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Journal articles on the topic 'Triple negative breast neoplasms/pathology'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Segovia-Mendoza, Mariana, Susana Romero-Garcia, Cristina Lemini, and Heriberto Prado-Garcia. "Determining Factors in the Therapeutic Success of Checkpoint Immunotherapies against PD-L1 in Breast Cancer: A Focus on Epithelial-Mesenchymal Transition Activation." Journal of Immunology Research 2021 (January 7, 2021): 1–18. http://dx.doi.org/10.1155/2021/6668573.

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Breast cancer is the most common neoplasm diagnosed in women around the world. Checkpoint inhibitors, targeting the programmed death receptor-1 or ligand-1 (PD-1/PD-L1) axis, have dramatically changed the outcome of cancer treatment. These therapies have been recently considered as alternatives for treatment of breast cancers, in particular those with the triple-negative phenotype (TNBC). A further understanding of the regulatory mechanisms of PD-L1 expression is required to increase the benefit of PD-L1/PD-1 checkpoint immunotherapy in breast cancer patients. In this review, we will compile the most recent studies evaluating PD-1/PD-L1 checkpoint inhibitors in breast cancer. We review factors that determine the therapeutic success of PD-1/PD-L1 immunotherapies in this pathology. In particular, we focus on pathways that interconnect the epithelial-mesenchymal transition (EMT) with regulation of PD-L1 expression. We also discuss the relationship between cellular metabolic pathways and PD-L1 expression that are involved in the promotion of resistance in TNBC.

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Segovia-Mendoza, Mariana, Susana Romero-Garcia, Cristina Lemini, and Heriberto Prado-Garcia. "Determining Factors in the Therapeutic Success of Checkpoint Immunotherapies against PD-L1 in Breast Cancer: A Focus on Epithelial-Mesenchymal Transition Activation." Journal of Immunology Research 2021 (January 7, 2021): 1–18. http://dx.doi.org/10.1155/2021/6668573.

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Breast cancer is the most common neoplasm diagnosed in women around the world. Checkpoint inhibitors, targeting the programmed death receptor-1 or ligand-1 (PD-1/PD-L1) axis, have dramatically changed the outcome of cancer treatment. These therapies have been recently considered as alternatives for treatment of breast cancers, in particular those with the triple-negative phenotype (TNBC). A further understanding of the regulatory mechanisms of PD-L1 expression is required to increase the benefit of PD-L1/PD-1 checkpoint immunotherapy in breast cancer patients. In this review, we will compile the most recent studies evaluating PD-1/PD-L1 checkpoint inhibitors in breast cancer. We review factors that determine the therapeutic success of PD-1/PD-L1 immunotherapies in this pathology. In particular, we focus on pathways that interconnect the epithelial-mesenchymal transition (EMT) with regulation of PD-L1 expression. We also discuss the relationship between cellular metabolic pathways and PD-L1 expression that are involved in the promotion of resistance in TNBC.

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3

Geyer, Felipe C., Samuel H. Berman, Caterina Marchiò, Kathleen A. Burke, Elena Guerini-Rocco, Salvatore Piscuoglio, Charlotte KY Ng, et al. "Genetic analysis of microglandular adenosis and acinic cell carcinomas of the breast provides evidence for the existence of a low-grade triple-negative breast neoplasia family." Modern Pathology 30, no. 1 (October 7, 2016): 69–84. http://dx.doi.org/10.1038/modpathol.2016.161.

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4

Nadhan, Revathy, Jayashree Vijaya Vaman, Satheesh Kumar Sengodan, Sreelatha Krishnakumar Hemalatha, Nirmala Chellappan, Santha Sadasivan, Aysha Pasuthottiyil Varkey, et al. "BRCA1 promoter hypermethylation in human placenta: a hidden link with β-hCG expression." Carcinogenesis 41, no. 5 (June 14, 2019): 611–24. http://dx.doi.org/10.1093/carcin/bgz117.

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AbstractGestational trophoblastic diseases (GTD) are group of pregnancy-related tumors characterized by abnormal levels of ‘β-hCG’ with higher incidence in South-East Asia, especially India. Our laboratory has reported that wild-type BRCA1 transcriptionally regulates β-hCG in triple negative breast cancers (TNBCs). These factors culminated into analysis of BRCA1 status in GTD, which would emanate into elucidation of BRCA1- β-hCG relationship and unraveling etio-pathology of GTD. BRCA1 level in GTD is down-regulated due to the over-expression of DNMT3b and subsequent promoter hypermethylation, when compared to the normal placentae accompanied with its shift in localization. There is an inverse correlation of serum β-hCG levels with BRCA1 mRNA expression. The effects of methotrexate (MTX), which is the first-line chemotherapeutic used for GTD treatment, when analyzed in comparison with plumbagin (PB) revealed that PB alone is efficient than MTX alone or MTX-PB in combination, in showing selective cytotoxicity against GTD. Interestingly, PB increases BRCA1 levels post-treatment, altering DNMT3b levels and resultant BRCA1 promoter methylation. Also, cohort study analyzed the incidence of GTD at Sree Avittom Thirunal (SAT) Hospital, Thiruvananthapuram, which points out that 11.5% of gestational trophoblastic neoplasia (GTN) cases were referred to Regional Cancer Centre, Thiruvananthapuram, for examination of breast lumps. This has lend clues to supervene the risk of GTD patients towards BRCA1-associated diseases and unveil novel therapeutic for GTD, a plant-derived naphthoquinone, PB, already reported as selectively cytotoxic against BRCA1 defective tumors.

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5

Livasy, Chad A. "Triple-Negative Breast Carcinoma." Surgical Pathology Clinics 2, no. 2 (June 2009): 247–61. http://dx.doi.org/10.1016/j.path.2009.02.005.

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6

Bose, Shikha. "Triple-negative Breast Carcinoma." Advances In Anatomic Pathology 22, no. 5 (September 2015): 306–13. http://dx.doi.org/10.1097/pap.0000000000000084.

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7

Lerma, Enrique, Agusti Barnadas, and Jaime Prat. "Triple Negative Breast Carcinomas." Applied Immunohistochemistry & Molecular Morphology 17, no. 6 (December 2009): 483–94. http://dx.doi.org/10.1097/pai.0b013e3181a725eb.

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8

Dietze, Eric C., Tanya A. Chavez, and Victoria L. Seewaldt. "Obesity and Triple-Negative Breast Cancer." American Journal of Pathology 188, no. 2 (February 2018): 280–90. http://dx.doi.org/10.1016/j.ajpath.2017.09.018.

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9

Shousha, Sami, David Peston, Ondrej Gojis, and Carlo Palmieri. "An unusual triple-negative breast carcinoma." Histopathology 55, no. 3 (September 2009): 364–66. http://dx.doi.org/10.1111/j.1365-2559.2009.03349.x.

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10

Geyer, Felipe C., Fresia Pareja, Britta Weigelt, Emad Rakha, Ian O. Ellis, Stuart J. Schnitt, and Jorge S. Reis-Filho. "The Spectrum of Triple-Negative Breast Disease." American Journal of Pathology 187, no. 10 (October 2017): 2139–51. http://dx.doi.org/10.1016/j.ajpath.2017.03.016.

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11

O'Toole, Sandra A., Jane M. Beith, Ewan K. A. Millar, Richard West, Anna McLean, Aurelie Cazet, Alexander Swarbrick, and Samantha R. Oakes. "Therapeutic targets in triple negative breast cancer." Journal of Clinical Pathology 66, no. 6 (February 22, 2013): 530–42. http://dx.doi.org/10.1136/jclinpath-2012-201361.

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12

Khan, Ashraf, and Otto Walter. "IMP3 expression in triple-negative breast carcinoma - Reply." Human Pathology 41, no. 9 (September 2010): 1356–57. http://dx.doi.org/10.1016/j.humpath.2010.05.005.

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13

Miller, Tiffany Renee, Ashlie Elizabeth Rubrecht, Jaya Ruth Asirvatham, Mehmet R. Genc, and Archana Shenoy. "Microscopic Placental Metastasis in Triple Negative Breast Carcinoma." International Journal of Surgical Pathology 28, no. 5 (October 15, 2019): 521–22. http://dx.doi.org/10.1177/1066896919880964.

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14

Rao, Deepthi, Bruce F. Kimler, Warren B. Nothnick, Marilyn K. Davis, Fang Fan, and Ossama Tawfik. "Transgelin: a potentially useful diagnostic marker differentially expressed in triple-negative and non–triple-negative breast cancers." Human Pathology 46, no. 6 (June 2015): 876–83. http://dx.doi.org/10.1016/j.humpath.2015.02.015.

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15

Jiagge, Evelyn, Dhananjay Chitale, and Lisa A. Newman. "Triple-Negative Breast Cancer, Stem Cells, and African Ancestry." American Journal of Pathology 188, no. 2 (February 2018): 271–79. http://dx.doi.org/10.1016/j.ajpath.2017.06.020.

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16

Jung, Hee Chan, Sung Hwan Kim, Jeong Hoon Lee, Ju Han Kim, and Sung Won Han. "Gene Regulatory Network Analysis for Triple-Negative Breast Neoplasms by Using Gene Expression Data." Journal of Breast Cancer 20, no. 3 (2017): 240. http://dx.doi.org/10.4048/jbc.2017.20.3.240.

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17

Romero, Pierre, Vanessa Benhamo, Gabrielle Deniziaut, Laetitia Fuhrmann, Frédérique Berger, Elodie Manié, Jaydutt Bhalshankar, et al. "Medullary Breast Carcinoma, a Triple-Negative Breast Cancer Associated with BCLG Overexpression." American Journal of Pathology 188, no. 10 (October 2018): 2378–91. http://dx.doi.org/10.1016/j.ajpath.2018.06.021.

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18

Matikas, Alexios, Georgios Lazaridis, and Sofa Agelaki. "Triple-Negative Breast Cancer: One Or More Entities?" Forum of Clinical Oncology 5, no. 2 (December 10, 2014): 20–31. http://dx.doi.org/10.2478/fco-2014-0010.

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Abstract Characterized by an aggressive clinical course and relatively poor prognosis, triple-negative breast cancer (TNBC) refers to a diverse group of tumors with distinct molecular characteristics rather than to a single entity. The recognition of distinct gene expression subtypes within the group of TNBC and the description of an ever-expanding set of genetic events has led to improved understanding of the underlying biology. However, the improvement of clinical results has been incremental despite undergoing efforts to evaluate the role of molecularly targeted agents in the treatment of TNBC. The relative rarity of each one of these genetic events increases the difficulty of conducting large clinical trials, further hindering our ability to identify meaningful, personalized treatment approaches. Herein, we summarize current knowledge on TNBC, focusing on molecular pathology and emerging treatment approaches.

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19

D'Alfonso, Timothy M., Jeffrey Hannah, Zhengming Chen, Yifang Liu, Pengbo Zhou, and Sandra J. Shin. "Axl receptor tyrosine kinase expression in breast cancer." Journal of Clinical Pathology 67, no. 8 (June 5, 2014): 690–96. http://dx.doi.org/10.1136/jclinpath-2013-202161.

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AimsTriple-negative breast cancer comprises a clinically aggressive group of invasive carcinomas. We examined a published gene expression screen of a panel of breast cancer cell lines to identify a potential triple-negative breast cancer-specific gene signature, and attempted to verify our findings by performing immunohistochemical analysis on tissue microarrays containing a large cohort of invasive breast carcinomas.MethodsThe microarray dataset for a panel of human breast cancer cell lines was interrogated for triple-negative breast cancer-specific genes. Membranous immunohistochemical expression of the protein product of the AXL gene was assessed semiquantitatively in 569 invasive breast carcinomas grouped according to molecular subgroup by immunohistochemistry.ResultsAXL was significantly upregulated in triple-negative/basal B cell lines compared with luminal or basal A cell lines. No significant difference was observed in the level of immunohistochemical expression of Axl protein between triple-negative breast cancers and other molecular subgroups (p=0.257). Axl expression was significantly associated with lymphovascular invasion (LVI) in all subgroups combined (p=0.033), and within the luminal A (p=0.002) and triple-negative breast cancer subgroups (p=0.026).ConclusionsDespite preferential upregulation of AXL in triple-negative/basal B cell lines, analysis of Axl protein expression in a large series of patients’ breast tumours revealed no association between Axl expression and triple-negative breast cancer or other subtype. The association of Axl expression with LVI supports previous work that implicates Axl as a promoter of invasiveness in breast cancer cell lines. Further studies are necessary to explore whether Axl expression of individual breast cancer tumours can be clinically useful.

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20

Downs-Kelly, Erinn, and Michael Z. Gilcrease. "Matrix-producing Carcinoma: Just Another Triple-negative Breast Cancer?" American Journal of Surgical Pathology 34, no. 1 (January 2010): 125–26. http://dx.doi.org/10.1097/pas.0b013e3181c4badf.

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21

Dusenbery, Anna C., Joseph L. Maniaci, Natalie D. Hillerson, Erik A. Dill, Timothy N. Bullock, and Anne M. Mills. "MHC Class I Loss in Triple-negative Breast Cancer." American Journal of Surgical Pathology 45, no. 5 (January 11, 2021): 701–7. http://dx.doi.org/10.1097/pas.0000000000001653.

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22

Thike, Aye Aye, Poh Yian Cheok, Ana Richelia Jara-Lazaro, Benita Tan, Patrick Tan, and Puay Hoon Tan. "Triple-negative breast cancer: clinicopathological characteristics and relationship with basal-like breast cancer." Modern Pathology 23, no. 1 (October 23, 2009): 123–33. http://dx.doi.org/10.1038/modpathol.2009.145.

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23

Hanna, Courtney A., Isam Eltoum, and Shantel Hebert-Magee. "Triple Negative Breast Cancer: Are There Rapidly Distinguishable Cytomorphological Features?" Journal of the American Society of Cytopathology 2, no. 1 (October 2013): S7—S8. http://dx.doi.org/10.1016/j.jasc.2013.08.017.

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24

Zhou, Ling, Ke Li, Yanli Luo, Ling Tian, Min Wang, Chuanyuan Li, and Qian Huang. "Novel prognostic markers for patients with triple-negative breast cancer." Human Pathology 44, no. 10 (October 2013): 2180–87. http://dx.doi.org/10.1016/j.humpath.2013.03.021.

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25

Guney Eskiler, Gamze, Gulsah Cecener, Unal Egeli, and Berrin Tunca. "Triple negative breast cancer: new therapeutic approaches andBRCAstatus." APMIS 126, no. 5 (April 25, 2018): 371–79. http://dx.doi.org/10.1111/apm.12836.

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26

Ameer, Amna, Farhan Akhtar, Hafeez Ud Din, and Rabia Ahmad. "IMMUNOHISTOCHEMICAL EXPRESSION OF ANDROGEN RECEPTOR IN TRIPLE NEGATIVE BREAST CARCINOMA AT ARMED FORCES INSTITUTE OF PATHOLOGY, RAWALPINDI." PAFMJ 71, no. 1 (February 23, 2021): 7–11. http://dx.doi.org/10.51253/pafmj.v71i1.4687.

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Objective: To determine the frequency of immunohistochemical expression of androgen receptor in triplenegative breast carcinoma. Study Design: Cross sectional study. Duration and Place of Study: This study included 30 cases confirmed as triple negative breast carcinoma atArmed Forces Institute of Pathology Rawalpindi, from Jan to Jul 2018. Methodology: Anti-androgen receptor antibody was applied and assessed. Positive expression was defined asgreater and equal to 10% nuclear immunostaining. SPSS-24 was used for analyzing data. Results: Out of 30 cases of triple negative breast carcinoma (TNBC), all patients were female. Patients’ agesranged between 21-72 years with a mean age of 46.35 years and a standard deviation of ± 13.4. Androgen receptor expression was positive in 8 cases (27%) of all triple negative breast carcinomas. Out of these androgen receptor (AR) triple negative breast carcinomas; all 8 cases were of histological subtype invasive ductal (mammary) carcinoma, non special type, 7 cases (23%) were of histological grade 3 and 1 was of histological grade 2. Conclusion: Androgen receptor expression is observed in 8 cases (27%) of triple negative breast carcinoma cases. Such patients can be selected as candidates for anti- androgen receptor targeted therapy.

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Tolba, NS, AS Alsedfy, SW Skandar, and YM El-Kerm. "Expression of Transgelin in Triple Negative and Non Triple Negative Breast Cancer: A Differential Study." Tumori Journal 106, no. 1_suppl (April 2020): 20. http://dx.doi.org/10.1177/0300891620914150.

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Introduction: Triple negative breast cancer (TNBC) is defined by the absence of ER expression, PR expression and HER2 amplification. No targeted treatment is available for TNBC and chemotherapy remains the best therapeutic option. However, in the case of recurrence or chemo-resistance, therapeutic options are very limited. TNBC presents a high rate of proliferation and is highly aggressive having low survival rate. As the complexity of this disease is being simplified over time, new targets are also being discovered for the treatment of this disease. Therefore, there is still need for new biomarkers, which would serve for targeted treatment. Transgelin was proposed as a new potential cancer biomarker. Altered expression of Transgelin has been described in a wide range of cancers, often with contradictory results. The aim of the study was to compare Transgelin expression across molecular subtypes of breast cancer, to identify if it can be used as a future molecular targeted protein for TNBC. Material and Methods: Transgelin immunohistochemistry was applied on 60 retrospectively collected paraffin blocks of patients presenting with invasive breast carcinoma (NST) having different molecular subtypes. Blocks were collected between 2015 and 2016 from Pathology department, Medical Research Institute, Egypt. Her2 equivocal cases were excluded from the study. Results: Transgelin expression was positive in 23 cases and negative in 37 cases. There was a statistically significant difference between (Transgelin +) and (Transgelin -) cases being highly expressed in TNBC in comparison to other molecular subtypes. It was also highly expressed in tumors with large size, high grade, positive lymph-vascular invasion status & lymph node metastasis. There was no statistically significant difference between (Transgelin+) and (Transgelin-) as regards age and Her2 status. Conclusions: Transgelin is an aggressive biomarker differentially expressed among the molecular breast cancer subtypes with high expression in TNBC. Transgelin may provide a potential target for future treatment of TNBC.

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Kala, Chayanika, Mohd Athar, Sanjay Kala, Lubna Khan, RamendraK Jauhari, and Amitabh Satsangi. "Clinical and cyto-morphological characterization of triple negative breast cancer." Journal of Cytology 36, no. 2 (2019): 84. http://dx.doi.org/10.4103/joc.joc_47_18.

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Vona-Davis, Linda, David P. Rose, Vijaya Gadiyaram, Barbara Ducatman, Gerald Hobbs, Hannah Hazard, Sobha Kurian, and Jame Abraham. "Breast Cancer Pathology, Receptor Status, and Patterns of Metastasis in a Rural Appalachian Population." Journal of Cancer Epidemiology 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/170634.

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Breast cancer patients in rural Appalachia have a high prevalence of obesity and poverty, together with more triple-negative phenotypes. We reviewed clinical records for tumor receptor status and time to distant metastasis. Body mass index, tumor size, grade, nodal status, and receptor status were related to metastatic patterns. For 687 patients, 13.8% developed metastases to bone (n=42) or visceral sites (n=53). Metastases to viscera occurred within five years, a latent period which was shorter than that for bone (P=0.042). More women with visceral metastasis presented with grade 3 tumors compared with the bone and nonmetastatic groups (P=0.0002). There were 135/574 women (23.5%) with triple-negative breast cancer, who presented with lymph node involvement and visceral metastases (68.2% versus 24.3%;P=0.033). Triple-negative tumors that metastasized to visceral sites were larger (P=0.007). Developing a visceral metastasis within 10 years was higher among women with triple-negative tumors. Across all breast cancer receptor subtypes, the probability of remaining distant metastasis-free was greater for brain and liver than for lung. The excess risk of metastatic spread to visceral organs in triple-negative breast cancers, even in the absence of positive nodes, was combined with the burden of larger and more advanced tumors.

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Liu, Huan-Tao, Rong Ma, Qi-Feng Yang, Gang Du, and Cui-Juan Zhang. "Lymphangiogenic Characteristics of Triple Negativity in Node-Negative Breast Cancer." International Journal of Surgical Pathology 17, no. 6 (June 3, 2009): 426–31. http://dx.doi.org/10.1177/1066896909337505.

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31

Yu, Kangjie, Joseph Rohr, Yang Liu, Mingyang Li, Junpeng Xu, Kaijing Wang, Jia Chai, et al. "Progress in triple negative breast carcinoma pathophysiology: Potential therapeutic targets." Pathology - Research and Practice 216, no. 4 (April 2020): 152874. http://dx.doi.org/10.1016/j.prp.2020.152874.

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32

Alsaleem, Mansour A., Graham Ball, Michael S. Toss, Sara Raafat, Mohammed Aleskandarany, Chitra Joseph, Angela Ogden, et al. "A novel prognostic two-gene signature for triple negative breast cancer." Modern Pathology 33, no. 11 (May 13, 2020): 2208–20. http://dx.doi.org/10.1038/s41379-020-0563-7.

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33

Ginter, Paula S., Zhiyan Fu, and Sandra J. Shin. "Low-grade variants of triple-negative breast carcinoma (TNBC): a review." Diagnostic Histopathology 26, no. 2 (February 2020): 51–60. http://dx.doi.org/10.1016/j.mpdhp.2019.10.019.

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Ueda, Ai, Keiki Oikawa, Koji Fujita, Akio Ishikawa, Eiichi Sato, Takashi Ishikawa, Masahiko Kuroda, and Kohsuke Kanekura. "Therapeutic potential of PLK1 inhibition in triple-negative breast cancer." Laboratory Investigation 99, no. 9 (April 17, 2019): 1275–86. http://dx.doi.org/10.1038/s41374-019-0247-4.

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Sullivan, Harold C., Gabriela Oprea-Ilies, Amy L. Adams, Andrew J. Page, Sungjin Kim, Jason Wang, and Cynthia Cohen. "Triple-negative Breast Carcinoma in African American and Caucasian Women." Applied Immunohistochemistry & Molecular Morphology 22, no. 1 (January 2014): 17–23. http://dx.doi.org/10.1097/pai.0b013e318281148e.

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Mrklić, Ivana, Zenon Pogorelić, Vesna Ćapkun, and Snježana Tomić. "Expression of Topoisomerase II-α in Triple Negative Breast Cancer." Applied Immunohistochemistry & Molecular Morphology 22, no. 3 (March 2014): 182–87. http://dx.doi.org/10.1097/pai.0b013e3182910967.

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O’Reilly, Elma A., Luke Gubbins, Shiva Sharma, Riona Tully, Matthew Ho Zhing Guang, Karolina Weiner-Gorzel, John McCaffrey, et al. "The fate of chemoresistance in triple negative breast cancer (TNBC)." BBA Clinical 3 (June 2015): 257–75. http://dx.doi.org/10.1016/j.bbacli.2015.03.003.

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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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Sahin Ozkan, Hulya, Mustafa Umit Ugurlu, Perran Fulden Yumuk, and Handan Kaya. "Prognostic Role of Immune Markers in Triple Negative Breast Carcinoma." Pathology & Oncology Research 26, no. 4 (July 17, 2020): 2733–45. http://dx.doi.org/10.1007/s12253-020-00874-4.

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Matsumoto, Hirofumi, Si-lin Koo, Rebecca Dent, Puay Hoon Tan, and Jabed Iqbal. "Role of inflammatory infiltrates in triple negative breast cancer: Table 1." Journal of Clinical Pathology 68, no. 7 (March 6, 2015): 506–10. http://dx.doi.org/10.1136/jclinpath-2015-202944.

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Liu, Rong-Zong, Kathryn Graham, Darryl D. Glubrecht, Devon R. Germain, John R. Mackey, and Roseline Godbout. "Association of FABP5 Expression With Poor Survival in Triple-Negative Breast Cancer." American Journal of Pathology 178, no. 3 (March 2011): 997–1008. http://dx.doi.org/10.1016/j.ajpath.2010.11.075.

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42

Krings, Gregor, Michael Nystrom, Irum Mehdi, Poonam Vohra, and Yunn-Yi Chen. "Diagnostic utility and sensitivities of GATA3 antibodies in triple-negative breast cancer." Human Pathology 45, no. 11 (November 2014): 2225–32. http://dx.doi.org/10.1016/j.humpath.2014.06.022.

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43

Vtorushin, S. V., N. V. Krakhmal, and M. V. Zavyalova. "Triple-negative breast cancer. Modern molecular genetic concepts and their clinical significance." Arkhiv patologii 83, no. 3 (2021): 46. http://dx.doi.org/10.17116/patol20218302146.

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44

Loo, Claudette E., Marieke E. Straver, Sjoerd Rodenhuis, Sara H. Muller, Jelle Wesseling, Marie-Jeanne T. F. D. Vrancken Peeters, and Kenneth G. A. Gilhuijs. "Magnetic Resonance Imaging Response Monitoring of Breast Cancer During Neoadjuvant Chemotherapy: Relevance of Breast Cancer Subtype." Journal of Clinical Oncology 29, no. 6 (February 20, 2011): 660–66. http://dx.doi.org/10.1200/jco.2010.31.1258.

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Purpose To evaluate the relevance of breast cancer subtypes for magnetic resonance imaging (MRI) markers for monitoring of therapy response during neoadjuvant chemotherapy (NAC). Patients and Methods MRI examinations were performed in 188 women before and during NAC. MRI interpretation included lesion morphology at baseline, changes in morphology, size, and contrast uptake kinetics (initial and late enhancement). By using immunohistochemistry, tumors were divided into three subtypes: triple negative, human epidermal growth factor receptor 2 (HER2) positive, and estrogen receptor (ER) positive/HER2 negative. Tumor response was assessed dichotomously (ie, presence or absence of residual tumor in the surgical specimen). Complementary, a continuous scale assessment was used (the breast response index [BRI], representing the relative change in tumor stage). Multivariate regression analysis and receiver operating characteristic analysis were employed to establish significant associations. Results Residual tumor at pathology was present in 31 (66%) of 47 triple-negative tumors, 23 (61%) of 38 HER2-positive tumors, and 96 (93%) of 103 ER-positive/HER2-negative tumors. Multivariate analysis of residual disease showed significant associations between breast cancer subtype and MRI (area under the curve [AUC], 0.84; P < .001). BRI also showed significant correlation among breast cancer subtype, MRI, and age (Pearson's r = 0.465; P < .001). In subset analysis, this was only significant for triple-negative tumors (P < .001) and HER2-positive tumors (P < .05). Residual tumor after NAC in the triple-negative and HER2-positive group is significantly associated with the change in largest diameter of late enhancement during NAC (AUC, 0.76; P < .001). No associations were found for ER-positive/HER2-negative tumors. Conclusion MRI during NAC to monitor response is effective in triple-negative or HER2-positive disease but is inaccurate in ER-positive/HER2-negative breast cancer.

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Kuroda, Naoto, Masahiko Ohara, Kaori Inoue, Keiko Mizuno, Nokiaki Fujishima, Nobumasa Hamaguchi, and Gang-Hong Lee. "The majority of triple-negative breast cancer may correspond to basal-like carcinoma, but triple-negative breast cancer is not identical to basal-like carcinoma." Medical Molecular Morphology 42, no. 2 (June 2009): 128–31. http://dx.doi.org/10.1007/s00795-008-0428-5.

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Kim, Ji Yeon, Taeeun Kim, and Eun Yoon Cho. "Comparative Study of Metaplastic Breast Carcinoma and Triple-Negative Breast Carcinoma Using Histologic and Immunohistochemical Analyses." Korean Journal of Pathology 44, no. 6 (2010): 605. http://dx.doi.org/10.4132/koreanjpathol.2010.44.6.605.

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Roitberg, G. E., J. V. Dorosh, and O. Yu Anikeeva. "Treatment of thrice-negative breast cancer in a patient with metabolic syndrome." Research and Practical Medicine Journal 8, no. 1 (March 10, 2021): 62–68. http://dx.doi.org/10.17709/2409-2231-2021-8-1-6.

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Breast cancer (BC) remains one of the most common diseases of the female population. According to statistics, breast cancer is detected in every eighth woman. Approximately 20‑24% of breast cancer patients are diagnosed with triple negative breast cancer. Triple‑negative breast cancer is characterized by an aggressive clinical course, a higher relapse rate, and low overall survival. According to statistics, the median survival rate for women with metastatic triple‑negative breast cancer is less than one year. We demonstrate a successful case of treatment of a 60‑year‑old woman diagnosed with triple negative breast cancer on the right, edematous‑infiltrative form, St IIIC cT4bN3M0 on the background of metabolic syndrome. Antitumor treatment lasted 1 year and consisted of three stages: systemic chemotherapy, surgical treatment (radical mastectomy), and adjuvant radiation therapy. After the treatment, remission was achieved. The patient is alive and has a relapse‑free period of 3 years. Conclusion. Despite the severe concomitant pathology in the observed patient, we received a positive result of multi‑ stage therapy, where cytotoxic chemotherapy was the basic treatment for a woman with triple negative breast cancer.

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Hashmi, Atif, Muhammad Edhi, Hanna Naqvi, Naveen Faridi, Amna Khurshid, and Mehmood Khan. "Clinicopathologic features of triple negative breast cancers: an experience from Pakistan." Diagnostic Pathology 9, no. 1 (2014): 43. http://dx.doi.org/10.1186/1746-1596-9-43.

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Li, Mingyang, Jingwei Liu, Sihui Li, Yanling Feng, Fei Yi, Liang Wang, Shi Wei, and Liu Cao. "Autophagy-related 7 modulates tumor progression in triple-negative breast cancer." Laboratory Investigation 99, no. 9 (April 15, 2019): 1266–74. http://dx.doi.org/10.1038/s41374-019-0249-2.

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Atchley, Deann P., Constance T. Albarracin, Adriana Lopez, Vicente Valero, Christopher I. Amos, Ana Maria Gonzalez-Angulo, Gabriel N. Hortobagyi, and Banu K. Arun. "Clinical and Pathologic Characteristics of Patients With BRCA-Positive and BRCA-Negative Breast Cancer." Journal of Clinical Oncology 26, no. 26 (September 10, 2008): 4282–88. http://dx.doi.org/10.1200/jco.2008.16.6231.

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Purpose Mutations in the BRCA1 and BRCA2 genes confer greater risk of developing breast cancer. We determined whether tumor pathologic features and clinical features differ in patients with and without BRCA mutations. Patients and Methods Tumor pathologic features and clinical characteristics were examined in 491 women with breast cancer who underwent genetic testing for BRCA mutations between 1997 and 2006. A retrospective review of medical records was conducted to determine clinical characteristics including ethnicity, age and clinical stage at diagnosis, age at parity, number of full-term pregnancies, use of oral contraceptives and hormone replacement therapy, and BRCA mutation status. Tumor pathology was reviewed to determine histologic type, tumor grade, and estrogen receptor, progesterone receptor, and HER-2/neu status. Results Of the 491 patients with identified breast cancers, 391 patients were BRCA negative, and 86 patients were BRCA positive. Triple-negative breast cancer (ie, those with negative estrogen receptor, progesterone receptor, and HER-2/neu status) was diagnosed in 57.1% of the BRCA1-positive patients, 23.3% of the BRCA2-positive patients, and 13.8% of the BRCA-negative patients. BRCA1 mutation carriers had higher nuclear grade tumors than the other two groups (P < .001). Of the triple-negative cancer patients, BRCA2 mutation carriers were older when diagnosed than BRCA1 mutation carriers and noncarriers (P < .01). Conclusion These results suggest that tumors associated with BRCA1 mutations may be divided into two distinct groups, triple-negative and non–triple-negative groups. Future studies should seek to determine whether patients with BRCA1 mutations and triple-negative breast cancer respond to treatment better than BRCA-negative patients with similar tumor pathology.

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