Relevant bibliographies by topics / Triple negative breast cancers

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Academic literature on the topic 'Triple negative breast cancers'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "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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Dissertations / Theses on the topic "Triple negative breast cancers"

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Kravalis, Saulius [Verfasser], and Elmar [Akademischer Betreuer] Stickeler. "MicroRNA signatures in triple-negative breast cancer." Freiburg : Universität, 2016. http://d-nb.info/1139977482/34.

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Perera, Don Franciscuge Thilini N. "Targeting Focal Adhesion Kinase (FAK) in Triple Negative Breast Cancer (TNBC)." Thesis, Griffith University, 2020. http://hdl.handle.net/10072/397040.

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Breast cancers are one of the most frequently diagnosed diseases in women and responsible for considerable mortality annually. Breast cancers are complex, with vast variations in terms of genetic, as well as epigenetic factors, which contribute to the ongoing challenges in developing efficacious treatments. The primary cause of mortality is due to metastasis and recurrence. Triple negative breast cancer (TNBC) is an aggressive subset of breast cancer which commonly metastasises to the lungs, liver, brain and bone, and lacks targeted therapeutics. Metastasis generally involves cancer cells penetrating the extracellular matrix (ECM), a major component of the cell microenvironment. The ECM is a dynamic and versatile part of the cell microenvironment which regularly interacts with cell membrane receptors, resulting in the regulation of cell proliferation, migration, invasion and metastasis. Focal adhesion kinase (FAK) is a cytoplasmic non-receptor protein tyrosine kinase that is up-regulated in many cancers including breast cancer. It is a signalling molecule regulated in tumour progression and metastasis and a key mediator in breast cancer cell survival. FAK can regulate the phosphorylation of downstream signalling pathways such as Akt and mitogen-activated protein kinase (MAPK). Moreover, FAK is also associated with cell metabolism, where, glucose consumption and lipogenesis can be upregulated due to FAK activity. Understanding the role ECM proteins have on the functionality of FAK and associated intracellular signalling pathways in TNBC, has the potential to improve therapeutic strategies. Moreover, targeting this essential signalling molecule is known to impact the metastasis and cell viability in breast cancer. By studying the interactions of TNBC cells with the surrounding ECM and involvement of key cellular signalling pathways such as FAK, will contribute to an improved understanding of the impact of these factors on breast cancer biology and potential therapeutic options. The aims of this project were to determine whether ECM components play a major role in FAK expression and activation in TNBC, and the impact of FAK inhibitors have in FAK activation, in the presence and absence of ECM components. In addition, the effect FAK inhibitors have on essential downstream signalling pathways, and vital cellular events such as cell cycle progression, oxidative stress and apoptosis in TNBC cells was assessed. The TNBC cell line, MDA-MB-231, grown with and without complete ECM Matrigel, and pure individual ECM proteins: Collagen IV, Fibronectin and Laminin were evaluated to determine the effect on FAK activation and expression. Collagen IV was selected for further exploration given the noticeable impact it had on FA related activities. As Collagen IV is a major constituent in the human mammary gland, its biological relevance to TNBC research was highlighted. FAK inhibitors with two distinct modes of action; Y15 (FAK inhibitor 14) and TAE226 were utilised to understand how FAK inhibition impacts FAK activation and expression in the presence of Collagen IV. Y15 is a small molecule FAK inhibitor that targets FAK specific 397 auto-phosphorylation sites, while TAE226 blocks the ATP binding site of FAK. The two inhibitors demonstrated differences in how they affect MDA-MB-231 cell metabolism as well as FA point formation. However, given that TAE226 has significant off-target effects, Y15 was selected to study specific FAK inhibition on FAK associated downstream pathways, cell cycle progression, oxidative stress and apoptosis. As FAK plays a vital role in cell attachment, FAK inhibition was investigated in cells treated both before and after cell attachment. A drastic reduction in FA point formation was observed when FAK inhibitors were added to attached cells. In contrast, this observation was not made for pre-adherent cells, with only minimal effects reported on FA point formation, in particular, in the presence of Collagen IV. Moreover, increased levels of apoptosis were observed following the FAK inhibition on the already attached cells, with less live cells present in comparison to the pre-adherent cells. Collectively, these results indicated that Y15 is more effective on adherent cells, resulting in changes to FA point formation and cell death. Nonetheless, the inhibitory concentrations of Y15 observed for the two conditions (i:e: Y15 treatment on pre and post attached cells) was very similar, both in the absence and presence of Collagen IV. This suggests that although a higher percentage of adherent cells had undergone cell death, the remaining live cells had an overall metabolic rate similar to that observed for pre-adherent cells, where the majority of the cell population was alive. The effects of FAK inhibition by Y15 also resulted in an upregulation of phosphorylation of Akt in the pre-adherent cells, which is an indication that MDA-MB-231 cells rely on the Akt pathway for survival. In addition, FAK inhibition using Y15 exhibited downregulation of reactive oxygen species (ROS) which is indicative of hindrance in breast cancer cell metabolism. Collectively, these findings suggest Collagen IV plays a pivotal role as an ECM component, in TNBC disease progression and the efficacy of FAK inhibition.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Environment and Sc
Science, Environment, Engineering and Technology
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Basree, Mustafa M. "Implications of Breastfeeding in Triple Negative Breast Cancer." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1492791260508232.

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Albukhari, Ashwag. "Targeting EGFR signalling pathway in triple negative breast cancer." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:85d4bb10-385e-4187-8576-cf04f15f2871.

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Epidermal growth factor receptor (EGFR) is frequently overexpressed in the majority of triple negative breast cancer patients (TNBC). However, the molecular determinants behind their limited response to EGFR-targeted therapies are poorly understood. Here, both the acute and chronic responses of TNBC to the EGFR-targeted therapy, cetuximab (CTX), have been investigated. The expression of EGFR has been analyzed in a cohort of 2000 breast cancer tumours from the public dataset as well as in a panel of breast cancer cell lines. Furthermore, the response of TNBC cell lines to CTX has been investigated using conventional biochemical methods. Finally, a comprehensive transcriptomic profiling of an acquired CTX-resistant TNBC model by RNA sequencing has been performed to understand the molecular determinants of acquired CTX resistance. The results confirmed that EGFR is highly expressed in TNBC in comparison to non-TNBC breast cancer tumours and cell lines, which was associated with adverse clinical outcomes. Targeting EGFR in TNBC cell lines using CTX failed to completely inhibit the EGFR signalling pathway and was associated with an increase in ADAMs-mediated release of endogenous EGFR ligands, EGF and TGFα. Inhibition of ADAMs (ADAM10 and ADAM17) significantly enhanced the anti tumour efficacy of CTX both in vitro and in vivo. Furthermore, transcriptomic profiling of the acquired CTX-resistant TNBC cell line (MDA-MB-468CR) revealed an activation of several key oncogenic pathways and genes, including the TGFβ/BMP pathway. Blocking BMP receptors (BMPRs) restored the sensitivity of resistant cells to CTX treatment. Collectively, current findings offer alternative strategies that could enhance the CTX response in TNBC. We further reported that simultaneous targeting of both EGFR and BMPR pathways could overcome CTX resistance, which might have important implications for the treatment of TNBC.
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Pipili, Aikaterini. "The role of IQGAP3 in triple negative breast cancer." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-iqgap3-in-triple-negative-breast-cancer(bb661f8b-46f8-4917-9734-8285c3c60867).html.

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Triple negative breast cancer refers to a spectrum of breast tumours which are characterised by the lack of overexpressing hormone or HER2 receptors. These tumours present as high grade and tend to have reduced progression free survival rates because of their aggressive and metastatic behaviour. The lack of targeted therapies for triple negative breast cancer also contributes to the observed poor outcomes. During a genetic profiling screen of aggressive breast tumours, mRNA levels of IQGAP3 were specifically found to be upregulated in triple negative tumours compared to other types of the disease and normal tissue samples. IQGAP3 is the most recently discovered member of the IQGAP family of scaffold proteins. Even though IQGAP1 is a well described effector for the Rho GTPases and has also been heavily associated with tumourigenesis and cancer cell motility, far less is known about IQGAP3. The aim of this project was to investigate the role of IQGAP3 in triple negative breast cancer cell behaviour. At first, IQGAP3 was found to be expressed across a panel of triple negative cell lines. Modulating expression levels of IQGAP3 conferred morphological changes, disrupted cell migration and inhibited the ability of cells to form specialised invasive adhesion structures, termed invadopodia. Reduced expression of IQGAP3 disrupted RhoA activity and actomyosin contractility. IQGAP3 was also found to interact with PAK6 and Filamin-A; proteins already associated with the regulation of cell morphology. Indeed, PAK6 overexpression rescued the IQGAP3 depletion phenotype. IQGAP domains have previously been suggested to have potential therapeutic value thus IQGAP3 could be a promising candidate to target in order to inhibit metastasis in triple negative breast cancer.
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Mohamad, Hanif Ezanee Azlina Binti. "The identification and characterisation of markers clinical outcome in triple negative breast cancers (TNBCs)." Thesis, Queen's University Belfast, 2017. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.728192.

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Triple Negative Breast Cancer (TNBC) is an aggressive and is associated with epithelial-mesenchymal transition (EMT)-like features and highly metastatic. TNBCs display negative expression for the estrogen (ER), progesterone (PR) and HER2 receptors with high heterogeneity and have no targeted therapies available (current treatment generic DNA damage chemotherapy cocktail (FEC)). Some TNBCs respond well, or refractory or initially respond but relapse quickly (<18 months). To date, there are no predictive markers that could represent relapse to TNBC. The study aims to identify predictive poor outcome markers to FEC in TNBCs and to identify associated genes/pathways driving this aggressive biology. This study was initiated by microarray analyses on Partek Genomic Suite Software, from an in­house TNBC dataset consisting of poor outcome patients (relapse <5 years post FEC) and good outcome outcome patients (no relapse >5 years post FEC). These profiles were analysed with high (Analysis I; removing non- discriminatory samples and FDR<0.05) and low (Analysis II; inclusive all samples without FDR) stringency settings. Consistent findings were MiR205 downregulation (Analysis I) and TGF02 upregulation (Analysis II) in poor outcome TNBCs. Both markers suggested that they played contrasting roles in the increase of EMT-like processes in TNBC cells which closely resembled TNBC tumours from the poor outcome subgroup (Basal B). We showed that MiR205 is p63-dependent in poor outcome TNBCs due to the action of mutant p53 proteins. Loss of MiR205 consistently results in upregulation of the transcription factor ZEB1, a known inducer of EMT. Conversely, the poor outcome TNBCs overexpress the TGFp2 ligand. Altered regulation of both markers resulted in increasing cell invasion of poor outcome/Basal B cell lines, relative to good outcome/Basal A. Taken together, quantification of these markers could provide valuable insights into how to predict which TNBC patients are likely to relapse following FEC and prediction of additional chemotherapeutic agents alongside FEC to minimize the risk of relapse. This new knowledge could also provide opportunities for the development of novel therapeutic strategies (such as targeting components of the TGFp/SMAD signaling pathway) to improve treatment responses and ultimately improve patient survival in this aggressive subtype of breast cancer.
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Sadacca, Benjamin. "Pharmacogenomic and High-Throughput Data Analysis to Overcome Triple Negative Breast Cancers Drug Resistance." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS538/document.

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Devant le grand nombre de tumeurs du sein triple négatif résistant aux traitements, il est essentiel de comprendre les mécanismes de résistance et de trouver de nouvelles molécules efficaces. En premier lieu, nous analysons deux ensembles de données pharmacogénomiques à grande échelle. Nous proposons une nouvelle classification basée sur des profils transcriptomiques de lignées cellulaires, selon un processus de sélection de gènes basé sur des réseaux biologiques. Notre classification moléculaire montre une plus grande homogénéité dans la réponse aux médicaments que lorsque l’on regroupe les lignées cellulaires en fonction de leur tissu d'origine. Elle permet également d’identifier des profils similaires de réponse aux traitements. Dans un second travail, nous étudions une cohorte de patients atteints d’un cancer du sein triple négatif ayant résisté à la chimiothérapie néoadjuvante. Nous effectuons des analyses moléculaires complètes basées sur du RNAseq et WES. Nous constatons une forte hétérogénéité moléculaire des tumeurs avant et après traitement. Bien que nous observons une évolution clonale sous traitement, aucun mécanisme récurrent de résistance n’a pu être identifié. Nos résultats suggèrent fortement que chaque tumeur a un profil moléculaire unique et qu'il est important d'étudier de grandes séries de tumeurs. Enfin, nous améliorons une méthode pour tester la surreprésentation de motifs connus de protéines de liaison à l'ARN, dans un ensemble donné de séquences régulées. Cet outil utilise une approche innovante pour contrôler la proportion de faux positifs qui n'est pas réalisé par l'algorithme existant. Nous montrons l'efficacité de notre approche en utilisant deux séries de données différentes
Given the large number of treatment-resistant triple-negative breast cancers, it is essential to understand the mechanisms of resistance and to find new effective molecules. First, we analyze two large-scale pharmacogenomic datasets. We propose a novel classification based on transcriptomic profiles of cell lines, according to a biological network-driven gene selection process. Our molecular classification shows greater homogeneity in drug response than when cell lines are grouped according to their original tissue. It also helps identify similar patterns of treatment response. In a second analysis, we study a cohort of patients with triple-negative breast cancer who have resisted to neoadjuvant chemotherapy. We perform complete molecular analyzes based on RNAseq and WES. We observe a high molecular heterogeneity of tumors before and after treatment. Although we highlighted clonal evolution under treatment, no recurrent mechanism of resistance could be identified Our results strongly suggest that each tumor has a unique molecular profile and that that it is increasingly important to have large series of tumors. Finally, we are improving a method for testing the overrepresentation of known RNA binding protein motifs in a given set of regulated sequences. This tool uses an innovative approach to control the proportion of false positives that is not realized by the existing algorithm. We show the effectiveness of our approach using two different datasets
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Kishi, Masae. "Strategies of Cancer Immunotherapy : Model of Triple Negative Breast Cancer." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS070.

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Les cellules souches cancéreuses (CSC) sont à l’origine de la progression tumorale, des métastases et rechutes tardives. Elles ont été identifiées dans de nombreux cancers, comme le cancer du sein triple négatif (TNBC) et cancers de grade III-IV. Elles sont résistantes aux chimiothérapies et radiothérapie et résident dans une niche immuno-répressive. Cette étude vise à évaluer une stratégie d’immunothérapie qui cible sélectivement les CSC dans le modèle murin 4T1-GFP-Luc mimant le TNBC. Le phénotype/ génotype des mamosphères a été initialement caractérisé. Basée sur l’analyse génomique des CSC, nous avons développé une immunothérapie active associée à des agents immuno-modulateurs. Nous avons mesuré la taille des tumeurs et suivi l’apparition des métastases par bioluminescence. Une étude immunologique et analyse génomique de la tumeur a été réalisée. La combinaison thérapeutique provoque le recrutement dans la tumeur de lymphocytes T (CD4 +, CD8 +) et lymphocytes B par augmentation de CXCL13, une réduction des lymphocytes T reg et cellules myéloïdes suppressives. Cette induction de réponse immunitaire provoque la diminution de la taille de la tumeur et des métastases. Cette nouvelle immunothérapie active de type vaccinale pourra être utilisée en association avec les traitements actuels pour des mesures prophylactiques et curatives dans une grande variété de cancers
Cancer stem cells (CSCs) are responsible for tumor progression, metastases, and late relapses. They have been identified in many cancers, such as triple negative breast cancer (TNBC) and grade III to IV cancers. They are resistant to chemotherapy and radiotherapy and reside in an immuno-repressive niche.This study aims to evaluate a immunotherapy strategy that selectively targets CSCs in the mouse model 4T1-GFP-Luc mimicking TNBC. The phenotype / genotype of mammosphere was initially characterized. Based on genomic analysis of CSC, we have developed an active immunotherapy associated with immunomodulatory agents. We measured the size of tumors and monitored the appearance of metastases by bioluminescence. We performed an immunological study and genomic tumor analysis. The therapeutic combination causes the recruitment of CD4 + and CD8 + T lymphocytes and B lymphocytes with increased CXCL13, the reduction of T reg cells and suppressive myeloid cells in the tumor. This induction of intra-tumor immune response leads to a decrease in tumor size and metastases.This new active immunotherapy can be used in combination with current treatments for prophylactic and curative measures in a wide variety of cancers
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Kishi, Masae. "Strategies of Cancer Immunotherapy : Model of Triple Negative Breast Cancer." Electronic Thesis or Diss., Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS070.

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Les cellules souches cancéreuses (CSC) sont à l’origine de la progression tumorale, des métastases et rechutes tardives. Elles ont été identifiées dans de nombreux cancers, comme le cancer du sein triple négatif (TNBC) et cancers de grade III-IV. Elles sont résistantes aux chimiothérapies et radiothérapie et résident dans une niche immuno-répressive. Cette étude vise à évaluer une stratégie d’immunothérapie qui cible sélectivement les CSC dans le modèle murin 4T1-GFP-Luc mimant le TNBC. Le phénotype/ génotype des mamosphères a été initialement caractérisé. Basée sur l’analyse génomique des CSC, nous avons développé une immunothérapie active associée à des agents immuno-modulateurs. Nous avons mesuré la taille des tumeurs et suivi l’apparition des métastases par bioluminescence. Une étude immunologique et analyse génomique de la tumeur a été réalisée. La combinaison thérapeutique provoque le recrutement dans la tumeur de lymphocytes T (CD4 +, CD8 +) et lymphocytes B par augmentation de CXCL13, une réduction des lymphocytes T reg et cellules myéloïdes suppressives. Cette induction de réponse immunitaire provoque la diminution de la taille de la tumeur et des métastases. Cette nouvelle immunothérapie active de type vaccinale pourra être utilisée en association avec les traitements actuels pour des mesures prophylactiques et curatives dans une grande variété de cancers
Cancer stem cells (CSCs) are responsible for tumor progression, metastases, and late relapses. They have been identified in many cancers, such as triple negative breast cancer (TNBC) and grade III to IV cancers. They are resistant to chemotherapy and radiotherapy and reside in an immuno-repressive niche.This study aims to evaluate a immunotherapy strategy that selectively targets CSCs in the mouse model 4T1-GFP-Luc mimicking TNBC. The phenotype / genotype of mammosphere was initially characterized. Based on genomic analysis of CSC, we have developed an active immunotherapy associated with immunomodulatory agents. We measured the size of tumors and monitored the appearance of metastases by bioluminescence. We performed an immunological study and genomic tumor analysis. The therapeutic combination causes the recruitment of CD4 + and CD8 + T lymphocytes and B lymphocytes with increased CXCL13, the reduction of T reg cells and suppressive myeloid cells in the tumor. This induction of intra-tumor immune response leads to a decrease in tumor size and metastases.This new active immunotherapy can be used in combination with current treatments for prophylactic and curative measures in a wide variety of cancers
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Brancato, Jennifer M. "Defining the Mechanism of Action of Bromodomain and Extraterminal Inhibitors in Triple-Negative Breast Cancers." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1522842642716411.

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Books on the topic "Triple negative breast cancers"

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Tan, Antoinette R., ed. Triple-Negative Breast Cancer. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-69980-6.

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U, Lin Nancy, ed. 100 questions and answers about triple negative breast cancer. Sudbury, Mass: Jones and Bartlett Publishers, 2012.

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Surviving triple negative breast cancer: Hope, treatment, and recovery. Oxford: Oxford University Press, 2013.

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Deng, Xiyun, Faqing Tang, and Thomas J. Rosol. Triple-Negative Breast Cancer. WORLD SCIENTIFIC, 2020. http://dx.doi.org/10.1142/11199.

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Deng, Xiyun, and Junjiang Fu. Triple-Negative Breast Cancer. World Scientific Publishing Co Pte Ltd, 2020.

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Tan, Antoinette R. Triple-Negative Breast Cancer: A Clinician’s Guide. Springer, 2019.

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Tan, Antoinette R. Triple-Negative Breast Cancer: A Clinician’s Guide. Springer, 2018.

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Mir, Manzoor Ahmad. Combinational Therapy in Triple Negative Breast Cancer. Elsevier Science & Technology Books, 2022.

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Mir, Manzoor Ahmad. Combinational Therapy in Triple Negative Breast Cancer. Elsevier Science & Technology, 2022.

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Yarbro, Connie Henke. 100 Q and As about Triple Negative Breast. Jones & Bartlett Learning, LLC, 2019.

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Book chapters on the topic "Triple negative breast cancers"

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Ismail-Khan, Roohi, Susan Minton, and Nazanin Khakpour. "Triple-Negative Breast Cancer." In Breast Disease, 463–72. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1145-5_29.

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Vohra, Poonam, Gregor Krings, and Yunn-Yi Chen. "Less Common Triple Negative Breast Cancers." In A Comprehensive Guide to Core Needle Biopsies of the Breast, 445–518. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26291-8_12.

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Vohra, Poonam, Yunn-Yi Chen, and Gregor Krings. "Less Common Triple-Negative Breast Cancers." In A Comprehensive Guide to Core Needle Biopsies of the Breast, 463–573. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-05532-4_12.

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Telli, Melinda L. "Triple-Negative Breast Cancer." In Molecular Pathology of Breast Cancer, 71–80. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41761-5_6.

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Paquette, Benoit. "Triple-Negative Breast Cancer." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_5981-2.

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Vankina, Ritika, and Yuan Yuan. "Triple-Negative Breast Cancer." In Oncology in the Precision Medicine Era, 209–23. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-31471-2_13.

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Paquette, Benoit. "Triple-Negative Breast Cancer." In Encyclopedia of Cancer, 4658–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_5981.

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Avery, Tiffany P. "Triple-Negative Breast Cancer." In Changing Paradigms in the Management of Breast Cancer, 155–66. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60336-0_11.

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Livasy, Chad A. "Pathologic Evaluation of Triple-Negative Breast Cancer." In Triple-Negative Breast Cancer, 1–22. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-69980-6_1.

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Duma, Narjust, Ciara C. O’Sullivan, Kathryn J. Ruddy, and Alexis D. Leal. "Special Issues in Young Women with Triple-Negative Breast Cancer." In Triple-Negative Breast Cancer, 141–58. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-69980-6_10.

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Conference papers on the topic "Triple negative breast cancers"

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Kern, P., and M. Rezai. "Abstract P2-10-14: Triple Negative Breast Cancer: prognosis of triple-negative breast cancers and non-triple-negative breast cancers in a large registry of certified breast units." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-p2-10-14.

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Sundqvist, M., L. De Koning, G. Rigaill, T. Dubois, and J. Chiquet. "PO-435 Proteomic classification of triple negative breast cancers." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.946.

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Souza, Fabiana Lúcia de Lima, Francielle Souza Silva Lopes, Hellen Karine Paes Porto, and Cesar Augusto Sam Tiago Vilanova Costa. "TRIPLE-NEGATIVE BREAST CANCER AND BRCA1 UNDEREXPRESSION ASSOCIATION: AN EVIDENCEBASED META-ANALYSIS OF CASE–CONTROL STUDIES." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2010.

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Objectives: This meta-analysis aims to evaluate the association of triple-negative breast cancer and BRCA1 gene underexpression by means of a meta-analysis. Methodology: Case–control studies, published between the years 2011 and 2015, were selected from three available databases (PubMed, Scopus, and Web of Science) and were analyzed using Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) recommendations. Literature search was performed using the key words “([triple-negative breast cancer] AND [BRCA1] AND [Associated] AND [expression]).” Study quality was assessed using the Grading of Recommendations, Assessment, Development, and Evaluations (GRADE). The quality of evidence of the studies was classified into four categories: high, moderate, low, or very low quality. We also analyzed the influence of possible conflicts of interest and any information on ethical approval of the studies. Results: A total of 11 studies, out of the 189 studies initially identified, were included in this meta-analysis after applying the inclusion and exclusion criteria. Results show a high prevalence of BRCA1 mutations and underexpression on triple-negative breast cancer patients (χ2 =33.814 and p=0.0001). Studies also show that chemotherapy remains the basis of systemic treatment for breast cancer patients with the BRCA1 mutations and after triple-negative breast cancer treatment, tumor recurrence and resistance to therapy remain a challenging problem. Conclusion: This meta-analysis corroborates other studies that the underexpressive BRCA1 carriers are linked to a higher risk to develop breast cancers that tend to be negative for estrogen (ER), progesterone (PgR), and HER-2 receptor (triple-negative).
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Yuan, Hebao, Hongwei Guo, Feng Li, Joseph Burnett, Miao He, Nathan Truchan, Ila Myers, and Duxin Sun. "Abstract 4788: Abraxane eliminates cancer stem cells in triple-negative breast cancers." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4788.

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Roesler, Alexander S., Smriti Malasi, Elizabeth Lenkiewicz, Barbara A. Pockaj, Michael T. Lewis, Lacey E. Dobrolecki, Lori Koslosky, Peter Hartmayer, Karen S. Anderson, and Michael T. Barrett. "Abstract 1790: PDJ amplicon heterogeneity in triple negative breast cancers." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1790.

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Erson-Bensan, Ayse Elif, Begum H. Akman, Merve Oyken, Hizlan H. Agus, Esra Yavuz, Murat Erdem, and Tolga Can. "Abstract 3374: APA isoform diversity in triple negative breast cancers." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3374.

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Elsberger, B., SM Tovey, BA Tan, SB Brown, VG Brunton, EA Mallon, TG Cooke, and J. Edwards. "Phosphorylated c-Src predicts clinical outcome in triple negative breast cancers." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-2076.

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Kurata, K., M. Kubo, H. Mori, H. Kawaji, Y. Motoyama, L. Kuroki, M. Yamada, K. Kaneshiro, M. Kai, and M. Nakamura. "Abstract P1-06-11: Microsatellite instability in triple negative breast cancers." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p1-06-11.

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Anwar, Talha, Heather Moore, Sarah Bergholtz, and Celina Kleer. "Abstract 4790: Noncanonical functions of EZH2 in triple-negative breast cancers." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4790.

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Agner, Shannon C., Jun Xu, Hussain Fatakdawala, Shridar Ganesan, Anant Madabhushi, Sarah Englander, Mark Rosen, et al. "Segmentation and classification of triple negative breast cancers using DCE-MRI." In 2009 IEEE International Symposium on Biomedical Imaging: From Nano to Macro (ISBI). IEEE, 2009. http://dx.doi.org/10.1109/isbi.2009.5193283.

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Reports on the topic "Triple negative breast cancers"

1

Qi, Chao. PPAR Delta as a Therapeutic Target in Triple-Negative Breast Cancers. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada568147.

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Qi, Chao. PPAR Delta as a Therapeutic Target in Triple-negative Breast Cancers. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada560836.

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Yee, Amy S. Triple Negative Breast Cancer and Metabolic Regulation. Fort Belvoir, VA: Defense Technical Information Center, August 2014. http://dx.doi.org/10.21236/ada612056.

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Gonzalez-Perez, Ruben R. Targeting Breast Cancer Stem Cells In Triple Negative Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613188.

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Gautier, Jean. Evaluating Interstrand Crosslink (ICL) Repair in Triple-Negative Breast Cancers to Guide Chemotherapy. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada586664.

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Richer, Jennifer K. Reversing Anoikis Resistance in Triple-Negative Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613479.

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Cecil, Denise. Development of a Vaccine Targeting Triple-Negative Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada567745.

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Russell, Tanya. Does Lactation Mitigate Triple Negative/Basal Breast Cancer Progression? Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada580133.

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Cecil, Denise. Development of a Vaccine Targeting Triple-Negative Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2013. http://dx.doi.org/10.21236/ada592218.

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Russell, Tanya. Does Lactation Mitigate Triple Negative/Basal Breast Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, November 2013. http://dx.doi.org/10.21236/ada594430.

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