Abstract
Breast cancer remains a leading cause of mortality among women globally, characterized by uncontrolled epithelial cell proliferation within breast tissue. This malignancy exhibits a range of histological subtypes, including invasive ductal and lobular carcinomas, and poses significant challenges in public health due to its complex biology and diverse clinical manifestations. Epidemiological data show higher incidence rates in developed countries, with genetic mutations in BRCA1 and BRCA2 notably increasing susceptibility. Hormonal influences and environmental factors further complicate risk assessment. The pathogenesis of breast cancer involves genetic and epigenetic alterations leading to malignant transformation, with critical molecular pathways such as HER2/neu and PI3K/AKT/mTOR playing pivotal roles. The metastatic process is facilitated by mechanisms including epithelial-to-mesenchymal transition (EMT) and extracellular matrix (ECM) degradation, with heparanase and integrins significantly contributing to metastasis. Recent advancements in circulating tumor cell (CTC) analysis offer promising insights into early detection and monitoring of metastasis. Tumor-induced pre-metastatic niches and angiogenesis also play crucial roles in the metastatic cascade. Despite progress in treatment strategies, including chemotherapy, hormone therapy, and targeted therapies, metastatic breast cancer remains challenging to cure. Ongoing research aims to enhance early detection, refine therapeutic approaches, and improve patient outcomes.
Keywords
Breast Cancer, Metastasis, HER2/neu Pathway, PI3K/AKT/mTOR Pathway, Epithelial-to-Mesenchymal Transition, Circulating Tumor Cells, Heparanase, Angiogenesis, Pre-Metastatic Niche, Targeted Therapy,
Introduction
Breast cancer is one of the most common and fatal malignancies affecting women worldwide [1]. This disease is characterized by uncontrolled proliferation of cells within breast tissue, originating from various epithelial cells, and can present as several histological subtypes, including invasive ductal carcinoma and invasive lobular carcinoma. Despite advancements in early detection and treatment, breast cancer remains a significant public health concern due to its complex biology and varied clinical manifestations [2-4]. The epidemiology of breast cancer reveals significant geographic variation, with higher incidence rates in developed countries compared to developing regions. It is the most frequently diagnosed cancer among women and ranks as the second leading cause of cancer-related deaths globally [5-7]. Risk factors for breast cancer are multifactorial, involving genetic predispositions, hormonal influences, and environmental factors. [8, 9] Notably, genetic mutations in BRCA1 and BRCA2 are linked to a higher risk of developing breast cancer due to their role in DNA repair [10, 11]. Other mutations in genes such as TP53 and PTEN also contribute to hereditary breast cancer syndromes [12, 13]. Hormonal factors, particularly the effects of estrogen and progesterone, are significant, with prolonged exposure through early menarche, late menopause, or hormone replacement therapy increasing risk. Additionally, environmental and lifestyle factors like obesity, physical inactivity, and alcohol consumption further influence breast cancer risk, interacting with genetic predispositions to complicate the disease [14-16].
The pathogenesis of breast cancer involves a series of genetic and epigenetic changes that lead to malignant transformation. The progression from benign lesions, such as ductal carcinoma in situ (DCIS) or lobular carcinoma in situ (LCIS), to invasive cancer is marked by genomic instability and the disruption of key cellular pathways [17-19]. Crucial molecular pathways include the HER2/neu pathway, characterized by the overexpression of the HER2 protein, which is associated with more aggressive disease and poor prognosis but can be targeted with therapies like trastuzumab [20-22]. The PI3K/AKT/mTOR pathway, involved in regulating cell growth and metabolism, is also frequently altered, contributing to tumor progression and therapy resistance [23,24]. The epithelial-to-mesenchymal transition (EMT) is another critical process, where epithelial cells gain mesenchymal traits, enhancing their ability to invade surrounding tissues and spread to distant sites [25-28]. This transition is controlled by transcription factors such as Snail, Twist, and ZEB1, which regulate cell adhesion and motility [29, 30]. Clinically, breast cancer may present with symptoms such as palpable lumps, changes in breast shape or texture, and abnormal nipple discharge, though it can also be asymptomatic and detected through screening [31, 32]. Diagnostic modalities include mammography, ultrasonography, and magnetic resonance imaging (MRI), with mammography being the primary method for early detection. Histopathological analysis of biopsy specimens provides essential information about tumor type, grade, and receptor status, guiding therapeutic decisions [33-35]. Immunohistochemical staining for estrogen receptors (ER), progesterone receptors (PR), and HER2 is critical for determining prognosis and treatment strategies. [36, 37].Treatment for breast cancer involves a multidisciplinary approach, encompassing surgery, radiation therapy, chemotherapy, hormone therapy, and targeted therapies. Surgical options range from breast-conserving surgery to mastectomy, depending on tumor characteristics and patient preferences. Adjuvant therapies aim to eliminate residual disease and prevent recurrence, with chemotherapy and radiation playing key roles [38, 39]. Hormone therapy, including agents like tamoxifen and aromatase inhibitors, targets hormone receptor-positive tumors, while targeted therapies, such as HER2 inhibitors and CDK4/6 inhibitors, offer improved outcomes for specific molecular subtypes [40-43]. Future research is focused on further elucidating the molecular mechanisms of breast cancer and developing novel therapeutic approaches. Advances in genomics and proteomics are enhancing our understanding of tumor biology, paving the way for personalized medicine. Ongoing efforts aim to improve early detection, minimize treatment-related side effects, and enhance patient quality of life. Despite significant progress in diagnosis and treatment, breast cancer remains a complex and challenging disease, necessitating continued research and innovation to ultimately achieve a cure [44, 45].

Fig. 1. Mechanism of Breast Cancer
MECHANISMS
- The Role of Circulating Tumor Cells
The detection of breast cancer metastasis relies on clinical presentations of distant organ involvement, biopsies of affected tissues, radiological assessments, imaging techniques, and serum tumor markers [46, 47]. The American Society of Clinical Oncology (ASCO) guidelines for breast cancer follow-up and management list symptoms of recurrence as new breast lumps, bone, chest, or abdominal pain, dyspnea, and persistent headaches. ASCO also recommends mammography for early detection of relapse [48-50]. According to a study the importance of serum tumor markers in postoperative monitoring of breast cancer patients. They suggest intensive postoperative follow-up including consultations every 4-6 months, physical examinations, and evaluations of serum carcinoembryonic antigen (CEA), tissue polypeptide antigen (TPA), and breast cancer-associated antigen 115 D8/DF3 (CA15.3) [51-53]. Imaging methods such as bone scintigraphy, liver echography, and chest X-ray are recommended biannually, with computed tomography and magnetic resonance imaging performed if earlier methods raise suspicion [54, 55]. Although mammographic screening has reduced mortality by facilitating early diagnosis, the aforementioned methods often fall short in detecting metastasis at the earliest stages and in accurately predicting clinical outcomes [56, 57]. An emerging method for metastasis detection is the analysis of circulating tumor cells (CTCs), which shows promise in addressing the limitations of other diagnostic techniques [58, 59]. CTCs are tumor cells originating from primary sites or metastases that circulate in the bloodstream and are rarely found in healthy individuals. They play crucial roles in carcinoma metastasis, enabling prediction of metastatic relapse and disease progression. CTCs are typically isolated and enriched using either morphological or immunological techniques [60-62]. Morphological-based isolation separates CTCs by size discrepancies or density, while immunological techniques, which are more widely used, employ immunomagnetic isolation targeting epithelial cell-specific markers or tumor markers specific to cancer types [63-65]. After isolation, the source and genetic composition of CTCs are characterized using nucleic acid-based methods, such as quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR), or cytometric-based methods, such as flow cytometry and enzyme-linked immunospot assay technology [66-68]. Clinical applications of CTC analysis have shown promising results. A specific research proposed that the number of CTCs could indicate ongoing metastasis [69, 70]. Evidence suggests that CTC counts correlate with clinical outcomes and survival in cancer patients. A study on patients with metastatic breast cancer before treatment found that those with more than five CTCs in 7.5 ml of blood had shorter progression-free and overall survival [71, 72]. A particular research demonstrated that the presence of one CTC in 7.5 ml blood after neoadjuvant chemotherapy could predict metastatic relapse. Despite promising results, the increasing number of CTC detection methods calls for standardization to ensure increased efficacy and quality [73, 74].

Fig. 2. Circulating Tumor Cells in the blood Stream
- The Metastatic Cascade and Invasion Mechanisms in Breast Cancer
The metastatic process involves a series of sequential steps. Failure to complete any of these steps halts the process. Metastasis begins with the local invasion of surrounding host tissue by cells originating from the primary tumor, followed by intravasation into blood or lymphatic vessels [75-77]. Tumor cells are then disseminated via the bloodstream or lymphatic system to distant organs, where they undergo cell cycle arrest and adhere to capillary beds within the target organ [78-80]. This is followed by extravasation into the organ parenchyma, proliferation, and promotion of angiogenesis [81-83]. Throughout these steps, tumor cells must evade the host’s immune response and apoptotic signals to survive. If successful, the process can be repeated to produce secondary metastases or ‘metastasis of metastases [84, 85].
- Invasion
Metastasis begins with the invasion of tumor cells into surrounding host tissue. Invasive tumor cells must alter cell-to-cell adhesion and adhesion to the extracellular matrix (ECM) [86]. The cadherin family plays a significant role in mediating cell-to-cell adhesion and is pivotal in breast cancer metastasis [87]. E-cadherin maintains cell-cell junctions, and its down-regulation is a determinant in the outgrowth of metastatic breast cancer cells. This down-regulation is associated with progression and metastasis in breast cancer, reflecting poor prognosis [88]. Mutations in E-cadherin that lead to functional loss are found in lobular breast carcinoma. N-cadherin, associated with mesenchymal cells, is related to epithelial-to-mesenchymal transition (EMT) during the gastrulation stage [89, 90]. EMT is increasingly linked to cancer progression, aiding invasion and intravasation into the bloodstream and inducing proteases involved in ECM degradation. N-cadherin expression in place of E-cadherin leads to fibrosis and cyst formation in mammary glands, eventually resulting in malignant breast tumors in mice [91-93]. Down-regulation of E-cadherin and up-regulation of N-cadherin are frequently observed in most epithelial cancers during stromal invasion [94, 95]. Loss of E-cadherin reduces adhesion between epithelial breast cancer cells, while increased N-cadherin promotes adhesion to stromal cells, facilitating invasion into the stroma [96, 97]. Tumor cell adhesion to the ECM is mediated by integrins, transmembrane receptors found on ECM components such as fibronectin, laminin, collagen, fibrinogen, and vitronectin [98, 99]. Invasion is preceded by ECM degradation to penetrate tissue boundaries [100]. This degradation is mainly carried out by metalloproteinases (MMPs) and the urokinase plasminogen activator (uPA) system [101]. In breast cancer patients, uPA is prognostically important for predicting the risk of distant metastases, even in patients with a good prognosis at diagnosis [102, 103]. Inhibition of uPA via small-interfering RNA (siRNA) restricts invasion and reduces MMP9 expression [104]. MMPs mediate ECM proteolysis at the invadopodial front of invasive breast cancer cell lines. Integrins also modulate tumor motility by participating in ECM-degrading enzyme activities, such as those of the MMPs. For instance, integrins ?5?1 and ?3?1 up-regulate MMP9 [105-107].

Fig. 3. Schematic showing the metastasis cascade of breast cancer
- Role of Heparanase in ECM Degradation and Breast Cancer Metastasis
Heparanase, a ?-glucuronidase, contributes to the degradation of the extracellular matrix (ECM) by breaking down heparan sulfate proteoglycan. Heparan sulfate proteoglycans, found in the ECM and on cell surfaces, are crucial for ECM assembly, integrity, cell matrix adhesion, and growth factor receptor interactions [108-110]. Heparan sulfate acts as a reservoir for heparin-binding growth factors and angiogenic factors. By degrading heparan sulfate, heparanase releases these substances, promoting tumor growth, invasion, and angiogenesis [111,112]. The expression of heparanase correlates with metastatic potential in breast cancer, and increased levels of heparan sulfate proteoglycans, such as glypican-1 and syndecan-1, are observed in advanced stages of breast cancer. Additionally, the overexpression of heparanase in MCF7 breast cancer cells has been shown to enhance cell proliferation, survival, and stromal infiltration both in vitro and in vivo [113-115].
- Migration and Motility in Tumor Cell Invasion
To achieve an invasive phenotype, tumor cells must migrate from the primary site. They can migrate either singly or in coordination. Coordinated migration is common in intermediate or highly differentiated lobular carcinomas of the breast [116, 117]. It is suggested that coordinated migration may switch to single-cell migration, particularly in poorly differentiated tumors, due to abnormalities in intercellular adhesion proteins [118]. Tumor cells that migrate collectively require intercellular junctions and often circulate as emboli in the blood or lymphatic vessels after invasion and intravasation [119, 120]. Cells at the leading edge of the migrating tumor create tube-like microtracks by cleaving and orienting collagen fibers using membrane type 1 (MT1) MMP, facilitating collective migration through the ECM [121, 122]. In contrast, single tumor cells migrate via two main mechanisms: protease-dependent mesenchymal movement or protease-independent amoeboid movement [123]. The epithelial-to-mesenchymal transition (EMT) is a critical pathway for the mesenchymal movement of single migratory cells [124, 125]. During EMT, cells transition from an epithelial phenotype to a mesenchymal-like phenotype, losing epithelial markers like E-cadherin and expressing mesenchymal markers such as vimentin [126]. This process involves transcriptional repressors of E-cadherin, including ZEB1, ZEB2, Twist, Snail, and Slug, which are linked to signaling pathways such as TGF-?, WNT, and PI3K/AKT [127-130]. These repressors are associated with poor prognosis in breast carcinoma. Following the loss of cell adhesion, cells alter their polarity from apical-basal to front-rear, initiating migration through changes in cortical actin and actin stress fibers that remodel the cytoskeleton. Proteolytic enzymes like MMPs are activated, altering cell-matrix adhesion. Cells undergoing EMT adopt an elongated fibroblast-like shape, moving through ECM channels created by matrix-degrading enzymes like MMPs [131, 132]. In contrast, cells with amoeboid movement are round and resemble primordial unicellular organisms. They push and squeeze through matrix pores, relying on shape deformations and structural changes in the ECM rather than actual degradation. These cells are loosely attached to the ECM, lose cell polarity, and move through paths of least resistance. The mechanical force for amoeboid movement is generated by active myosin/actin contractions and cortical actin via signaling pathways such as RhoA/Rho kinase (ROCK) [133-135].
- Regulation of Tumor Cell Migration Modes: Mesenchymal-to-Amoeboid Transition and Amoeboid-to-Mesenchymal Transition
Tumor cells predominantly employ mesenchymal motility for migration. However, under specific conditions, changes in molecular pathways can lead to a shift in migration mode. This shift can occur either from mesenchymal to amoeboid movement, known as mesenchymal-to-amoeboid transition (MAT), or from amoeboid to mesenchymal movement, termed amoeboid-to-mesenchymal transition (AMT) [136, 137]. At the molecular level, AMT is induced by the inhibition of pro-amoeboid pathways, such as those involving Rho/ROCK, PI3K, and cell division control protein 42 homolog (CDC42) [138, 139]. Conversely, molecules such as ras-related C3 botulinum toxin substrate (Rac) and SMAD-specific E3 ubiquitin protein ligase 1 (Smurf1), which promote mesenchymal movement, are associated with MAT. Additionally, inhibition of pericellular proteolysis or elevated levels of Rho/ROCK signaling can also drive MAT [140-142]. The spatial organization of collagen fibers in the tumor extracellular matrix (ECM) boundary influences the migration mode of tumor cells [143-144]. When collagen fibers are pre-aligned perpendicularly to the ECM boundary, amoeboid movements of MDA-MB-231 mesenchymal cells do not engage the Rho/ROCK pathway. However, if collagen fibers are not aligned with the tumor ECM boundary, activation of the Rho/ROCK pathway is observed in these cells [145-147].
- Role of Stromal Cells and Tumor Microenvironment in Tumor Cell Migration and Metastasis
Stromal cells play a significant role in facilitating tumor cell migration. In breast cancer, the predominant stromal cells are fibroblasts, often referred to as carcinoma-associated fibroblasts (CAFs) [148, 149]. Conditioned media derived from CAFs has been shown to enhance cell motility and invasion in breast cancer models in vitro [150-151]. Furthermore, studies in immunodeficient nude mice have demonstrated that injection of human CAFs along with MCF7-ras human breast cancer cells leads to increased tumor growth and angiogenesis compared to injection with normal human fibroblasts [151, 152].
- Tumor Microenvironment
Stephen Paget's 'seed and soil' theory of metastasis, proposed in the 1980s, posits that tumor cells ('seeds') can only grow when they encounter a favorable environment ('soil'). This theory is being reevaluated, with growing evidence highlighting the tumor microenvironment as a crucial determinant of metastasis [153, 154]. The microenvironment is essential for tumor cell proliferation, and a supportive microenvironment is necessary for tumor growth and malignant progression. The tumor microenvironment comprises various specialized cells, including fibroblasts, immune cells, endothelial cells, and mural cells of blood and lymphatic vessels, as well as the extracellular matrix (ECM) [155-158]. These components collectively influence tumor progression. Malignant cells interact continuously with microenvironmental cells at both primary and metastatic sites, facilitating the transition from 'in situ' to metastatic breast cancer. For instance, macrophages recruited by non-invasive breast tumor cells can induce angiogenesis and promote malignant transformation [159, 160]. Tissue-associated macrophages, which impact tumor invasion, angiogenesis, immune evasion, and migratory behavior, form interactive niches with breast cancer cells and endothelial cells, aiding in intravasation and metastatic spread [161-163]. In bone, interactions between tumor cells and stromal components, such as osteoclasts and osteoblasts, affect tumor cell growth and dormancy. Consequently, the successful outgrowth of metastatic cells in bone is heavily influenced by the bone stroma [164-165].
- Tumor-Induced Pre-Metastatic Niche Formation and Tissue Tropism in Breast Cancer Metastasis
It is proposed that tumor cells may secrete factors to modify the microenvironment and create a 'pre-metastatic niche' that facilitates future metastasis. A research demonstrated that signals from the primary tumor can induce the expression of matrix metalloproteinase 9 (MMP9) in lung endothelial cells and macrophages before metastasis occurs, thereby promoting the preferential invasion of tumor cells into the lungs [166, 167]. Additionally, clusters of vascular endothelial growth factor receptor 1 (VEGFR-1)-positive hematopoietic progenitor cells were identified in pre-metastatic lymph nodes of breast cancer patients prior to the arrival of tumor cells, indicating the establishment of a pre-metastatic niche [168, 169]. Breast cancer is known to predominantly metastasize to the bone and lungs, while metastasis to other organs such as the liver and brain is less frequent [170, 171]. Gene expression profiles associated with the preferential metastasis of breast cancer cells to bone marrow and lungs have been identified, suggesting that metastasis exhibits tissue-specific tropism [172, 173]. Furthermore, chemokines play a role in directing tumor cells to specific organs. For instance, breast cancer tissues express high levels of the chemokine receptor CXCR4, while its ligand, CXCL12, is predominantly expressed in lymph nodes, lungs, liver, and bone marrow, but at lower levels in the small intestine, kidney, brain, skin, and skeletal muscle [174, 175]. Organs with elevated CXCL12 expression are common sites for breast cancer metastasis. Muller et al. demonstrated that the interaction between CXCR4 and CXCL12 facilitates the migration of breast cancer cells to these frequently targeted organs [176, 177].

Fig. 4. Epithelial–to-mesenchymal transition (EMT). The epithelial cells undergo phenotypic changes to take on mesenchymal-like characteristics
- Role of Angiogenesis in Tumor Metastasis and the Angiogenic Switch
The development of tumor vasculature is a crucial factor in metastasis, as angiogenesis significantly contributes to tumor progression and the growth of metastases. Angiogenesis is considered a key adaptation of the tumor microenvironment and is recognized as a hallmark of cancer. During tumorigenesis, the equilibrium between pro-angiogenic and anti-angiogenic factors becomes disrupted, favoring pro-angiogenic signalling [178-180]. This shift, often referred to as the 'angiogenic switch,' is driven by genetic mutations, mechanical stress, inflammatory responses, tumor expression of angiogenic proteins, and predominantly, hypoxia. Unlike normal physiological conditions, tumor vasculature is irregular and differs structurally, functionally, and genetically from healthy blood vessels. These abnormal blood vessels are inadequate in delivering sufficient oxygen to the tumor, leading to a state of tumor hypoxia. In response, tumor cells increase the production of pro-angiogenic factors, which further exacerbates the formation of dysfunctional vasculature. This creates a feedback loop where the persistent hypoxic environment triggers invasive and metastatic programs, promoting tumor progression and metastasis [181-183].
- Hypoxia-Induced Angiogenesis and the Role of Vascular Endothelial Growth Factor (VEGF)
Hypoxic conditions in tumors activate factors such as hypoxia-inducible factor-1 (HIF-1), which in turn stimulate the production of angiogenic proteins. Vascular endothelial growth factor (VEGF) and its receptors (VEGFRs) are among the most extensively studied of these proteins. VEGF is a key member of a growth factor family that includes VEGF-A, -B, -C, -D, and -E, as well as placental growth factor. VEGF plays a critical role in both vasculogenesis and angiogenesis, exerting its effects through various VEGFRs [184, 185]. It promotes endothelial cell proliferation, invasion, and migration, and increases microvascular permeability. The elevated expression of VEGF in solid tumors is often associated with poor prognosis and a higher propensity for metastasis [186, 187].
CURRENT STRATEGIES AND CHALLENGES IN THE TREATMENT OF METASTATIC BREAST CANCER
Despite significant advancements in treatment, metastatic breast cancer remains a largely incurable disease. Therapeutic approaches are generally categorized into standard chemotherapy and targeted therapies.
Standard Chemotherapy:
Traditional chemotherapy for metastatic breast cancer includes the use of anthracyclines, taxanes, and 5-fluorouracil, often administered in a sequential manner. Anthracyclines, while effective, are associated with the risk of cardiac dysfunction. Newer cytotoxic agents such as epothilones and ixabepilone have shown increased efficacy in patients previously treated with anthracyclines and taxanes [188, 189].
Targeted Therapies: This category encompasses hormone therapy, immunotherapy, and antiangiogenic therapy [190].
Hormone Therapy:
Hormone-based treatments aim to block estrogen receptors or reduce estrogen levels. Aromatase inhibitors, such as letrozole, anastrozole, and exemestane, inhibit the enzyme aromatase, which converts adrenal androgens to estrogen. Aromatase inhibitors have demonstrated superior therapeutic outcomes compared to tamoxifen, particularly as first-line treatments in post-menopausal women [191- 193].
Immunotherapy:
Trastuzumab, a monoclonal antibody targeting the extracellular domain of the human epidermal growth factor receptor 2 (HER-2), is used to inhibit the growth of tumors overexpressing HER-2. When combined with chemotherapy, trastuzumab has been shown to improve overall survival rates, response rates, and progression-free survival. Newer HER-2-targeting antibodies, such as trastuzumab-MCC-DM1 and pertuzumab, are also showing promising results [194-196].
Antiangiogenic Therapy:
Antiangiogenic agents target the formation of new blood vessels, a process crucial for tumor growth. Bevacizumab, a humanized monoclonal antibody that inhibits vascular endothelial growth factor A (VEGF-A), reduces endothelial cell proliferation and limits the tumor's blood supply. The combination of bevacizumab with other chemotherapeutic agents has been associated with increased progression-free survival. However, this therapy can also lead to adverse effects such as severe hypertension, bleeding, and heart failure [197-200].
CONCLUSION:
Breast cancer continues to be a significant global health issue, marked by its diverse histological subtypes, complex pathogenesis, and challenging clinical management. Despite substantial advancements in early detection and treatment modalities, the multifactorial nature of breast cancer, encompassing genetic, hormonal, and environmental risk factors, necessitates ongoing research and innovation. The progression from benign lesions to invasive carcinoma involves critical molecular pathways, such as HER2/neu and PI3K/AKT/mTOR, which underscore the complexity of tumor biology and contribute to resistance against conventional therapies. The metastatic cascade, driven by processes such as epithelial-to-mesenchymal transition (EMT) and extracellular matrix (ECM) degradation, is crucial for the spread of breast cancer cells. Emerging techniques for detecting circulating tumor cells (CTCs) and understanding their role in metastasis hold promise for earlier diagnosis and more effective monitoring of disease progression. Additionally, the formation of pre-metastatic niches and the role of angiogenesis in tumor growth and metastasis highlight the intricate interactions between tumor cells and their microenvironment. Despite the progress made in targeted therapies, hormone treatments, and antiangiogenic agents, metastatic breast cancer remains difficult to cure, underscoring the need for continued research. Future efforts should focus on refining detection methods, developing personalized treatment strategies, and improving patient outcomes through a deeper understanding of the molecular mechanisms underlying tumor progression and metastasis. The ultimate goal is to achieve more effective therapies that can significantly enhance survival rates and quality of life for patients with breast cancer.
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