421-3.

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Abstract Purpose of Review This review summarizes the most recent data on the management of small, node-negative Her2+ and triple-negative breast cancer. Recent Findings Both Her2+ and triple-negative breast cancers are characterized by high rates of recurrence and worse survival outcomes compared to hormone-positive cancers. De-escalation of systemic therapy in early-stage breast cancer is a recent national trend in clinical research. Recent prospective trials support the scaling back of cytotoxic agents and maximization of targeted therapy regimens. Similarly, large retrospective studies on small, node-negative triple-negative breast cancer report the omission of chemotherapy in women with T1a,N0 triple-negative cancers with favorable short term outcomes. Summary De-escalation of systemic therapy for Her2+ breast cancer is effective in the management of early-stage, node-negative disease. Future prospective studies on the omission of systemic therapy for triple-negative breast cancer are required to safely adopt into consensus guidelines.

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Anderson, Kristin, Patricia Thompson, Betsy Wertheim, Lorena Martin, Ian K. Komenaka, Melissa Bondy, Adrian Daneri-Navarro, et al. "Family history and breast cancer subtype among women of Mexican descent." Journal of Clinical Oncology 32, no. 26_suppl (September 10, 2014): 41. http://dx.doi.org/10.1200/jco.2014.32.26_suppl.41.

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41 Background: A family history of breast cancer in a first-degree relative is associated with a 2-fold increase in breast cancer risk; however, breast cancer is a heterogeneous disease and there may be differences in risk profiles driven by tumor subtype or by racial/ethnic group. Methods: We assessed prevalence of familial breast cancer and its association with tumor subtype among 914 women with breast cancer of Mexican descent enrolled in the Ella Study, a case-only, binational (U.S.-Mexico) breast cancer study. Logistic regression was conducted to compare odds of triple negative breast cancers to non triple-negative breast cancers according to family history. Results: The prevalence of family history of breast cancer in a first- or second-degree relative was 24.1%, with 13.1% having an affected first-degree relative. Among participants who were diagnosed at age < 50, prevalence of family history of breast cancer in a first- or second-degree relative was 27.4%. After adjustment for age and country of residence, women with a first-degree relative with breast cancer were significantly more likely to be diagnosed with triple-negative breast cancers compared to non triple-negative breast cancers (OR = 1.98; 95% CI, 1.26-3.11). Similar results were seen for odds of triple-negative breast cancers compared to non-triple negative breast cancers for women with affected first- or second-degree relatives (OR=2.04; 95% CI, 1.40–2.98). The odds of triple-negative breast cancer compared to non-triple negative breast cancer was 1.93 (95% CI, 1.26–2.97) for women with first-degree relatives affected with breast or ovarian cancer. Conclusions: Findings suggest that familial cancers are most likely to be associated with triple negative subtype, supporting etiologic heterogeneity by tumor subtype in this population of Hispanic women. This association may be related to the prevalence of BRCA1 founder mutations in this population, which are strongly associated with triple-negative breast cancers. Identification of such differences in risk factors can help personalize screening and prevention approaches.

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STADALNYKAITĖ, Sigutė, and Rūta BRIEDIENĖ. "Radiological diagnostics of triple negative breast cancer: a review." Acta medica Lituanica 18, no. 2 (April 1, 2011): 98–106. http://dx.doi.org/10.6001/actamedica.v18i2.1822.

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Background. Triple negative breast cancer has a poor prognosis. Therefore, it is vital to detect this subtype of breast cancer in its early stage. The imaging features of this clinically important subtype of breast cancer are not well known. There have been no published reports about radiological diagnostics of triple negative breast tumour in Lithuania. The purpose of this study was to review the imaging characteristics of triple receptor negative cancers in mammography, ultrasonography and magnetic resonance imaging (MRI). Materials and methods. The published data for the period 2006–2011 concerning the imaging of triple negative breast cancer were analyzed. There were ten retrospective, ten prospective studies and five reviews. Five studies were on mammography imaging, three on both mammography and ultrasonography imaging, and five studies dealt with MR imaging data. Two studies analysed all three diagnostic methods. Results. In mammography, triple negative breast (TRN) cancers often present as a mass and are most frequently round, oval or lobular in shape, less frequently being irregular. TRN tumours aren’t associated with calcifications. Moreover, architectural distortion is not a characteristic feature of triple negative breast cancer. In ultrasonography, TRN cancer appears as a parallel. TRN breast tumours mostly are irregular in shape and have a circumscribed margin. Attenuating posterior echoes and hypervascularity are not their characteristic features. In MR imaging, TRN breast cancer tends to have a lobulated, round or oval mass shape. Rim enhancement is identified in most of TRN tumours. Initially, rapid enhancement with a washout pattern (a sign of malignancy) does not usually apply to triple-negative breast cancers. Conclusions. TRN breast cancer is difficult to diagnose, because usually it has no specific imaging signs typical of breast cancer. In mammography, TRN cancers aren’t associated with microcalcifications. In ultrasonography, attenuating posterior echoes and hypervascularity are not characteristic features of TRN tumours. In MRI, initially rapid enhancement with a washout pattern does not usually apply to triple-negative breast cancers. Keywords: triple negative breast cancer, mammography, ultrasonography, magnetic resonance imaging

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Lu, Boya, Elango Natarajan, Hanumantha Rao Balaji Raghavendran, and Uma Devi Markandan. "Molecular Classification, Treatment, and Genetic Biomarkers in Triple-Negative Breast Cancer: A Review." Technology in Cancer Research & Treatment 22 (January 2023): 153303382211452. http://dx.doi.org/10.1177/15330338221145246.

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Breast cancer is the most common malignancy and the second most common cause of cancer-related mortality in women. Triple-negative breast cancers do not express estrogen receptors, progesterone receptors, or human epidermal growth factor receptor 2 and have a higher recurrence rate, greater metastatic potential, and lower overall survival rate than those of other breast cancers. Treatment of triple-negative breast cancer is challenging; molecular-targeted therapies are largely ineffective and there is no standard treatment. In this review, we evaluate current attempts to classify triple-negative breast cancers based on their molecular features. We also describe promising treatment methods with different advantages and discuss genetic biomarkers and other prediction tools. Accurate molecular classification of triple-negative breast cancers is critical for patient risk categorization, treatment decisions, and surveillance. This review offers new ideas for more effective treatment of triple-negative breast cancer and identifies novel targets for drug development.

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Bhatti, Abu Bakar Hafeez, Amina Iqbal Khan, Neelam Siddiqui, Narjis Muzaffar, and Mazhar Ali Shah. "Outcomes of triple-negative versus non-triple-negative breast cancers managed with breast-conservative therapy." Journal of Clinical Oncology 31, no. 26_suppl (September 10, 2013): 70. http://dx.doi.org/10.1200/jco.2013.31.26_suppl.70.

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70 Background: Triple-negative breast cancer represents a subgroup of breast cancer associated with aggressive behavior and high risk of local and regional failure. Aggressive surgical intervention is considered optimal for this cancer which has made role of Breast conservative therapy (BCT) debatable in these patients. The objective of this study was to compare outcome of BCT for triple negative versus non-triple–negative breast cancers. Methods: Data of patients who underwent breast conservative therapy between 1997-2009 at Shaukat Khanum Cancer Hospital and had complete receptor status information were extracted. Patients were divided into triple-negative breast cancer (TNBC) and non-TNBC. Patient characteristics, medical treatment modalities and adverse events between two groups were compared. Five year locoregional recurrence free, disease free and overall survival was calculated. Univariate and multivariate analysis was done to identify independent predictors of outcome. Results: A total of 194 patients with TNBC and 443 with non-TNBC were compared. Significant differences was present for age at presentation (p<0.0001), family history (p=0.005), grade (p<0.0001) and use of hormonal therapy (p<0.0001). The actual number of locoregional failures, distant failures, and mortalities were not significantly different. No significant difference was present in 5-year locoregional recurrence free (96% vs. 92%, p=0.3), disease free (75% vs. 74%, p=0.7) and overall survival (78% vs. 83%, p=0.2). Tumor size, nodal involvement and hormonal treatment were independent predictors of survival on multivariate analysis. Conclusions: Breast-conservative therapy has comparable outcomes for triple-negative and non-triple–negative breast cancers.

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Kuo, Wen-Hung, Yao-Yin Chang, Ming-Feng Hou, Eric Y. Chuang, and King-Jen Chang. "Molecular characteristics and metastasis predictor genes of triple-negative breast cancer." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): 1043. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.1043.

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1043 Background: Triple-negative breast cancer(TNBC) is a subtype of breast cancer with aggressive tumor behavior and distinct disease etiology. Due to the lack of an effective targeted medicine, treatment options for triple-negative breast cancer are few and recurrence rates are high. Although various multi-gene prognostic markers have been proposed for the prediction of breast cancer outcome, most of them were proven clinically useful only for estrogen receptor-positive breast cancers. Reliable identification of triple-negative patients with a favorable prognosis is not yet possible. Methods: Clinicopathological information and microarray data from 157 invasive breast carcinomas were collected at National Taiwan University Hospital from 1995 to 2008. Gene expression data of 51 triple-negative and 106 luminal breast cancers were generated with oligonucleotide microarrays. A prognostic 45-gene signature for triple-negative breast cancer was identified using Student’s t test and receiver operating characteristic analysis. Results: Hierarchical clustering analysis revealed that the majority (94%) of triple-negative breast cancers were tightly clustered together carrying strong basal-like characteristics. A novel 45-gene signature giving 98% predictive accuracy in distant metastasis recurrence was identified in our triple-negative patient cohort. External validation of the prognostic signature in an independent microarray dataset of 59 early-stage triple-negative patients also obtained statistical significance (hazard ratio 2.29, 95% CI 1.04-5.06, Cox P = 0.04), outperforming five other published breast cancer prognostic signatures. The prognostic signature was statistically predictive with the node-negative triple-negative patients in the validation cohort. Conclusions: The 45-gene prognostic signature identified in this study revealed that TGF-β signaling in immune/inflammatory regulation may be critically involved in distant metastatic invasion of TNBC. The 45-gene signature, if further validated, may be a clinically useful tool in risk assessment of metastasis recurrence for early-stage triple-negative patients.

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Chirappapha, Prakasit, Thongchai Sukarayothin, Yodying Wasuthit, Ronnarat Suvikapalornkul, Panuwat Lertsithichai, and Youwanush Kongdan. "Disease-free Probability and Triple-Negative Breast Cancer." Ramathibodi Medical Journal 35, no. 1 (March 30, 2012): 5–13. http://dx.doi.org/10.33165/rmj.2012.35.1.117663.

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Objective: To compare the probabilities of local recurrence and distant metastasis between women with triple-negative and non- triple negative breast cancers. Methods: Medical and pathological records of breast cancer patients treated between the years 2002 and 2006 were reviewed. Results: There were 256 patients with complete data on estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2) expression determinations. There were 54 patients (21%) with triple-negative (ER-, PR-, HER2 -) cancers. Triple-negative patients were more likely to have larger tumors with higher histologic grade. The median fallow-up time was 4 years. The probabilities of local and distant recurrence were similar between the two groups of patients. Only two factors were independently and significantly associated with overall recurrence: tumor stage and tumor size. Conclusion: Triple-negative breast cancer did not have a higher risk for both local recurrence and distant metastasis when compared with non-triple negative cancer.

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Zoghi, Behyar, and Peter Ravdin. "Improving the efficacy of chemotherapy drugs for the treatment of triple-negative breast cancers." Journal of Clinical Oncology 30, no. 27_suppl (September 20, 2012): 107. http://dx.doi.org/10.1200/jco.2012.30.27_suppl.107.

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107 Background: Approximately 15-20% of all breast cancers account for triple-negative breast cancers that exhibit aggressive, distinct metastatic pattern and poor prognosis. More than 50% of patients with triple negative breast cancers develop chemoresistance and do not respond to chemotherapeutic drugs, leading to early relapse and shorter survival. Understanding the mechanisms underlying such resistance is therefore crucial for the development of new, efficacious cancer drugs. Methods: Through high-throughput miRNA inhibitor library screens, we have identified miRNA inhibitors that sensitize resistant triple negative breast cancer cells to paclitaxel, a drug commonly used to treat triple negative breast cancers. Results: Through high-throughput miRNA inhibitor library screens, we have identified miRNA inhibitors that sensitize resistant triple negative breast cancer cells to paclitaxel, a drug commonly used to treat triple negative breast cancers. Since miRNAs are endogenously expressed and can be easily manipulated using synthetic oligoribonucleotides, we believe that they represent more attractive targets than the single gene or gene product that is the target of conventional cancer treatments that are typically prone to drug resistance. Supporting this, we have recently demonstrated that miRNAs can be systemically delivered to treat breast cancer lung metastasis without any hepatotoxicity. In addition to being a potent therapeutic regimen, our preliminary analyses reveal that miRNAs can be bonafide early prognostic markers to monitor treatment response to specific drugs in triple-negative breast cancers. Conclusions: Taken together, these findings suggest that miRNA can serve as potent therapeutic adjuvants and although the data content of miRNA profiles is far less than that of gene expression profiles, by virtue of their ability to modulate entire spectrum of genes and pathways miRNAs have potential to be better classifiers for the prognosis and response to treatment of cancers. We believe that the identification of miRNAs that mediate chemoresistance could lead to more efficient treatment selection at the patient level and an improved response rates at the population level.

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Andre, F., P. Dessen, B. Job, S. Delaloge, L. Pusztai, and V. Lazar. "Functional pathways analyses to identify candidate therapeutic targets in triple-negative breast cancer." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 569. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.569.

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569 Background: In the present study, we have analyzed dysregulated pathways in triple-negative breast cancers. Methods: Two datasets of cDNA arrays were used to identify differentially expressed genes between triple negative breast cancer and either normal/benign breast tissue or other molecular classes. The first dataset (I) was included 165 samples. The second data set (II) included 148 samples. Pathway analyses (gene set) were done based using BRB array tool and a software developed in house (SBIME). Results: Fifteen and 27 patients presented a triple negative breast cancer in the dataset I and II respectively. Ten and eleven pathways were significantly different between triple negative and other molecular classes in dataset I and II respectively (LS permutation p value<0.01). Six pathways were common between the two datasets (p53, cyclin E, E2F1, p27 phosphorylation, Ran, cycle regulation). We then focused the analyses on differential pathways between triple negative and normal/benign tissue. In the dataset I, targetable pathways were identified (hotelling t-test <10–7) including VEGF signalling pathway, proteasome, Hedgehog and Notch pathway. In addition, an enrichment of histone overexpression was observed in triple negative breast cancer (3% of overexpressed genes, ratio expression >2). In the dataset II, histone (p = 2x10–6), chromosome organization (p = 2x10–4) gene sets were enriched in triple negative breast cancer. We then assessed whether such pathway dysregulations could be linked to genomic aberration enriched in triple negative breast cancer. Using high resolution CGH arrays (Agilent, 4*44K) on 53 triple negative breast cancers, we detected that 31% of triple negative tumors presented a gene gain in 6p21 and 6p22, two regions that contain VEGFA gene (6p21) and a cluster of histones (6p22). Conclusions: Triple negative breast cancers present dysregulation of targetable pathways, including VEGF signaling and chromosome organization. Dysregulation of these two pathways could be related to gene gains in 6p21–22 regions observed in 30% of triple negative breast cancer. No significant financial relationships to disclose.

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Sener Dede, D., S. Aksoy, N. Bulut, O. Dizdar, Z. Arik, I. Gullu, Y. Ozisik, and K. Altundag. "Comparison of serum levels of CEA and CA 15–3 in triple-negative breast cancer at the time of metastases and serum levels at the time of first diagnosis." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e12017-e12017. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e12017.

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e12017 Background: Cancer antigen 15–3 (CA 15–3) and carcinoembryonic antigen (CEA), are often used in follow up care of breast cancer and provide important clues to the clinicians for disease progression in metastatic and recurrent breast cancer. Triple-negative breast cancers are frequently defined as a single group identifiable using routine clinical tests. They are negative for estrogen receptor (ER), progesterone receptor (PR), and the human epidermal growth factor receptor 2 (HER-2), the so-called triple-negative breast cancers. In this study we compared the tumor markers of triple negative breast cancer and non-triple negative patients. Methods: We retrospectively analyzed serum CEA and CA 15–3 levels of both triple negative and non-triple negative breast cancer patients at the time of first diagnosis and when they developed metastatic disease. Results: 544 consecutive nonmetastatic breast cancer patients presenting at Hacettepe University Institute of Oncology, Ankara, Turkey, with a median age of 49 were evaluated. 15.1% of the patients were triple negative breast cancer. At the time of diagnosis triple negative group had lower serum CEA (2.5 ± 5.9 vs 4.0 ±16.4 p = 0.35) and CA 15–3 (23.7 ± 14.6 vs 37.1 ± 117; p = 0.021) levels compared to non-triple negative group. In patients who developed metastasis during follow up; the CEA (3.2 ± 3.8 vs 29.6 ± 106.4 p = 0.022) and CA15–3 (46.9 ± 46.3 vs 203.2 ± 534 p = 0.008) levels were also significantly lower in triple negative breast cancer group compared to non-triple negative group.In non-triple negative breast cancer patients who developed metastasis, mean serum levels of CEA and CA15–3 significantly increased compared to baseline, whereas in triple negative group who developed metastasis CEA and CA 15–3 levels did not differ significantly. Conclusions: While being a good laboratory parameter in the follow-up of patients with breast cancer metastases, tumor markers may not show the increased tumor burden in the triple-negative breast cancer patients. No significant financial relationships to disclose.

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Minami, Christina A., Debra U. Chung, and Helena R. Chang. "Management Options in Triple-Negative Breast Cancer." Breast Cancer: Basic and Clinical Research 5 (January 2011): BCBCR.S6562. http://dx.doi.org/10.4137/bcbcr.s6562.

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Notorious for its poor prognosis and aggressive nature, triple-negative breast cancer (TNBC) is a heterogeneous disease entity. The nature of its biological specificity, which is similar to basal-like cancers, tumors arising in BRCA1 mutation carriers, and claudin-low cancers, is currently being explored in hopes of finding the targets for novel biologics and chemotherapeutic agents. In this review, we aim to give a broad overview of the disease's nomenclature and epidemiology, as well as the basic mechanisms of emerging targeted therapies and their performance in clinical trials to date.

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Gierach, Gretchen L., Aileen Burke, and William F. Anderson. "Epidemiology of triple negative breast cancers." Breast Disease 32, no. 1-2 (March 15, 2011): 5–24. http://dx.doi.org/10.3233/bd-2010-0319.

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Hubalek, Michael, Theresa Czech, and Hannes Müller. "Biological Subtypes of Triple-Negative Breast Cancer." Breast Care 12, no. 1 (2017): 8–14. http://dx.doi.org/10.1159/000455820.

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Triple-negative breast cancers (TNBCs) are defined as tumors that are negative for estrogen, progesterone and HER-2 receptor. At a percentage of 10-20% TNBCs represent a minority in all breast cancers. However, because of the poor prognosis this particular subtype, triple negative disease accounts for a disproportionate number of metastatic cases and breast cancer deaths. Identification of its subtypes is essential for understanding the biological characteristics and clinical behavior of TNBC, as well as for developing personalized treatments. This review will focus on the great progress that has been made in the past few years on identifying new targets in TNBC subtypes and a variety of new treatment options that are on the verge of routine clinical application.

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Tsang, J., T. L. Lai, D. H. Lau, G. K. Au, and D. T. Chua. "Triple-negative breast cancer in Hong Kong Chinese patients." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e22127-e22127. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e22127.

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e22127 Background: There is increasing data showing that breast cancer is a heterogeneous disease which should be assessed separately in different populations, as it differs substantially between Chinese and Caucasian women. Triple-negative breast tumours which are negative for ER, PR and HER-2 neu receptors are associated with younger age at presentation, tumour of higher grade with larger size and a poorer prognosis. There is recent suggestion that the prognostic outlook of Chinese triple-negative breast cancers might be somewhat different from those in the Western population, but few studies have attempted to understand the role of ethnic factor in the triple-negative entity. Methods: We conducted a preliminary retrospective comparison of 170 Hong Kong Chinese primary breast cancer patients seen as new cases during January 2004 and December 2004 in a teaching hospital. Clinico-pathological features of triple-negative tumours were compared to their non-triple-negative counterpart. Results: Triple negative breast cancer accounted for 12.4% of all breast cancer patients seen in the year of 2004 (n = 21). It is associated with more cancers with grade 3 tumour (68.4% vs 36.8%; p = 0.02) but there was no statistically difference between the age of presentation, tumour size, extensive intraductal component, lymph node status and rate of local relapse or metastasis after adjuvant therapy. Subset analysis further revealed that when triple negative breast cancer patients (n = 21) were compared to the HER-2 positive patients (n = 40) in the studied population, HER-2 positive patients were still associated with higher proportion of node positive disease (57.5% vs 30.0%; p = 0.04). Disease free survival and overall survival were not studied due to limited follow-up time. Conclusions: Our preliminary findings suggested that Hong Kong Chinese triple-negative breast cancers are associated with a more favourable outlook and might behave differently when compared to their Western counterpart. Further large-scale study of the ethnic factor with long-term follow-up is warranted. No significant financial relationships to disclose.

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Gadi, Vijayakrishna K., and Nancy E. Davidson. "Practical Approach to Triple-Negative Breast Cancer." Journal of Oncology Practice 13, no. 5 (May 2017): 293–300. http://dx.doi.org/10.1200/jop.2017.022632.

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Triple negative is a term applied to breast cancers that do not meaningfully express the estrogen or progesterone hormone receptors or overexpress the human epidermal growth factor receptor 2 tyrosine kinase. At present, the only proven method for systemic management of triple-negative breast cancer for both early-stage and metastatic settings is cytotoxic chemotherapy. Here, we provide a comprehensive review of management strategies that are best supported by available data. We also review recent advances most likely to affect treatment of triple-negative breast cancer in the coming years with particular emphasis on targeted agents, biologics, and immunotherapy.

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Nandini, Dey, Aske Jennifer, and De Pradip. "Therapeutic Strategies for Metastatic Triple-Negative Breast Cancers: From Negative to Positive." Pharmaceuticals 14, no. 5 (May 12, 2021): 455. http://dx.doi.org/10.3390/ph14050455.

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Metastatic triple-negative breast cancer (TNBC) is a distinct and immensely complex form of breast cancer. Among all subtypes of breast cancers, TNBC has a comparatively high rate of relapse, a high rate of distant metastasis, and poor overall survival after standard chemotherapy. Chemotherapy regimens are an essential component of the management of this estrogen receptor-negative, progesterone receptor-negative, and epidermal growth factor receptor2 negative subtype of breast cancers. Chemotherapy is critical for preventing the recurrence of the disease and for achieving long-term survival. Currently, a couple of agents are approved for the management of this disease, including chemotherapy like eribulin, targeted therapy like PARP inhibitor, as well as an antibody-drug conjugate (ADC) to target TROP2. Like many other metastatic cancers, immune checkpoint inhibitors (ICIs) have also been approved for TNBC patients with PD-L1 positive tumors and high tumor mutational burden. In this review article, we discuss these newly approved and promising novel agents that may change the therapeutic landscape for advanced/metastatic TNBC patients.

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Kubouchi, Koichi, Kyosuke Shimada, Takamichi Yokoe, and Yutaka Tsutsumi. "Avoidance and Period-Shortening of Neoadjuvant Chemotherapy Against Triple-Negative Breast Cancer in Stages I and II: Importance of Ki-67 Labeling Index and the Recognition of Apocrine-Type Lesions." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382094324. http://dx.doi.org/10.1177/1533033820943246.

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Background: Triple-negative breast cancer encompasses heterogeneous subtypes. Neoadjuvant chemotherapy is ineffective against some triple-negative breast cancers, while others show a favorable prognosis despite chemoresistance. Methods: A total of 51 cases with stages I and II triple-negative breast cancer were analyzed; 34 triple-negative breast cancers treated with neoadjuvant chemotherapy were divided into “good responders” (n = 22), showing therapeutic effect G2b or G3 in surgical specimens, and “poor responders” with therapeutic effect G0, G1a, G1b, and G2a (n = 12). Neoadjuvant chemotherapy was spared in 17 cases (non-neoadjuvant chemotherapy group). Apocrine-type triple-negative breast cancer was defined as triple-negative breast cancer immunoreactive for both androgen receptor and forkhead-box protein A1. Triple-negative breast cancer other than apocrine-type (n = 16) and special types (myoepithelial, medullary, adenoid cystic, and spindle cell carcinomas, n = 6) was categorized as basal-like subtype (n = 29). Prognosis was evaluated in each category. Results: Neoadjuvant chemotherapy provoked significant effects against basal-like triple-negative breast cancer with high Ki-67 labeling (≧50%), and tumor-infiltrating lymphocytes predicted high chemosensitivity. Neoadjuvant chemotherapy was avoidable in triple-negative breast cancer of apocrine- and special types showing low (<50%) Ki-67 labeling. Ten (59%) lesions in the non-neoadjuvant chemotherapy group belonged to the apocrine-type. When clinical complete remission shown by contrast-enhanced magnetic resonance imaging was reached in the course of neoadjuvant chemotherapy against basal-like triple-negative breast cancer, the neoadjuvant chemotherapy period was shortened in 14 (64%) of 22 good responders. Disease-free and overall survival rates were excellent in all groups. Conclusions: The following 2 hypothetical proposals should be proven by large-scale clinical trials. Immunohistochemical recognition of apocrine-type triple-negative breast cancer with low Ki-67 labeling is important for avoiding ineffective/unnecessary neoadjuvant chemotherapy. By employing appropriate clinical imaging, period-shortening is achievable in basal-like triple-negative breast cancer with high Ki-67 labeling.

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Bredel, Markus, Hyunsoo Kim, Nanda K. Thudi, Denise M. Scholtens, James A. Bonner, and Branimir I. Sikic. "NFKBIA deletion in triple-negative breast cancer." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 1012. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.1012.

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1012 Background: While effective, target-directed therapies are available for ER-positive and HER2-amplified breast cancer, adjuvant therapeutic options for triple-negative breast cancer (TNBC) are limited in the absence of well-defined molecular targets. Constitutive activation of oncogenic nuclear factor kB (NFkB) has been associated with ER-negative or basal-like (BL) breast cancers, but the underlying mechanism of this activation remains undefined. We previously showed that deletion of the endogenous NFkB repressor gene NFKBIA associates with EGFR non-amplified glioblastoma multiforme and portends unfavorable clinical outcome (Bredel et al. NEJM 2011). Methods: We analyzed >5,000 human breast cancers for deletions, mutations and/or expression of NFKBIA. We studied tumor suppressor activity of NFKBIA and the effect of targeted NFkB inhibition in cell culture with various NFKBIA genotypes. We compared molecular results with outcomes of affected persons. Results: NFKBIA is often (10.8%) deleted but not mutated in breast cancer. NFKBIA deletions are significantly associated with TNBC (32.8%) and particularly frequent in the BL subtype (36.7%). Loss of NFKBIA exerts a haploinsufficient effect on NFKBIA expression and the transactivation of several NF-kB target genes with important roles in breast carcinogenesis. Restoration of NFKBIA expression or pharmacologic NFkB inhibition attenuates the malignant phenotype of cells cultured from TNBC with NFKBIA deletion. Deletion and low expression of NFKBIA are highly associated with unfavorable overall survival, independent of patient age, tumor stage, nodal status, and tumor subtype. Loss of NFKBIA expression portends significantly poorer disease-specific survival, recurrence-free survival, and distant metastasis-free survival. Moreover, NFKBIA expression is significantly associated with duration of metastasis-free survival in subgroups of patients with brain or lung metastases from breast cancer. Conclusions: NFKBIA is a new, prognostically relevant, molecular target in TNBC, which remains a clinically challenging subtype of breast cancer with limited treatment options.

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Amirifard, Nasrin, Edris Sadeghi, and Mansour Choubsaz. "Triple-Negative Breast Cancer Survival in Kurdish Patients." Scholars Journal of Applied Medical Sciences 4, no. 7 (July 2016): 2732–35. http://dx.doi.org/10.21276/sjams.2016.4.7.89.

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Parry, S., K. Savage, C. Marchiò, and J. S. Reis-Filho. "Nestin is expressed in basal-like and triple negative breast cancers." Journal of Clinical Pathology 61, no. 9 (July 19, 2008): 1045–50. http://dx.doi.org/10.1136/jcp.2008.058750.

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Aims:To analyse the distribution of nestin expression in different breast tumours and to determine the prognostic impact of nestin expression.Methods:Nestin expression was immunohistochemically analysed in a cohort of 245 invasive breast cancer patients treated with therapeutic surgery followed by anthracycline-based chemotherapy using a semi-quantitative scoring system.Results:Nestin was exclusively expressed in grade III breast carcinoma and preferentially expressed in basal-like and triple negative cancers. Nestin-positive tumours displayed high proliferation rates and p53 nuclear expression. Lymph-node positive patients with nestin-positive cancers had a shorter breast cancer specific survival; however nestin was not an independent prognostic factor on multivariate analysis.Conclusions:Nestin expression is preferentially found in basal-like and triple negative breast carcinomas. Further studies are warranted to define the biological role played by nestin in these subgroups of breast cancers.

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Wu, Jiande, Tarun Karthik Kumar Mamidi, Lu Zhang, and Chindo Hicks. "Unraveling the Genomic-Epigenomic Interaction Landscape in Triple Negative and Non-Triple Negative Breast Cancer." Cancers 12, no. 6 (June 12, 2020): 1559. http://dx.doi.org/10.3390/cancers12061559.

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Background: The recent surge of next generation sequencing of breast cancer genomes has enabled development of comprehensive catalogues of somatic mutations and expanded the molecular classification of subtypes of breast cancer. However, somatic mutations and gene expression data have not been leveraged and integrated with epigenomic data to unravel the genomic-epigenomic interaction landscape of triple negative breast cancer (TNBC) and non-triple negative breast cancer (non-TNBC). Methods: We performed integrative data analysis combining somatic mutation, epigenomic and gene expression data from The Cancer Genome Atlas (TCGA) to unravel the possible oncogenic interactions between genomic and epigenomic variation in TNBC and non-TNBC. We hypothesized that within breast cancers, there are differences in somatic mutation, DNA methylation and gene expression signatures between TNBC and non-TNBC. We further hypothesized that genomic and epigenomic alterations affect gene regulatory networks and signaling pathways driving the two types of breast cancer. Results: The investigation revealed somatic mutated, epigenomic and gene expression signatures unique to TNBC and non-TNBC and signatures distinguishing the two types of breast cancer. In addition, the investigation revealed molecular networks and signaling pathways enriched for somatic mutations and epigenomic changes unique to each type of breast cancer. The most significant pathways for TNBC were: retinal biosynthesis, BAG2, LXR/RXR, EIF2 and P2Y purigenic receptor signaling pathways. The most significant pathways for non-TNBC were: UVB-induced MAPK, PCP, Apelin endothelial, Endoplasmatic reticulum stress and mechanisms of viral exit from host signaling Pathways. Conclusion: The investigation revealed integrated genomic, epigenomic and gene expression signatures and signing pathways unique to TNBC and non-TNBC, and a gene signature distinguishing the two types of breast cancer. The study demonstrates that integrative analysis of multi-omics data is a powerful approach for unravelling the genomic-epigenomic interaction landscape in TNBC and non-TNBC.

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Sharma, D., B. B. Knight, R. Yacoub, T. Liu, L. Taliaferro-Smith, A. Nagalingam, and R. M. O'Regan. "Using epigenetic reprogramming to target triple-negative breast cancer." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): e14565-e14565. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e14565.

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e14565 Background: The outcome for patients with breast cancer has been significantly improved by the use of targeted agents. The prognosis of triple negative (TN) breast cancers, which do not express hormone receptors (ER, PR) or Her2, is poor, because of an aggressive clinical course and lack of targeted therapeutic agents. Epigenetic silencing of specific genes has been observed in breast cancer and some of these genes are more important due to available targeted therapies such as ER. Since all endocrine therapies are designed to block ER function in some way, the identification of new therapies or strategies that could sensitize TN breast cancers to existing endocrine therapy could provide a revolutionary means of treating this aggressive subtype of cancer Methods: We examined the efficacy of combined treatment of HDAC inhibitor LBH589 and DNMT inhibitor decitabine to regenerate ER and PR in TN breast cancer cells using RT-PCR and immunoblotting. Changes in growth and proliferation of TN breast cancer cells in response to LBH589 and decitabine treatment were determined by XTT, BrdU incorporation and colony formation assay. Changes in apoptotic proteins were determined by western blotting. Athymic nude mice were used to establish pre-clinical models for TN breast cancer cells and effectiveness of combined treatment of LBH589 and decitabine was determined. Tumors biopsies were analyzed for ER and PR re-expression by western blot analysis and immunohistochemistry at the end of the treatment. Results: Combined treatment of LBH589 and decitabine resulted in re-expression of ER and PR in TN breast cancers in vitro and in vivo. Although re-expression of ER and PR were noted following LBH589 treatment alone, re-expression was more robust with the combination. TN breast cancer cells showing re-expressed ER can be targeted with tamoxifen. Tamoxifen inhibits growth of TN breast cancer cells re- expressing ER by triggering apoptosis. Conclusions: The importance of epigenetic events such as DNA methylation and HDAC inhibition in tumor progression is becoming increasingly evident. A trial evaluating the ability of LBH589 and decitabine to re- express ER, which can then be targeted by tamoxifen, is planned in patients with metastatic TN breast cancer. No significant financial relationships to disclose.

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EZZET, Alaa Anwer, Isik Didem KARAGOZ, Sibel CANGI, and Tulay KUS. "DNA Profiling of ING1 Gene in Triple Negative Breast Cancer." Eurasia Proceedings of Science Technology Engineering and Mathematics 22 (August 30, 2023): 280–84. http://dx.doi.org/10.55549/epstem.1350983.

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Breast cancer is among the most common cancers and the second in death caused from cancers in women. Triple negative breast cancer (TNBC) is a subgroup which not expressed estrogen (ER), progesterone (PR) and HER2 receptors in breast cancer. It has 15% rate of all breast cancer and has been more aggressive and has poor prognosis. For this reason, early diagnosis has a key role because of TNBC’s high relapse. Investigation of DNA methylation pattern in TNBC likewise all types of breast cancer has become an important prognostic vehicle besides assessment of gene expression profile in diagnosis cancer subtypes. DNA methylation pattern of tumor suppressor genes which is one of the epigenetic modifications has highly importance. In this study, we aimed to investigate the relationship DNA methylation pattern of ING1 (inhibitor of growth family member 1), a tumor suppressor gene and TNBC. For this purpose, we searched the methylation pattern of ING1 and breast cancer patients especially TNBC. As a result, we discussed and tried to clarified the relationship between epigenetic modifications of ING1 gene and TNBC.

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Voutsadakis, Ioannis A. "EMT Features in Claudin-Low versus Claudin-Non-Suppressed Breast Cancers and the Role of Epigenetic Modifications." Current Issues in Molecular Biology 45, no. 7 (July 19, 2023): 6040–54. http://dx.doi.org/10.3390/cimb45070381.

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Background: Breast cancers are heterogeneous and are classified according to the expression of ER, PR and HER2 receptors to distinct groups with prognostic and therapeutic implications. Within the triple-negative group, with no expression of these three receptors, molecular heterogeneity exists but is currently not exploited in the clinic. The claudin-low phenotype is present in a subset of triple-negative breast cancers and constitutes together with basal-like cancers the most extensive groups within triple-negative breast cancers. Suppression of epithelial cell adhesion molecules in claudin-low cancers is also a hallmark of Epithelial Mesenchymal Transition (EMT). Methods: The groups of claudin-low and claudin-non-suppressed breast cancers from the extensive publicly available genomic cohorts of the METABRIC study were examined to delineate and compare their molecular landscape. Genetic and epigenetic alterations of key factors involved in EMT and potentially associated with the pathogenesis of the claudin-low phenotype were analyzed in the two groups. Results: Claudin-low cancers displayed up-regulation of several core transcription factors of EMT at the mRNA level, compared with claudin-non-suppressed breast cancers. Global promoter DNA methylation was increased in both groups of triple-negative cancers and in claudin-low ER-positive cancers compared with the rest of ER-positive cancers. Histone modifier enzymes, including methyltransferases, demethylases, acetyltransferases and deacetylases displayed amplifications more frequently in claudin-non-suppressed triple-negative cancers than in claudin-low counterparts and the expression of some of these enzymes differed significantly between the two groups. Conclusion: Claudin-low and claudin-non-suppressed triple-negative breast cancers differ in their landscape of EMT core regulators and epigenetic regulators. These differences may be explored as targets for therapeutic interventions specific to the two groups of triple-negative breast cancers.

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Riaz, Fauzia. "New strategies for the management of triple-negative breast cancer." Current Opinion in Obstetrics & Gynecology 36, no. 1 (December 8, 2023): 40–44. http://dx.doi.org/10.1097/gco.0000000000000927.

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Purpose of review This review highlights important changes in our understanding of triple-negative breast cancer. It highlights important novel approaches in treatment and reviews predicts potential challenges facing the treatment of triple-negative breast cancer. Recent findings There is a clear shift away from chemotherapy-centric approaches to the treatment of breast cancer, and instead, a move towards incorporating immune checkpoint inhibitors, antibody-drug conjugates, and other targeted therapies. There is a focus on understanding biomarkers and leveraging novel targets in drug development. Summary It is now standard of care to use neoadjuvant combination immunotherapy-chemotherapy in patients with Stage 1 and 2 breast cancers. Chemo-immunotherapy combinations when appropriate biomarkers are present (PD-L1) are standard first-line therapy in metastatic triple-negative breast cancer. Antibody-drug conjugates are now a mainstay in the treatment of this disease. These findings have shifted the treatment paradigm of the treatment of triple-negative breast cancer.

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Perou, Charles M. "Molecular Stratification of Triple‐Negative Breast Cancers." Oncologist 15, S5 (November 2010): 39–48. http://dx.doi.org/10.1634/theoncologist.2010-s5-39.

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Perou, Charles M. "Molecular Stratification of Triple‐Negative Breast Cancers." Oncologist 16, S1 (January 2011): 61–70. http://dx.doi.org/10.1634/theoncologist.2011-s1-61.

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Joensuu, H., and J. Gligorov. "Adjuvant treatments for triple-negative breast cancers." Annals of Oncology 23 (August 2012): vi40—vi45. http://dx.doi.org/10.1093/annonc/mds194.

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Vaidyanathan, Kannan. "The Challenge of Triple Negative Breast Cancers." Indian Journal of Clinical Biochemistry 29, no. 3 (June 14, 2014): 267–68. http://dx.doi.org/10.1007/s12291-014-0453-1.

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Byrne, David J., Siddhartha Deb, Elena A. Takano, and Stephen B. Fox. "GATA3 expression in triple-negative breast cancers." Histopathology 71, no. 1 (April 19, 2017): 63–71. http://dx.doi.org/10.1111/his.13187.

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Alluri, Prasanna, and Lisa A. Newman. "Basal-Like and Triple-Negative Breast Cancers." Surgical Oncology Clinics of North America 23, no. 3 (July 2014): 567–77. http://dx.doi.org/10.1016/j.soc.2014.03.003.

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Boukerroucha, M., C. Josse, S. ElGuendi, P. Freres, R. Marée, S. Wenric, K. Segers, J. Collignon, G. Jerusalem, and V. Bours. "Genetic study of triple negative breast cancers." Annals of Oncology 26 (May 2015): iii10. http://dx.doi.org/10.1093/annonc/mdv116.11.

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Xu, Hong, Peter Eirew, Sarah C. Mullaly, and Samuel Aparicio. "The Omics of Triple-Negative Breast Cancers." Clinical Chemistry 60, no. 1 (January 1, 2014): 122–33. http://dx.doi.org/10.1373/clinchem.2013.207167.

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Abstract BACKGROUND Triple-negative breast cancers (TNBC) do not represent a single disease subgroup and are often aggressive breast cancers with poor prognoses. Unlike estrogen/progesterone receptor and HER2 (human epidermal growth factor receptor 2) breast cancers, which are responsive to targeted treatments, there is no effective targeted therapy for TNBC, although approximately 50% of patients respond to conventional chemotherapies, including taxanes, anthracyclines, cyclophosphamide, and platinum salts. CONTENT Genomic studies have helped clarify some of the possible disease groupings that make up TNBC. We discuss the findings, including copy number–transcriptome analysis, whole genome sequencing, and exome sequencing, in terms of the biological properties and phenotypes that make up the constellation of TNBC. The relationships between subgroups defined by transcriptome and genome analysis are discussed. SUMMARY TNBC is not a uniform molecular or disease entity but a constellation of variably well-defined biological properties whose relationship to each other is not understood. There is good support for the existence of a basal expression subtype, p53 mutated, high–genomic instability subtype of TNBC. This should be considered a distinct TNBC subtype. Other subtypes with variable degrees of supporting evidence exist within the nonbasal/p53wt (wild-type p53) TNBC, including a group of TNBC with PI3K (phosphoinositide 3-kinase) pathway activation that have better overall prognosis than the basal TNBC. Consistent molecular phenotyping of TNBC by whole genome sequencing, transcriptomics, and functional studies with patient-derived tumor xenograft models will be essential components in clinical and biological studies as means of resolving this heterogeneity.

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Malorni, L., P. B. Shetty, S. G. Hilsenbeck, M. F. Rimawi, R. M. Elledge, C. De Angelis, C. K. Osborne, S. De Placido, and G. Arpino. "Triple-negative breast cancers: Biomarkers and outcomes." Journal of Clinical Oncology 28, no. 15_suppl (May 20, 2010): 10621. http://dx.doi.org/10.1200/jco.2010.28.15_suppl.10621.

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Džoić Dominković, Martina, Gordana Ivanac, Tomislav Kelava, and Boris Brkljačić. "Elastographic features of triple negative breast cancers." European Radiology 26, no. 4 (August 1, 2015): 1090–97. http://dx.doi.org/10.1007/s00330-015-3925-7.

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Bertucci, François, Pascal Finetti, Nathalie Cervera, Benjamin Esterni, Fabienne Hermitte, Patrice Viens, and Daniel Birnbaum. "How basal are triple-negative breast cancers?" International Journal of Cancer 123, no. 1 (2008): 236–40. http://dx.doi.org/10.1002/ijc.23518.

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Sasaki, Yuka, and Hitoshi Tsuda. "Clinicopathological characteristics of triple-negative breast cancers." Breast Cancer 16, no. 4 (August 6, 2009): 254–59. http://dx.doi.org/10.1007/s12282-009-0153-5.

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Regua, Angelina T., Dongqin Zhu, Daniel L. Doheny, Grace L. Wong, Sara G. Manore, Calvin J. Wagner, Austin Arrigo, Mariana Najjar, and Hui-Wen Lo. "Abstract 1039: TrkA and JAK2-STAT3 pathway crosstalk promotes breast cancer stem cells in HER2-enriched and triple-negative breast cancers." Cancer Research 82, no. 12_Supplement (June 15, 2022): 1039. http://dx.doi.org/10.1158/1538-7445.am2022-1039.

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Abstract Breast cancer is the most commonly diagnosed cancer in American women and accounts for ~15% of cancer-related deaths. Despite the current standard of care, metastatic HER2-enriched breast cancer and triple-negative breast cancer remain difficult to treat due to poor response to treatment, lack of actionable targets, or eventual acquired resistance. The high mortality rate of metastatic HER2-enriched breast cancers and triple-negative breast cancers highlights the need for novel actionable targets for improved response to therapeutic intervention. Through datamining of publicly available breast cancer patient datasets, we recently found that Tropomyosin receptor kinase A (TrkA) and Janus kinase 2 (JAK2)-STAT3 pathways are co-activated and co-enriched in HER2-enriched breast cancers and triple-negative breast cancers (Cancers 10:2340-2360, 2021). We also found that TrkA, a receptor tyrosine kinase, directly interacts with and phosphorylates STAT3 on Y705 residue, resulting in STAT3 activation, nuclear translocation, and increased transcription of STAT3 target genes SOX2 and c-MYC, which are associated with breast cancer stem cell formation as well as tumor recurrence and metastasis. In this study, we aimed to further characterize the effects of the TrkA-JAK2/STAT3 pathway crosstalk on breast cancer stem cells. Our data showed that overexpression of TrkA enhances mammosphere formation and ALDH activity of breast cancer cells, which are further enhanced upon co-overexpression of STAT3. Our study further revealed that TrkA and JAK2 inhibitors synergize to reduce breast cancer stemness since co-inhibition of TrkA and JAK2 significantly reduces the CD44high/CD24low cell subpopulation, mammosphere formation, and ALDH activity to a greater extent compared to vehicle or monotherapies. Western blot analysis of breast cancer cells treated with TrkA and/or JAK2 inhibitors showed that co-inhibition of these two kinases significantly reduces levels of p-STAT3 (Y705), as well as stemness markers SOX2, MYC, and CD44. Taken together, these findings suggest that TrkA cooperates with the JAK2-STAT3 signaling pathway to promote breast cancer stem cells through increasing expression of SOX2, c-MYC, and CD44, and that co-inhibition of TrkA and JAK2 significantly suppressed breast cancer stemness, suggesting its future utility as a promising new treatment modality for patients with HER2-enriched breast cancers and triple-negative breast cancers. Citation Format: Angelina T. Regua, Dongqin Zhu, Daniel L. Doheny, Grace L. Wong, Sara G. Manore, Calvin J. Wagner, Austin Arrigo, Mariana Najjar, Hui-Wen Lo. TrkA and JAK2-STAT3 pathway crosstalk promotes breast cancer stem cells in HER2-enriched and triple-negative breast cancers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1039.

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Gucalp, Ayca, and Tiffany A. Traina. "Triple-Negative Breast Cancer: Adjuvant Therapeutic Options." Chemotherapy Research and Practice 2011 (June 21, 2011): 1–13. http://dx.doi.org/10.1155/2011/696208.

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Triple-negative breast cancer (TNBC), a subtype distinguished by negative immunohistochemical assays for expression of the estrogen and progesterone receptors (ER/PR) and human epidermal growth factor receptor-2(HER2) represents 15% of all breast cancers. Patients with TNBC generally experience a more aggressive clinical course with increased risk of disease progression and poorer overall survival. Furthermore, this subtype accounts for a disproportionate number of disease-related mortality in part due to its aggressive natural history and our lack of effective targeted agents beyond conventional cytotoxic chemotherapy. In this paper, we will review the epidemiology, risk factors, prognosis, and the molecular and clinicopathologic features that distinguish TNBC from other subtypes of breast cancer. In addition, we will examine the available data for the use of cytotoxic chemotherapy in the treatment of TNBC in both the neoadjuvant and adjuvant setting and explore the ongoing development of newer targeted agents.

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Bhatti, Abu Bakar Hafeez, Amina Iqbal Khan, Neelam Siddiqui, Nargis Muzaffar, Aamir Ali Syed, Mazhar Ali Shah, and Arif Jamshed. "Outcomes of Triple-Negative Versus Non-Triple-Negative Breast Cancers Managed with Breast-Conserving Therapy." Asian Pacific Journal of Cancer Prevention 15, no. 6 (March 30, 2014): 2577–81. http://dx.doi.org/10.7314/apjcp.2014.15.6.2577.

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42

Pareja, Fresia, and Jorge S. Reis-Filho. "Triple-negative breast cancers — a panoply of cancer types." Nature Reviews Clinical Oncology 15, no. 6 (March 19, 2018): 347–48. http://dx.doi.org/10.1038/s41571-018-0001-7.

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Núñez Abad, Martín, Silvia Calabuig-Fariñas, Miriam Lobo de Mena, María José Godes Sanz de Bremond, Clara García González, Susana Torres Martínez, José Ángel García-García, Vega Iranzo González-Cruz, and Carlos Camps Herrero. "Update on systemic treatment in early triple negative breast cancer." Therapeutic Advances in Medical Oncology 13 (January 2021): 175883592098674. http://dx.doi.org/10.1177/1758835920986749.

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Triple negative breast cancer (TNBC) is a heterogeneous disease representing about 15% of all breast cancers. TNBC are usually high-grade histological tumors, and are generally more aggressive and difficult to treat due to the lack of targeted therapies available, and chemotherapy remains the standard treatment. There is a close relationship between pathological complete response after chemotherapy treatment and higher rates of disease-free survival and overall survival. In this review of systemic treatment in early triple negative breast cancer, our purpose is to analyze and compare different therapies, as well as to highlight the novelties of treatment in this breast cancer subtype.

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Kim, Isaac, Katherine Sanchez, Heather L. McArthur, and David Page. "Immunotherapy in Triple-Negative Breast Cancer: Present and Future." Current Breast Cancer Reports 11, no. 4 (November 20, 2019): 259–71. http://dx.doi.org/10.1007/s12609-019-00345-z.

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Abstract Purpose of Review Immunotherapy is emerging as an effective treatment option for metastatic triple-negative breast cancer. In this review, we summarize clinical data of immunotherapy in triple-negative breast cancer and comment on future directions in the field. Recent Findings IMpassion130 was a phase III trial that demonstrated progression-free survival benefit, and potentially overall survival benefit, of first-line chemotherapy (nab-paclitaxel) plus anti-programmed death ligand 1 (PD-L1) atezolizumab, among PD-L1-positive metastatic triple-negative breast cancers. Studies are ongoing to evaluate other combination therapies with immune checkpoint blockade in TNBC, and to evaluate efficacy in PD-L1-negative tumors and in later lines of therapy. Summary Immunotherapy is now a standard option in the treatment of triple-negative breast cancer. Ongoing trials may expand the degree of clinical benefit. Further work is ongoing to identify novel predictive biomarkers, which in the future may enable a personalized approach of combination immunotherapy.

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Khandekar, Durga, and Venkataswarup Tiriveedhi. "Role of BET Inhibitors in Triple Negative Breast Cancers." Cancers 12, no. 4 (March 25, 2020): 784. http://dx.doi.org/10.3390/cancers12040784.

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Bromodomain and extraterminal domain (BET) proteins have evolved as key multifunctional super-regulators that control gene expression. These proteins have been shown to upregulate transcriptional machinery leading to over expression of genes involved in cell proliferation and carcinogenesis. Based on favorable preclinical evidence of BET inhibitors in various cancer models; currently, 26 clinical trials are underway in various stages of study on various hematological and solid organ cancers. Unfortunately, preliminary evidence for these clinical studies does not support the application of BET inhibitors as monotherapy in cancer treatment. Furthermore, the combinatorial efficiency of BET inhibitors with other chemo-and immunotherapeutic agents remain elusive. In this review, we will provide a concise summary of the molecular basis and preliminary clinical outcomes of BET inhibitors in cancer therapy, with special focus on triple negative breast cancer.

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Hu, Taobo, Yiqiang Liu, Jinbo Wu, Xuejiao Lina Hu, Guiyang Zhao, Baosheng Liang, Shu Wang, and Mengping Long. "Triple-Negative Apocrine Breast Carcinoma Has Better Prognosis despite Poor Response to Neoadjuvant Chemotherapy." Journal of Clinical Medicine 11, no. 6 (March 14, 2022): 1607. http://dx.doi.org/10.3390/jcm11061607.

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Apocrine carcinoma is a rare subtype of invasive ductal breast cancer that shows apocrine differentiation and largely triple-negative immunohistology. Triple-negative breast cancers are known to have more aggressive clinical courses. However, unlike most other subtypes, it is reported that triple-negative apocrine carcinoma (TNAC) has a better prognosis. Due to the scarcity of reported studies, our knowledge regarding its clinical behavior, prognosis and response to therapy is very limited. In this study, we retrospectively retrieved 41 triple-negative apocrine carcinoma cases from our breast cancer database, with an average follow-up of 32.8 months. It was found that TNAC had a poorer response to neoadjuvant therapy but a better prognosis than other nonapocrine types of triple-negative breast cancer. Meanwhile, TNAC has a low proliferative nature, as indicated by its low Ki-67 index. An updated analysis of the Surveillance, Epidemiology, and End Results database showed that chemotherapy did not improve breast-cancer-specific survival in TNAC patients. Our results suggest that TNAC is a special subtype of triple-negative breast cancer with a better short-term prognosis despite poor response to neoadjuvant chemotherapy.

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Manna, Subrata, and Marina K. Holz. "Tamoxifen Action in ER-Negative Breast Cancer." Signal Transduction Insights 5 (January 2016): STI.S29901. http://dx.doi.org/10.4137/sti.s29901.

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Breast cancer is a highly heterogeneous disease. Tamoxifen is a selective estrogen receptor (ER) modulator and is mainly indicated for the treatment of breast cancer in postmenopausal women and postsurgery neoadjuvant therapy in ER-positive breast cancers. Interestingly, 5-10% of the ER-negative breast cancers have also shown sensitivity to tamoxifen treatment. The involvement of molecular markers and/or signaling pathways independent of ER signaling has been implicated in tamoxifen sensitivity in the ER-negative subgroup. Studies reveal that variation in the expression of estrogen-related receptor alpha, ER subtype beta, tumor microenvironment, and epigenetics affects tamoxifen sensitivity. This review discusses the background of the research on the action of tamoxifen that may inspire future studies to explore effective therapeutic strategies for the treatment of ER-negative and triple-negative breast cancers, the latter being an aggressive disease with worse clinical outcome.

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Ahmed, Muneer, A. Basit, R. Kirby, S. Narayanan, and J. Adjogatse. "A comparison of triple negative versus triple positive breast cancers." European Journal of Surgical Oncology (EJSO) 37, no. 11 (November 2011): 986. http://dx.doi.org/10.1016/j.ejso.2011.08.040.

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Keenan, Tanya E., and Sara M. Tolaney. "Role of Immunotherapy in Triple-Negative Breast Cancer." Journal of the National Comprehensive Cancer Network 18, no. 4 (April 2020): 479–89. http://dx.doi.org/10.6004/jnccn.2020.7554.

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Immune checkpoint inhibitors (ICIs) have led to durable clinical remissions in many metastatic cancers. However, the single-agent efficacy of ICIs in breast cancer is low, including in triple-negative breast cancer (TNBC), which has several key characteristics that enhance ICI responses. Strategies to improve anticancer immune responses in TNBC are urgently needed to extend survival for patients with metastatic disease. This review presents ICI monotherapy response rates and discusses combination strategies with chemotherapy, targeted therapies, and novel immunotherapies. It concludes with a summary of immunotherapy biomarkers in TNBC and a call to action for future directions of research critical to advancing the efficacy of immunotherapy for patients with TNBC.

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Tryfonopoulos, Dimitrios, Georgios Oikonomopoulos, Stamatina Demiri, Lazaros Lekakis, Nikolaos Fragkiskos Pistamaltzian, George Koumakis, Chris G. Panopoulos, et al. "Clinicopathologic characteristics of triple-negative breast cancer and relationship to basal markers." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e11519-e11519. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e11519.

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e11519 Background: Triple negative breast cancers are immunohistochemical surrogates of basal-like breast cancers. There is no complete overlap between triple negative and basal-like tumors and as gene expression studies evolve, further subclassification bearing clinical relevance is underway. Our purpose was to correlate clinicopathologic characteristics of triple negative breast cancer tumors with expression of basal markers in an effort to define immunohistochemically subgroups of this heterogenous disease Methods: Data were retrieved and analysed using our electronic databank. Patient samples were reviewed by an expert breast cancer pathologist and stained additionally for EGFR and CK 5/6 antibodies. Results: Sixty-five women with triple negative breast cancer were identified. Mean age was 58.3±12.9 years. Most tumors (86%) were of ductal histology, 53% grade 3, 48% having high Ki-67 index (>14%). 10% of patients presented with Stage IV, 25% with Stage III, 38% with stage II and 27% with stage I disease. 63% of patients were postmenopausal. EGFR staining was present in 43% of tumor samples, whereas CK 5/6 in 38.5%. Both EGFR and CK 5/6 expression was found in 18.5%, whereas 37% of tumors expressed neither EGFR or CK 5/6. No difference was observed between tumors expressing any of these 2 basal markers as compared to EGFR and CK 5/6 negative tumors in terms of Ki-67 index, grade, tumor size and nodal involvement. Lymphovascular invasion and non-ductal histology tended to occur more frequently (p=ns) in non-basal tumors. Additionally, patients with expression of any of the basal markers tended to be more obese than the non-basal triple negative breast cancer patients (p=ns). Conclusions: Further immunohistochemical markers apart from EGFR and CK 5/6 are needed in order to further define clinically meaningful subgroups of triple negative breast cancer.

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Journal articles on the topic 'Triple negative breast cancers'

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