Malignant Breast Cells Research Articles

Acetylation of Steroidogenic Acute Regulatory Protein Sensitizes 17β-Estradiol Regulation in Hormone-Sensitive Breast Cancer Cells.

An imbalance in estrogen signaling is a critical event in breast tumorigenesis. The majority of breast cancers (BCs) are hormone-sensitive; they majorly express the estrogen receptor (ER+) and are activated by 17β-estradiol (E2). The steroidogenic acute regulatory protein (StAR) mediates the rate-limiting step in steroid biosynthesis. The dysregulation of the epigenetic machinery, modulating E2 levels, is a primary occurrence for promoting breast tumorigenesis. StAR expression, concomitant with E2 synthesis, was reported to be aberrantly high in human and mouse hormone-dependent BC cells compared with their non-cancerous counterparts. However, the mechanism of action of StAR remains poorly understood. We discovered StAR as an acetylated protein and have identified a number of lysine (K) residues that are putatively acetylated in malignant and non-malignant breast cells, using LC-MS/MS (liquid chromatography-tandem mass spectrometry), suggesting they differently influence E2 synthesis in mammary tissue. The treatment of hormone-sensitive MCF7 cells with a variety of histone deacetylase inhibitors (HDACIs), at therapeutically and clinically relevant doses, identified a few additional StAR acetylated lysine residues. Among a total of fourteen StAR acetylomes undergoing acetylation and deacetylation, K111 and K253 were frequently recognized either endogenously or in response to HDACIs. Site-directed mutagenesis studies of these two StAR acetylomes, pertaining to K111Q and K253Q acetylation mimetic states, resulted in increases in E2 levels in ER+ MCF7 and triple negative MB-231 BC cells, compared with their values seen with human StAR. Conversely, these cells carrying K111R and K253R deacetylation mutants diminished E2 biosynthesis. These findings provide novel and mechanistic insights into intra-tumoral E2 regulation by elucidating the functional importance of this uncovered StAR post-translational modification (PTM), involving acetylation and deacetylation events, underscoring the potential of StAR as a therapeutic target for hormone-sensitive BC.

Nuclear rupture induced by capillary constriction forces promotes differential effects on metastatic and normal breast cells

During metastatic dissemination, circulating tumour cells (CTCs) enter capillary beds, where they experience mechanical constriction forces. The transient and persistent effects of these forces on CTCs behaviour remain poorly understood. Here, we developed a high-throughput microfluidic platform mimicking human capillaries to investigate the impact of mechanical constriction forces on malignant and normal breast cell lines. We observed that capillary constrictions induced nuclear envelope rupture in both cancer and normal cells, leading to transient changes in nuclear and cytoplasmic area. Constriction forces transiently activated cGAS/STING and pathways involved in inflammation (NF-κB, STAT and IRF3), especially in the non-malignant cell line. Furthermore, the non-malignant cell line experienced transcriptional changes, particularly downregulation of epithelial markers, while the metastatic cell lines showed minimal alterations. These findings suggest that mechanical constriction forces within capillaries may promote differential effects in malignant and normal cell lines.

Structural Design, Anticancer Evaluation, and Molecular Docking of Newly Synthesized Ni(II) Complexes with ONS-Donor Dithiocarbazate Ligands.

The current article reports the investigation of three new Ni(II) complexes with ONS-donor dithiocarbazate ligands: [Ni(L1)PPh3] (1), [Ni(L2)PPh3] (2), and [Ni(L2)Py] (3). Single-crystal X-ray analyses revealed mononuclear complexes with a distorted square planar geometry and the metal centers coordinated with a doubly deprotonated dithiocarbazate ligand and coligand pyridine or triphenylphosphine. The non-covalent interactions were investigated by the Hirshfeld surface and the results revealed that the strongest interactions were π⋅⋅⋅π stacking interactions and non-classical hydrogen bonds C-H···H and C-H···N. Physicochemical and spectroscopic methods indicate the same structures in the solid state and solution. The toxicity effects of the free ligands and Ni(II) complexes were tested on the human breast cancer cell line MCF-7 and non-malignant breast epithelial cell line MCF-10A. The half-maximal inhibitory concentration (IC50) values, indicating that the compounds were potent in inhibiting cell growth, were obtained for both cell lines at three distinct time points. While inhibitory effects were evident in both malignant and non-malignant cells, all three complexes demonstrated lower IC50 values for malignant breast cell lines than their non-malignant counterparts, suggesting a stronger impact on cancerous cell lines. Furthermore, molecular docking studies were performed showing the complex (2) as a promising candidate for further therapeutic exploration.

The analysis of transcriptomic signature of TNBC—searching for the potential RNA-based predictive biomarkers to determine the chemotherapy sensitivity

AbstractNeoadjuvant chemotherapy is the foundation treatment for triple-negative breast cancer (TNBC) and frequently results in pathological complete response (pCR). However, there are large differences in clinical response and survival after neoadjuvant chemotherapy of TNBC patients. The aim was to identify genes whose expression significantly associates with the efficacy of neoadjuvant chemotherapy in patients with TNBC. Transcriptomes of 46 formalin-fixed paraffin-embedded (FFPE) tumor samples from TNBC patients were analyzed by RNA-seq by comparing 26 TNBCs with pCR versus 20 TNBCs with pathological partial remission (pPR). Subsequently, we narrowed down the list of genes to those that strongly correlated with drug sensitivity of 63 breast cancer cell lines based on Dependency Map Consortium data re-analysis. Furthermore, the list of genes was limited to those presenting specific expression in breast tumor cells as revealed in three large published single-cell RNA-seq breast cancer datasets. Finally, we analyzed which of the selected genes were significantly associated with overall survival (OS) in TNBC TCGA dataset. A total of 105 genes were significantly differentially expressed in comparison between pPR versus pCR. As revealed by PLSR analysis in breast cancer cell lines, out of 105 deregulated genes, 42 were associated with sensitivity to docetaxel, doxorubicin, paclitaxel, and/or cyclophosphamide. We found that 24 out of 42 sensitivity-associated genes displayed intermediate or strong expression in breast malignant cells using single-cell RNAseq re-analysis. Finally, 10 out of 24 genes were significantly associated with overall survival in TNBC TCGA dataset. Our RNA-seq-based findings suggest that there might be transcriptomic signature consisted of 24 genes specifically expressed in tumor malignant cells for predicting neoadjuvant response in FFPE samples from TNBC patients prior to treatment initiation. Additionally, nine out of 24 genes were potential survival predictors in TNBC. This group of 24 genes should be further investigated for its potential to be translated into a predictive test(s).

Design and Evaluation of a Double-Gate Tunnel Field Effect Transistor for the Detection of Breast Cancer Cells

This research paper investigates the application of a Double Gate (DG) Tunnel Field-Effect Transistor (DG-TFET) for the detection of cell lines derived from breast cancer tissue, namely Hs578T, MDA-MB-231, MCF-7, and T47D. The device incorporates two nanocavities positioned beneath the two gate electrodes, significantly enhancing detection capabilities. The study emphasizes the differentiation between healthy non-tumorigenic cells (MCF-10A) and breast cancer-derived cell lines by incorporating gate engineering into the TFET. Furthermore, the research explores the impact of changes in dielectric values specific to different breast malignant cell types on the biosensor's detection capabilities. Additionally, the investigation delves into the influence of variations in device geometry, including cavity dimensions and dielectric layer thickness, on critical parameters such as drain current sensitivity, transconductance sensitivity, and ION/IOFF sensitivity. Sensitivity analysis concerns drive current, ION/IOFF ratio, threshold voltage (Vth), and transconductance. The structural design of the device is tailored to facilitate array-based diagnosis and screening of cell lines derived from breast cancer tissue. This design offers several advantages, including a simplified transduction process, compatibility with CMOS processes, cost-effectiveness, reproducibility, and adjustable electrical responses. The researchers employed ATLAS, a two-dimensional (2D) device simulator from Silvaco, to model and define the device structure. The numerical simulations validate the device's performance, demonstrating favorable ON-OFF transition profiles.

A New Series of Indole and Azaindole Derivatives with Oxo-dihydropyridines: Synthesis, Characterization and Cytotoxicity Studies against Breast Malignant Cell Lines

In this investigation, a novel series of indole and azaindole comprising oxo-dihydropyridine derivatives was synthesized. From their spectral (1H NMR and FTIR) as well as elemental (MS) investigations, the structures of all the synthesized 12 oxo-dihydropyridine derivatives were determined. Cytotoxicity of synthesized twelve compound was evaluated against MDA-MB-231 malignant breast cells had been assessed. Compound 1,6-diamino-4-(1H-indol-3-yl)-2-oxo-1,2-dihydropyridine-3,5-dicarbonitrile showed more percent of inhibition of growth and four more derivatives showed moderate percent of inhibition of growth counter to MDA-MB-231 malignant breast cells. The derivative 1,6-diamino-4-(1H-indol-3-yl)-2-oxo-1,2-dihydropyridine-3,5-dicarbonitrile showed the highest effectiveness when assessing the IC50 value against the malignant breast cell line MDA-MB-231. Each of the compounds synthesized has a druggable character and meets Lipinski’s criteria of five.

Determining the degree of chromosomal instability in breast cancer cells by atomic force microscopy.

Chromosomal instability (CIN) is a source of genetic variation and is highly linked to the malignance of cancer. Determining the degree of CIN is necessary for understanding the role that it plays in tumor development. There is currently a lack of research on high-resolution characterization of CIN and the relationship between CIN and cell mechanics. Here, a method to determine CIN of breast cancer cells by high resolution imaging with atomic force microscopy (AFM) is explored. The numerical and structural changes of chromosomes in human breast cells (MCF-10A), moderately malignant breast cells (MCF-7) and highly malignant breast cells (MDA-MB-231) were observed and analyzed by AFM. Meanwhile, the nuclei, cytoskeleton and cell mechanics of the three kinds of cells were also investigated. The results showed the differences in CIN between the benign and cancer cells. Also, the degree of structural CIN increased with enhanced malignancy of cancer cells. This was also demonstrated by calculating the probability of micronucleus formation in these three kinds of cells. Meanwhile, we found that the area of the nucleus was related to the number of chromosomes in the nucleus. In addition, reduced or even aggregated actin fibers led to decreased elasticities in MCF-7 and MDA-MB-231 cells. It was found that the rearrangement of actin fibers would affect the nucleus, and then lead to wrong mitosis and CIN. Using AFM to detect chromosomal changes in cells with different malignancy degrees provides a new detection method for the study of cell carcinogenesis with a perspective for targeted therapy of cancer.

Abstract 16391: Pro-Neoplastic Properties of Small Extracellular Vesicles From Failing Hearts

Background: Heart diseases are associated with an increased incidence of cancer independently of shared risk factors. The mechanism beyond this link is complex, unclear and limits our ability to develop effective therapies. We aimed to test the hypothesis that small cardiac extracellular vesicles (sEVs) contribute to the link between HF and cancer. Methods & Results: We used mouse models of heterotopic and orthotopic lung cancer and post-myocardial infarction (MI) heart failure (HF). sEVs were isolated by size exclusion chromatography. To determine the role of cardiac EVs in tumor growth, we focused on sEVs from cardiac mesenchymal stromal cells (cMSCs). cMSCs after MI secreted twice more sEVs, characterized with a unique proteome, compared with cMSCs from sham-MI ( Fig 1A ). cMSC-sEVs from post-MI HF harbored more tumor-promoting cytokines and microRNA (miR), such as periostin, osteopontin, IL-6, TNFα, galectin-3, and miR's 221 and 21. The pro-neoplastic effects of cMSC-sEVs on cancer cells were depended on cancer type, with a marked increase in proliferation and migration of lung and colon cancer cells but only a modest increase with more malignant triple-negative breast and melanoma cancer cells. Next, we inoculated lung cancer cells into mice and found that post-MI HF accelerated tumor growth. Furthermore, adoptive transfer of cMSC-sEVs from failing hearts accelerated tumor growth with and without systemic EV depletion ( Fig 1B ). Finally, we found that spironolactone mitigated the neoplastic effects of HF, attenuated tumor growth ( Fig 1C ), and reduced the number of cMSC-sEVs by 26%. Conclusions: We show, for the first time, that cardiac extracellular vesicles from post-MI failing heart harbor pro-neoplastic properties and promote tumor growth independently of other secreted factors. Spironolactone reduces the number of cardiac extracellular vesicles and the pro-neoplastic effects of post-MI heart failure.

Biogenic Synthesis and Characterization of Biocompatible Iron Oxide Nanoparticles:In VitroStudy of Selective Antiproliferative Efficacy Against MCF-7 Cells and Antibacterial Potential

The accelerating fatality rate of breast cancer patients has led to the idea of unconventional therapeutic approach in this work. Here, we report the facile, eco-benign and economically advantageous route for producing iron oxide nanoparticles employing triphala extract (TR-IONPs). MTT assay was used to assess the in-vitro anticancer effectiveness of TR-IONPs against the multi-drug-resistant breast malignant cell (MCF-7). TR-IONPs revealed a concentration-dependent effect on MCF-7 viability, with an IC[Formula: see text] value of 6.8[Formula: see text][Formula: see text]g/mL for a 24-h treatment. Thus, the cytotoxic ability was established at a much lower half-maximal inhibitory concentration. As the TR-IONPs did not show remarkable toxicity toward L929 fibroblast cells, they can be trusted as a biocompatible material for real-time biomedical applications. Apoptotic death of MCF-7 cells caused by the release of Reactive Oxygen Species (ROS) was affirmed by DCFH-DA staining, DNA fragmentation assay and cell cycle analysis. Through Kirby–Bauer Disk Diffusion assay, TR-IONPs were found to hold potent antibacterial efficacy against S. aureus, E. coli and P. aeruginosa bacterial pathogens. With the demonstrated favorable results, TR-IONPs may serve as a reliable multi-functional material in the field of nanobiotechnology.

The Role of MicroRNAs in Breast Cancer and the Challenges of Their Clinical Application.

MicroRNAs (miRNAs) constitute a subclass of non-coding RNAs that exert substantial influence on gene-expression regulation. Their tightly controlled expression plays a pivotal role in various cellular processes, while their dysregulation has been implicated in numerous pathological conditions, including cancer. Among cancers affecting women, breast cancer (BC) is the most prevalent malignant tumor. Extensive investigations have demonstrated distinct expression patterns of miRNAs in normal and malignant breast cells. Consequently, these findings have prompted research efforts towards leveraging miRNAs as diagnostic tools and the development of therapeutic strategies. The aim of this review is to describe the role of miRNAs in BC. We discuss the identification of oncogenic, tumor suppressor and metastatic miRNAs among BC cells, and their impact on tumor progression. We describe the potential of miRNAs as diagnostic and prognostic biomarkers for BC, as well as their role as promising therapeutic targets. Finally, we evaluate the current use of artificial intelligence tools for miRNA analysis and the challenges faced by these new biomedical approaches in its clinical application. The insights presented in this review underscore the promising prospects of utilizing miRNAs as innovative diagnostic, prognostic, and therapeutic tools for the management of BC.

Performance assessment of dielectrically modulated negative capacitance germanium source vertical tunnel FET biosensor for detection of breast cancer cell lines

The paper presents a dielectrically modulated negative capacitance Germanium source vertical tunnel FET (DM-NC-Ge-vTFET) biosensor for detection of non-tumorigenic breast cell line (MCF-10A) and breast cancer cell lines of Hs578T, MDA-MB-231, MCF-7 and T47D. The proposed biosensor exploits the incorporation of ferroelectric (FE) layer with lateral and vertical band-to-band tunneling for improved detection sensitivity. The detecting strategy is determined by variations in the dielectric constant of various breast malignant cell lines. Sensitivity (Sn) is determined for both neutral and charged (positive/negative) biomolecules fordistinctive breast cell lines. Sn is determined by evaluating the shiftsin drain current. Sensitivity of 1.16 × 105 is attained for MCF-10A whereas Sn of 1.04 × 108 is realised for the T47D breast cell line for a completely filled nanogap. Additionally, the impact of FE layer thickness on the biosensor has been evaluated. It is observed that Sn of the proposed biosensor isenhanced for increase infill factor from partially to completely filled nanogap with a peak SNR value of approximately 61100. The biosensor’s selectivity and linearity have been evaluated. Lastly, the DM-NC-Ge-vTFET biosensor is benchmarked against existing published literatures andyields superior results in terms of its approximate sensitivity.

Expression of genes related to iron homeostasis in breast cancer

The dysfunctions in the metabolism of iron have an important role in many pathological conditions, ranging from disease with iron deposition to cancer. Studies on malignant diseases of the breast reported irregular expression in genes associated with iron metabolism. The variations are related to findings that have prognostic significance. This study evaluated the relationship of the expression levels of transferrin receptor 1 (TFRC), iron regulatory protein 1 (IRP1), hepcidin (HAMP), ferroportin 1 (FPN1), hemojuvelin (HFE2), matriptase 2 (TMPRSS6), and miR-122 genes in the normal and malignant tissues of breast cancer patients. The normal and malignant tissues from 75 women with breast malignancies were used in this study. The patients did not receive any treatment previously. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used in figuring the levels of gene expression associated with iron metabolism. When the malignant and normal tissues gene expression levels were analyzed, expression of TFRC increased (1.586-fold); IRP1 (0.594 fold) and miR-122 (0.320 fold) expression decreased; HAMP, FPN1, HFE2, and TMPRSS6 expressions did not change. FPN1 and IRP1 had a positive association, and this association was statistically significant (r = 0.266; p = 0.022). IRP1 and miR-122 had a positive association, and this association had statistical significance (r = 0.231; p = 0.048). Our study portrayed the important association between genes involved in iron hemostasis and breast malignancy. The results could be used to establish new diagnostic techniques in the management of breast malignancies. The alterations in the metabolism of malignant breast cells with normal breast cells could be utilized to achieve advantages in treatment.

Altered expression of anti-apoptotic protein Api5 affects breast tumorigenesis

BackgroundApoptosis or programmed cell death plays a vital role in maintaining homeostasis and, therefore, is a tightly regulated process. Deregulation of apoptosis signalling can favour carcinogenesis. Apoptosis inhibitor 5 (Api5), an inhibitor of apoptosis, is upregulated in cancers. Interestingly, Api5 is shown to regulate both apoptosis and cell proliferation. To address the precise functional significance of Api5 in carcinogenesis here we investigate the role of Api5 in breast carcinogenesis.MethodsInitially, we carried out in silico analyses using TCGA and GENT2 datasets to understand expression pattern of API5 in breast cancer patients followed by investigating the protein expression in Indian breast cancer patient samples. To investigate the functional importance of Api5 in breast carcinogenesis, we utilised MCF10A 3D breast acinar cultures and spheroid cultures of malignant breast cells with altered Api5 expression. Various phenotypic and molecular changes induced by altered Api5 expression were studied using these 3D culture models. Furthermore, in vivo tumorigenicity studies were used to confirm the importance of Api5 in breast carcinogenesis.ResultsIn-silico analysis revealed elevated levels of Api5 transcript in breast cancer patients which correlated with poor prognosis. Overexpression of Api5 in non-tumorigenic breast acinar cultures resulted in increased proliferation and cells exhibited a partial EMT-like phenotype with higher migratory potential and disruption in cell polarity. Furthermore, during acini development, the influence of Api5 is mediated via the combined action of FGF2 activated PDK1-Akt/cMYC signalling and Ras-ERK pathways. Conversely, Api5 knock-down downregulated FGF2 signalling leading to reduced proliferation and diminished in vivo tumorigenic potential of the breast cancer cells.ConclusionTaken together, our study identifies Api5 as a central player involved in regulating multiple events during breast carcinogenesis including proliferation, and apoptosis through deregulation of FGF2 signalling pathway.

The Role of Isoflavones in the Prevention of Breast Cancer and Prostate Cancer

This narrative review summarizes epidemiological studies on breast cancer and prostate cancer with an overview of their global incidence distribution to investigate the relationship between these diseases and diet. The biological properties, mechanisms of action, and available data supporting the potential role of isoflavones in the prevention of breast cancer and prostate cancer are discussed. Studies evaluating the effects of isoflavones in tissue cultures of normal and malignant breast and prostate cells, as well as the current body of research regarding the effects of isoflavones attained through multiple modifications of cellular molecular signaling pathways and control of oxidative stress, are summarized. Furthermore, this review compiles literature sources reporting on the following: (1) levels of estrogen in breast and prostate tissue; (2) levels of isoflavones in the normal and malignant tissue of these organs in European and Asian populations; (3) average concentrations of isoflavones in the secretion of these organs (milk and semen). Finally, particular emphasis is placed on studies investigating the effect of isoflavones on tissues via estrogen receptors (ER).

Bone Marrow Mesenchymal Stem Cells Restrain the Migration and Invasion of Breast Cancer Cells by Up-Regulating miR-2158 and Inactivating RAI2/NLRP3 Pathway

Exosomes are the key mediator for intercellular communication and participate in malignancies. Short non-coding RNAs derived from BMSCs-originated exosomes (BMSCs-exosomes) can be employed as biomolecules for tumor treatment. Here to we aim to dissect the function of microRNA-2158 from BMSCs-exosomes in breast malignant disease. Breast malignant cells received a separated transfection of miR-2158-mimics and miR-2158-inhibitor, and also treated with BMSCoriginated exosomes followed by analysis of cell viability by MTT method, cell invading and migrating capabilities via Transwell assays and protein levels of EMT-related and RAI2/NLRP3-related proteins by Western-blot. Breast cancer cells exhibited a significantly enhanced miR-2158 expression after transfection with miR-2158-mimics or treatment with BMSC-EXO, while it was reduced by miR-2158-inhibitor. As the miR-2158 was up-regulated, a significant impediment of proliferation and migration was denoted, along with a down-regulation of RAI2/NLRP3 signal transduction pathway and a retarded EMT process. Furthermore, cell proliferating and migrating capabilities were strengthened by miR-2158-inhibitor, together with an enhanced RAI2/NLRP3 signal and a strengthened EMT process. In conclusion, miR-2158 retarded the in vitro proliferating and migrating activities of breast malignant cells, leading to the inactivation of RAI2/NLRP3 signal transduction pathway, thereby exerting its tumor-suppressing function.

Folic acid-chitosan coated stylosin nanostructured lipid carriers: fabrication, in vitro–in vivo assessment in breast malignant cells

Synthesis of targeted nanostructure lipid carriers for stylosin (STY-CFN-NPs) delivery to MCF-7 cells. STY-CFN-NPs were formulated via the homogenization and ultra-sonication technique. After evaluating the amount of drug encapsulation and FA binding, the toxicity effect of the STY and STY-CFN-NPs on MCF-7 cells was measured by the MTT method. Cell cycle analysis, AO/PI staining and qPCR to assess the inducing of apoptosis as well as Tubo cancer cell inoculated mouse model for antitumor properties of STY-CFN-NPs were used. Significant increases in nanoparticle size and changes in zeta potential were observed after FA-CS coating on nanoparticles. Slow release of the STY within 144 h as well as the acceptable rate for STY encapsulation efficiency (92.4% and FA binding (52.5%) to the STY-CFN-NPs (PS: 66.26 ± 3.02 nm, ZP: 29.54 ± 1.01 mV and PDI: 0.32 ± 0.01) was reported. STY-CFN-NPs exhibited higher toxicity compared to STY suspension and treatment with STY-CFN-NPs was lead to increased apoptotic cells, stopped cells in the SubG1 phase, and also increased caspase and BAX expression and decreased BCL-2 and BCL-XL expression in in vitro and decreased the size of murine tumors (54.57% in 16 days) in in vivo. The results showed STY-CFN-NPs have good potential for breast cancer management.

Dual-Channel Fluorescent Probe for the Detection of Peroxynitrite and Glutathione in Mitochondria: Accurate Discrimination of Inflammatory and Progressing Tumor Cells.

Distinguishing between normal, inflammatory, and progressing tumor cells plays a vital role in early diagnoses and clinical studies. The simultaneous quantification of multiple biomarkers in cells can reveal cellular heterogeneity, which contributes to the discrimination of different types of cells. Herein, a dual-channel fluorescent probe has been developed for monitoring peroxynitrite (ONOO-) and glutathione (GSH) to accurately discriminate normal cells, inflammatory cells, and progressing cancer cells. The probe can monitor exogenous and endogenous mitochondrial GSH and ONOO- in living cells and zebrafish by green (530 nm, G530) and red (630 nm, R630) emission based on its good selectivity and low biotoxicity. GSH and ONOO- are visualized via fluorescence imaging, and the corresponding output signals can be employed to differentiate nontumorigenic, malignant, and metastatic breast cells in cocultured cells. Furthermore, the accurate discrimination among normal, inflammatory, and cancerous cells is achieved through the changes in the dual-channel fluorescence signal, which shows great potential for the diagnosis of inflammation and cancer diseases.

Breast Cancer Diagnosis By IoB Implanted Tag Design And Machine Learning

Breast cancer is one of the worst diseases in the world and the most common cancer affected by women. Early detection of cancers allows for faster treatments. Recent studies have focused on early breast cancer diagnosis utilizing non-invasive UWB technologies. This article proposed to use metamaterials as an Implantable antenna to detect breast cancer in filed of IOB. With non-toxic materials,and safity frequency range from 1 to 10 GH three different compact and comfortable sizes for metamaterial antennas have been used for implanted within the breast tissue. Two models for compressed breast tissue were created using the CST Microwave studio simulator. These models generated patient data set with differing dielectric properties similar to human tissue. These dataset are used to train several appropriate supervised machine learning algorithms: Decision tree (DT), support vector machine (SVM), and nearest neighbour (NN) in order to develop an intelligent classification model that can assist doctors in identifying malignant breast cells. As a result SVM can classify the breast data to detect the tumor affactivly with 93%accuracy .

The Value of DPAS in the Detection of Breast Malignant Cells

Background: Fine-needle aspiration (FNA) has become an essential, critical test for breast masses. This study aimed to determine the value of diastase-resistant periodic acid-Schiff (DPAS) staining in the detection of malignant breast cells. Methods: This prospective cross-sectional study was conducted in Khartoum state (Sudan) among Sudanese women who suffered from breast lumps. FNA samples were collected from each patient, and the material was simultaneously smeared onto two labeled glass slides. The DPAS score and aspiration cytology (AC) grade are expressed as mean +/- SD, and the 95% confidence intervals of the means were calculated. Results: The findings revealed the following DPAS score frequencies among the studied women: negative (+/-) (28, 13.9%), one plus (+) (114, 56.7%), two plus (++) (27, 13.4%), and three-plus (+++) (32, 15.9%). Comparison of DPAS scores with the cytological categories (cytology results) revealed that DPAS positivity (++, +++) correlated best with malignancy. Of the 201 patients, the AC grades according to the International Academy of Cytology (IAC) system were: AC2 (30, 14.9%), AC3 (112, 55.7%), AC4 (27, 13.4%), and AC5 (32, 15.9%). Conclusions: DPAS positivity in atypical cells in FNA aspirates may assist in upgrading from a suspicious to a malignant diagnosis in women with breast lumps.

Dual-miRNA-Propelled Three-Dimensional DNA Walker for Highly Specific and Rapid Discrimination of Breast Cancer Cell Subtypes in Clinical Tissue Samples

Dual-miRNA-Propelled Three-Dimensional DNA Walker for Highly Specific and Rapid Discrimination of Breast Cancer Cell Subtypes in Clinical Tissue Samples