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Monaco, M.L.; Idris, O.A.; Essani, K. Basic Biology of Triple-Negative Breast Cancer. Encyclopedia. Available online: https://encyclopedia.pub/entry/43892 (accessed on 02 July 2024).
Monaco ML, Idris OA, Essani K. Basic Biology of Triple-Negative Breast Cancer. Encyclopedia. Available at: https://encyclopedia.pub/entry/43892. Accessed July 02, 2024.
Monaco, Michael L., Omer A. Idris, Karim Essani. "Basic Biology of Triple-Negative Breast Cancer" Encyclopedia, https://encyclopedia.pub/entry/43892 (accessed July 02, 2024).
Monaco, M.L., Idris, O.A., & Essani, K. (2023, May 05). Basic Biology of Triple-Negative Breast Cancer. In Encyclopedia. https://encyclopedia.pub/entry/43892
Monaco, Michael L., et al. "Basic Biology of Triple-Negative Breast Cancer." Encyclopedia. Web. 05 May, 2023.
Basic Biology of Triple-Negative Breast Cancer
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This entry is adapted from the peer-reviewed paper 10.3390/cancers15082393

Triple-negative breast cancer (TNBC) is an aggressive as well as the most dangerous form of breast cancer. Due to the lack of biomarkers that can be targeted by specific molecular therapeutics, treatment is usually limited to chemotherapy and surgery where applicable. 

triple-negative breast cancer metastasis cancer biology standard of care pathogenesis of cancer

1. Triple-Negative Breast Cancer (TNBC)

Breast cancer (BC) is the most diagnosed cancer in the United States for women, and is also the number two killer among cancers in women [1][2]. The biggest challenge with BC treatment lies in the heterogeneity of the tumors. There are three different receptors that define different BC subtypes: estrogen receptors (ERs, inside cells), progesterone receptors (PRs, inside cells), and human epidermal growth factor receptor 2 (HER-2, also named CD340, a cell surface receptor) [3][4]. Of all of the new cases of BC each year, approximately 10–20% are negative for all 3 receptors and are categorized as triple-negative breast cancer (TNBC) [5][6]; however, within TNBC itself, there are several different subtypes based on differential gene expression. These types are as follows: basal-like (BL1 and BL2), mesenchymal (M), mesenchymal-stem-cell-like (MSL), immunomodulatory (IM), and luminal androgen receptor (LAR) [7][8][9][10].
The BL1 and BL2 subtypes differ in that BL1 has elevated gene expression for DNA damage response, proliferation signaling, and cell cycle checkpoint loss, whereas BL2 has elevated growth factor (GF) signaling, glycolysis/gluconeogenesis signaling, and myoepithelial surface receptors. This suggests that cells of the BL1/2 subtypes may be of basal or myoepithelial origin. The M subtype has elevated expression of cell motility pathways, receptor interaction with the extracellular matrix (ECM), and cell differentiation pathways. The MSL subtype shares expression with the M subtype, but it also uniquely expresses pathways related to GF signaling (inositol phosphate metabolism, platelet-derived growth factor (PDGF), epidermal growth factor receptor (EGFR), calcium (Ca2+), G-protein-coupled receptor (GPCR), and extracellular-related kinase (ERK 1 and 2)), epithelial–mesenchymal transition (EMT), and Wnt/β-catenin. The MSL subtype also has a reduced expression of genes for cell proliferation. The IM subtype has an elevated expression of pathways involving immune cell signaling, cytokine signaling, antigen processing/presentation, and immune signal transduction. Finally, the LAR subtype has a heavily elevated expression of pathways related to hormone regulation, particularly with androgen receptor signaling (which can be approximately nine times as much as that of other TNBC subtypes) [8]. These extremely diverse genetic regulation conditions define tumor heterogeneity within TNBC, which helps to explain why TNBC is extremely difficult to treat in comparison with other BCs [8][11].

2. Development of Heterogeneity in Triple-Negative Breast Cancer

There have been a few theories to describe how heterogeneity in TNBC is established and maintained. The two main concepts are the cancer stem cell (CSC) hypothesis and the clonal evolution model (CEM). Other concepts, such as the deregulation of adult mammary stem cells (aMSCs), are described as contributing to developing TNBC in its initial stages [12][13][14][15].
The division of aMSCs gives rise to progenitors that further differentiate into basal or luminal progenitor cells. Under normal conditions, if basal or luminal progenitor cells are made, they further develop into mature basal or luminal cells; however, when the development of luminal progenitors is disrupted, cancer cells may develop. This is believed to occur via the improper regulation of Wnt/β-catenin pathways, transcription factors (TFs), such as Snail, and embryonic stem cell (ESC) markers (Sox2, Nanog, and Oct4). Combinations of genetic alterations to these pathways can make the progenitor cells de-differentiate and return to a proliferative state, which, when combined with other mutations, may result in TNBC [15].
The CSC model proposes that there is a hierarchy within cancers of tumorigenic cancer cells and their non-tumorigenic progeny. Within these subpopulations, the CSCs are hypothesized to be the driving forces behind the growth of a tumor, its progression, resistance to certain treatments, and metastasis [12][16][17][18][19]. This model does not address how to account for the massive variability in tumor heterogeneity between cancers of the same type in different individuals. Early characterizations of tumorigenic CSCs in BCs were via the expression of CD44 and not CD24 (including the opposite expression pattern); however, these characterizations have not held because many subtypes do not follow these marker patterns [12]. Moreover, the alteration of aldehyde dehydrogenase 1 (ALDH1) expression has also been independently reported to have tumorigenic potential in BCs [20].
The CEM presumes that there is one original clone that becomes cancerous, which then divides and, as carcinogenesis progresses, the cell as well as its subsequent progeny accumulate mutations in each cycle of clonal expansion, which results in the heterogeneity of the tumor. This model also assumes that there is no hierarchy among the cells and that, instead, natural selection determines which clones are successful and continue to divide. The cells that cannot undergo division are maintained as part of the tumor or will senesce, eventually being eliminated via necrosis [13][14]. Tumor heterogeneity may originate via some combination of the two models and several additional variables, including environmental factors, genetic background, and immune status. Hence, additional studies are needed to define the role of these contributing factors in individual cancers in order to formulate a more comprehensive model in the future.

3. Triple-Negative Breast Cancer Pathogenesis

Among the approximately 268,600 new cases of BC in the United States in 2019, about 10–20% of these were TNBC [21]. Estimates for 2022 suggested 287,850 new cases of BC in women of the United States, resulting in approximately 43,250 deaths [1]. TNBC, as a whole, is more aggressive, has more p53 mutations, has higher mitotic indices, has less defined nuclear pleomorphisms, has a higher average grade, and demonstrates higher rates of proliferation than typical BCs [22]. In addition to the above, TNBC has a high risk for relapsing in a patient following therapy, which factors into its high mortality compared to other BCs [23].
In the development and progression of carcinogenesis, epithelial–mesenchymal transition (EMT) has been repeatedly shown to be important in changing cell profile, metastasis, and even tumor recurrence [24][25][26]. Two genes, SLUG (a transcriptional repressor and regulator) and SOX10 (a TF), have been shown to have increased and preferential expression within TNBC. It has been shown that, when ALDH1 is simultaneously expressed with SLUG, there is an association with shorter disease-free survival rates and the conversion from EMT into mesenchymal–epithelial transition (MET) in metastatic sites. MET is the reverse of EMT, and it is denoted by the reacquisition of epithelial characteristics [27][28]. Of the TNBC subtypes, M and MSL have been linked to metaplastic BCs expressing some of these characteristics [29].
Another factor that contributes to the difficulty in treating TNBCs is the high degree of variance among the mutations acquired. The most common mutations are to p53 (up to 80%), followed by phosphatase and tensin homolog (PTEN) (35%) as well as inositol-polyphosphate-4-phosphatase type 2 (INPP4B, 30%) [30][31][32]. So far, none of the mutations described in TNBCs have been determined to be the “driver” of carcinogenesis [33]. The BRCA1 and BRCA2 genes have been shown to contribute to carcinogenesis particularly in BCs with a familial linkage (15–20%) or in those who are already carriers of one mutation in breast tissue [34][35][36]. Other risk factors are numerous, and lifestyle habits, such as diet and obesity, can increase the likelihood of developing TNBC [37]. During metastasis, TNBC has been documented to go to the lungs, liver, and brain more often than bone, which is the typical site for other BCs [38]. In a separate study, it was observed that, of 116 patients diagnosed with TNBC between 2000 and 2006 at the Dana–Farber Cancer Institute, 46% of the patients were diagnosed with metastases to parts of the central nervous system (CNS), and the median survival rate following prognosis was 4.6 months [39].

4. Triple-Negative Breast Cancer Ecology

Neoplastic cells must compete for resources with nearby healthy cells; however, these neoplastic clones also often compete amongst themselves. This is because different mutations acquired in these neoplasms impact replication and resource acquisition rates. It has been shown that neoplastic TNBC cell clones injected into opposite flanks of mice and rats can inhibit the growth of one another or that one set of clones can completely inhibit the other [40][41]. Neoplastic cells have also been described as parasites working towards establishing independence [14]. It has been suggested that the stimulation of fibroblasts and macrophages towards angiogenesis and the release of growth factors could aid TNBC clones in establishing tumors. The release of elastases and matrix metalloproteinases (MMPs) by macrophages for ECM degradation has also been suggested to be a contributing factor in establishing tumor beds and metastasis [42][43]. Additionally, it has been suggested that neoplastic TNBC clones participate in a commensal interaction with nearby non-metastatic clones where diffusible factors are absorbed, allowing them to take up a metastatic phenotype without needing to accumulate genetic mutations first [40][44][45][46].
Furthermore, data acquired from studying cocultures of different BC cell lines in vitro show that certain interactions between cells can impact growth, both positively and negatively. MDA-MB-231 cells coincubated with supernatants of MCF-7 cells increased proliferation over time, whereas coincubation with BT-474 cells or simply other MDA-MB-231 cells hampered growth [47]. Potential explanations for these observations were hypothesized as distant cell interactions where cell culture medium differences created competitively favorable environmental conditions or that ER−/PR− cells can utilize auto and paracrine self-regulation pathways to synthesize their own GFs more frequently than BC cells that express ER and/or PR [48]. Therefore, these cells could independently sustain their growth without an autocrine loop. Neoplasms also have important interactions with the TME in supporting the growth of a developing tumor. These interactions are complex as differing TME conditions have varied impacts on carcinogenesis; normal epithelial cells can become carcinomas [49] and teratocarcinomas can have their phenotype suppressed [50] or even potentially reverted [51] based on conditions present in the TME.

5. Current Standard Therapies for Triple-Negative Breast Cancer

Due to the extreme heterogeneity of TNBC, chemotherapy with anthracyclines or taxanes remains the standard for the treatment of TNBC. There are a few mechanistic targets for therapy such as DNA repair, cell proliferation, and p53 [52]. Patients with TNBC have been documented to receive significant benefit from and even respond better to chemotherapy than other BC types do, despite the more aggressive phenotypes [53][54][55]. Ultimately, if a patient’s TNBC becomes metastatic, particularly during a recurrence, survival falls to 0%; even combinatorial therapies that trade increased toxicity for potentially elevated responses result in no benefit to survival rates [56][57].
However, in March 2019, the US FDA granted accelerated approval for an immunotherapy regimen for patients with BC. The treatment includes the use of atezolizumab (Tecentriq®) combined with nanoparticle albumin-bound paclitaxel (Abraxane®, nab-paclitaxel) in patients with metastatic TNBC where ≥1% of the tumor area is positive for immune cells expressing programmed cell death-ligand 1 (PD-L1) [58][59]. Atezolizumab is a humanized IgG1 monoclonal antibody that binds directly to PD-L1 and blocks a receptor’s interaction with PD-1 as well as the costimulatory protein B7-1 [60]. Nab-paclitaxel is a microtubule inhibitor that, when bound to nanoparticle albumin, increases solubility, minimizes hypersensitivity reactions, has better transport across endothelial tissue, greater tissue penetration, and a slower elimination time as compared to unbound paclitaxel [61][62][63][64][65][66]. Results from a double-blind, randomized, and placebo phase III clinical trial lead to this regimen’s accelerated approval [60]. When the combination of atezolizumab and nab-paclitaxel was compared with the placebo plus nab-paclitaxel for the primary treatment group, patients had an average increased progression-free survival (PFS) of 1.7 months and a 20% reduction in risk for disease progression and/or death. In the PD-L1-positive subgroup, the PFS increased further to 2.5 months as well as further decreased the risk for disease progression and/or death to 38% [60]. Even though this new therapy shows promise to increase the lifespan of patients slightly, this may merely delay the inevitable in most cases; therefore, new targeted therapies are still needed for TNBC.

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Subjects: Cell Biology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Michael L. Monaco
,
Omer A. Idris
,
Karim Essani
View Times: 305
Revisions: 2 times (View History)
Update Date: 06 May 2023
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