Strategy For Treatment Of Breast Cancer Research Articles

DFT and molecular docking research on the effects of lichen metabolites

Breast cancer remains a significant public health problem worldwide and requires the investigation of new treatment methods. Lichens, symbiotic organisms rich in bioactive compounds, have emerged as promising sources of natural anticancer agents. This study investigates the anticancer effects of lichen metabolites derived from Xanthoparmelia wyomingica on breast cancer cell lines MCF-7 and MDA-MB231. High-performance liquid chromatography (HPLC) was used to measure specific lichen acids in the extract; this revealed the presence of Gyrophoric acid (GA), Norstictic acid (NA), Protocetraric acid (PA), Stictic acid (SA), and Usnic acid (UA). Cytotoxicity analysis showed significant reductions in cell viability, particularly in the MDA-MB231 cell line, with IC50 values ranging from 21.67 to 36.71 µg/mL. Molecular docking studies elucidated the interaction mechanisms between these metabolites and target proteins, highlighting NA as the most promising compound with the lowest binding energy (−9.5 kcal/mol) and inhibition constant (0.108755 μM). ADMET analysis of the molecules was then performed. Molecular electrostatic potential (MEP) and HOMO-LUMO analysis provided further information about the reactivity and electron distribution of the compounds. This study has the potential to provide novel therapeutic agents for breast cancer to tackle the increasing resistance to conventional therapies. Lichen metabolites enable the development of effective therapies in targeting aggressive subtypes such as triple-negative breast cancer with limited treatment options. This research highlights the anticancer properties of lichen metabolites and their potential in the development of innovative strategies for breast cancer treatment. The findings offer a promising avenue to address the urgent need for effective therapies in oncology.

Inhibition of XIST restrains paclitaxel resistance in breast cancer cells by targeting hsa-let-7d-5p/ATG16L1 through regulation of autophagy

Breast cancer is a fatal malignant tumor in women worldwide. The development of paclitaxel resistance remains a challenge. Autophagy is considered to have a significant part in the chemotherapeutic stress mechanism. This study aimed to investigate the function of long non-coding RNA (lncRNA) in breast cancer cell chemoresistance and autophagy. The paclitaxel (PTX)-resistant breast cancer cells were established. The function of X-inactive specific transcript (XIST) was demonstrated using in vitro and in vivo experiments. Transmission electron microscope (TEM) was used to observe autophagy vesicles. Protein and mRNA levels were determined using western blotting and quantitative real time polymerase chain reaction (qRT-PCR). We discovered that autophagic activity was correlated with chemoresistance in PTX-resistant breast cancer cells. In vitro and in vivo studies showed that XIST inhibition reduced cell resistance to paclitaxel, caused autophagy to be suppressed by regulating hsa-let-7d-5p and ATG16L1 expression. Mechanically, threonine protein kinase B (PKB; also known as AKT) - mammalian target of rapamycin (mTOR) pathway was activated when knockdown of XIST, while was reversed by inhibition of hsa-let-7d-5p. Our results verified that XIST played a significant role in developing chemoresistance via mediating autophagy in PTX-resistant breast cancer cells. It may be a potential target for breast cancer treatment strategies.

The Hippo Pathway in Breast Cancer: The Extracellular Matrix and Hypoxia

As one of the most prevalent malignant neoplasms among women globally, the optimization of therapeutic strategies for breast cancer has perpetually been a research hotspot. The tumor microenvironment (TME) is of paramount importance in the progression of breast cancer, among which the extracellular matrix (ECM) and hypoxia are two crucial factors. The alterations of these two factors are predominantly regulated by the Hippo signaling pathway, which promotes tumor invasiveness, metastasis, therapeutic resistance, and susceptibility. Hence, this review focuses on the Hippo pathway in breast cancer, specifically, how the ECM and hypoxia impact the biological traits and therapeutic responses of breast cancer. Moreover, the role of miRNAs in modulating ECM constituents was investigated, and hsa-miR-33b-3p was identified as a potential therapeutic target for breast cancer. The review provides theoretical foundations and potential therapeutic direction for clinical treatment strategies in breast cancer, with the aspiration of attaining more precise and effective treatment alternatives in the future.

Breast cancer cell resistance to hormonal and targeted therapeutics is correlated with the inactivation of the NR6A1 axis.

Aim: Resistance to hormonal and targeted therapies in breast cancer limits treatment efficacy. Epigenetic alterations, including changes mediated by DNA methyltransferases, play a key role in this process. Previously, we identified that resistance to tamoxifen and rapamycin is associated with the suppression of DNMT3A. This study aims to further explore the mechanisms underlying this suppression, with a focus on identifying NR6A1 as a novel regulatory factor. Methods: Acquisition of resistant breast cancer cell sublines, MTT-test, immunoblotting, transient transfection and reporter analysis, lentiviral infection, qRT-PCR, and analysis of methylation using bisulfite pyrosequencing. Results: Our findings indicate that the development of cross-resistance in breast cancer cells to hormonal and targeted therapies involves a shift in cell signaling to alternative AKT pathways, marked by a localized suppression of the NR6A1/DNMT3A axis and associated DNA methylation changes. We demonstrated the critical role of NR6A1 downregulation in resistance development. Additionally, we observed activation of Snail - a key regulator in the epithelial-mesenchymal transition - as a mediator of the effects of NR6A1 depletion, establishing a direct link between Snail expression and resistance formation. Conclusion: The coordinated suppression of NR6A1 and DNMT3A may contribute to sustaining the resistant phenotype in breast cancer cells. This pathway could serve as a predictive marker, helping guide the selection of optimal therapeutic strategies for breast cancer treatment in the future.

Inequality in breast cancer: Global statistics from 2022 to 2050

This study evaluates the global inequalities of breast cancer incidence and mortality from 2022 to 2050 with the latest GLOBOCAN estimates. It focuses on disparities across continents, age groups and Human Development Index (HDI) levels. In 2022, Africa shows the highest positive slope values of age-standardized rates (world) of mortality vs. incidence, both for those under 40 (0.346) and those 40 and older (0.335). These values contrast with those for Asia (0.085, 0.208), Europe (0.002, −0.014), Latin America and the Caribbean (0.17, 0.303), Northern America (−0.078, −0.188), and Oceania (0.166, −0.001). In both age groups, lower HDI levels are correlated with higher slope values and vice versa. Projections to 2050 indicate significant increases in the burden of breast cancer, with persistent yet varied disparities and differences. This highlights the need for differentiated strategies in breast cancer prevention, early-stage diagnosis, and treatment.

Treatment and Prevention Strategies of Breast Cancer

Abstract. With the increasing trend of late childbearing and low childbearing, the incidence of breast cancer is increasing rapidly worldwide. At present, breast cancer has become one of the more frequent malignant tumor diseases in women and has aroused widespread concern in society. The cause of the disease is not completely clear, with the deepening of research, the relevant detection methods are constantly updated, as far as possible early diagnosis. At present, the main methods of breast cancer prevention are lifestyle adjustment, including reducing alcohol intake, maintaining a healthy weight and chemical prevention, but the methods are limited, so the research on breast cancer prevention is particularly important. At the same time, medical workers should educate the majority of women about disease prevention, so that women can establish a correct concept of prevention and treatment, so as in order to lower the prevalence of breast cancer and improve the women health.

EfficientNet-resDDSC: A Hybrid Deep Learning Model Integrating Residual Blocks and Dilated Convolutions for Inferring Gene Causality in Single-Cell Data.

Gene Regulatory Networks (GRNs) reveal complex interactions between genes in organisms, crucial for understanding the life system's operation. The rapid development of biotechnology, especially single-cell RNA sequencing (scRNA-seq), has generated a large amount of scRNA-seq data, which can be analyzed to explore the regulatory relationships between genes at the single-cell level. Previous models used to construct GRNs mainly aim at constructing associative relationships between genes, but usually fail to accurately reveal the causality between genes. Therefore, we present a hybrid deep learning model called EfficientNet-resDDSC (the EfficientNet with Residual Blocks and Depthwise Separable Dilated Convolutions) to infer causality between genes. The model inherits the basic structure of EfficientNet-B0 and incorporates residual blocks as well as dilated convolutions. The model's ability to extract low-level features at the primary stage is enhanced by introducing residual blocks. The model combines Depthwise Separable Convolution (DSC) in the inverted linear bottleneck layers with the dilated convolutions to expand the model's receptive fields without increasing the computational effort. This design enables the model to comprehensively reveal potential relationships among different genes in high-dimensional and high-noise single-cell data. In comparison with the five existing deep learning network models, EfficientNet-resDDSC's overall performance is significantly better than others on four datasets. In this study, EfficientNet-resDDSC was further applied to construct GRNs for breast cancer patients, focusing on the related regulatory genes of the key gene BRCA1, which contributes to the advancement of breast cancer research and treatment strategies.

The effects of Omega-3 fatty acids and vitamin D supplementation on the quality of life and blood inflammation markers in newly diagnosed breast cancer women: An open-labelled randomised controlled trial

Background and aimsNutritional intervention is one of the primary steps to improvement of health status and quality of life (QoL) in patients with cancer treated by chemotherapy. There is limited evidence on the potential nutritional intervention to complement active oncological treatment strategies in breast cancer (BC) patients in developing countries. The aim of the present study was to assess the effects of omega-3 fatty acids (ω3) and vitamin D3 (VitD) supplementations on the QoL and blood inflammation markers of tumor necrosis factor-alpha (TNF-α) and high-sensitive C-reactive protein (hsCRP) assessed among women newly diagnosed with BC in the Gaza Strip, Palestine MethodsA total of 88 BC women were randomly assigned into one of four groups: i) omega-3 fatty acid (ω3) group; ii) vitamin D (VitD) group; iii) ω3+VitD group, and iv) the control. Participants were received either two 300mg ω3 capsules daily, or one 50,000IU VitD tablet weekly, or both supplementation for 9-weeks. The QoL status was assessed by the European Organization for Research and Treatment of Cancer (EORTC) instruments of QLQ-C30 and QLQ-BR23 tools, while blood inflammatory markers of TNF-α hsCRP were used. All measurements were taken from baseline to the end of the intervention period. The detailed procedures of the present study were registered on ClinicalTrial.gov with the identifier NCT05331807. ResultsAt the end of the trial, participants in the ω3+VitD group showed a significant increase in overall global health status (p <0.01) compared to other groups. Additionally, this group showed significantly higher functional scores (all p <0.05) and lower scores for fatigue (p <0.01), nausea and vomiting, pain, and appetite loss (all p <0.05) at the end of the trial compared to baseline. Furthermore, comparisons between the intervention groups revealed a significant difference in blood concentrations of TNF-α and hsCRP (p <0.05). These significant differences were identified in hsCRP between ω3 and control groups (p <0.01). The ω3+VitD group demonstrated a significant reduction in both hsCRP and TNF-α levels (both p <0.05) from baseline. No significant changes in blood inflammatory markers were observed within the ω3 or VitD groups alone. ConclusionParticipants receiving daily ω3 and weekly VitD supplementation for 9 weeks showed a significant improved in QoL and blood inflammation markers among the newly diagnosed BC during their chemotherapy treatment.

Targeting ferroptosis reveals a new strategy for breast cancer treatment: a bibliometric study

BackgroundStudies exploring the role of ferroptosis in the pathogenesis of breast cancer have proliferated over the past decade, especially in 2023, with a staggering 217 publications in related studies. However, there are still significant gaps in comprehensive scientometric analysis and mapping of scientific studies, especially in terms of temporal and study area tracking, principal investigators, and the emergence of new hotspots.ObjectiveThis study aims to summarize the role of ferroptosis in the development of breast cancer and the latest research results on the ferroptosis-targeted treatment of breast cancer and to use bibliometric methods to draw a visual map to explore future research trends.MethodsOn May 11, 2024, this study updated the research progress related to ferroptosis and breast cancer over the past 11 years by retrieving data from January 1, 2014, to May 1, 2024, from the Web of Science database. In this research, many scientific analysis software including VOSviewer, chorddiag R Language Pack, Scimago Graphica, Citespace 6.3.R1, Cluster Profiler, enrichplot, ggplot2 R Language Pack, Cytoscape, and STRING online platform are used to make in-depth scientific analysis and visualization of the measurement results.ResultsStatistical analysis of these data showed that China accounted for 74.43% of the total publications, highlighting China’s dominant role in research on the relationship between ferroptosis and breast cancer. Several research institutions, including Sun Yat-sen University, Zhejiang University, and Shanghai Jiao Tong University, have achieved impressive results. Efferth, Thomas is the most prominent author in this field and has the highest number of publications in the subfield of oncology. This study clearly shows that ferroptosis plays a crucial role in the development of triple-negative breast cancer, hepatocellular carcinoma, glioma, leukemia, mitochondrial disease, lymphoma, bladder tumors, lung adenocarcinoma, and esophageal tumors.ConclusionThis study provides a comprehensive bibliometric evaluation that deepens our understanding of the role of ferroptosis in the pathogenesis of breast cancer and the current status of targeting ferroptosis for treating breast cancer. Thus, it helps researchers in related fields explore new research directions by comprehensively extracting important information and research hotspots.

Choice of treatment strategy for metastatic luminal HER2-negative breast cancer with germline mutations in the BRCA1/2 genes. Experience of the use of olaparib in clinical practice

Choice of treatment strategy for metastatic luminal HER2-negative breast cancer with germline mutations in the BRCA1/2 genes. Experience of the use of olaparib in clinical practice

Precision Cancer Therapy Enabled Anti-Epidermal Growth Factor Receptor-Conjugated Manganese Core Phthalocyanine Bismuth Nanocomposite for Dual Imaging-Guided Breast Cancer Treatment.

Cancer remains a formidable global health challenge, demanding the exploration of innovative treatment modalities with minimized side effects. One promising avenue involves the synergistic integration of targeted photothermal/photodynamic therapy (PTT/PDT), utilizing specially designed functional nanomaterials for precise cancer diagnosis and treatment. This study introduces a composite biomaterial, anti-epidermal growth factor receptor-conjugated manganese core phthalocyanine bismuth (anti-EGFR-MPB), synthesized for precise cancer imaging and treatment. The biomaterial, synthesized via a solvothermal process, effectively treats and images breast cancer in mouse models. Its biomimetic design targets cancer cells precisely, with dual imaging for real-time monitoring. The biomimetic design of the composite enables precise targeting of cancer cells, whereas the dual imaging allows for real-time visualization and monitoring of the treatment. Invivo examinations confirm substantial damage to tumor tissues with no recurrence following 808-nm laser irradiation. The composite shows strong fluorescence/photoacoustic imaging (PAI) contrast, aiding malignancy detection. Biological assays and histological analyses confirmed the efficacy of the nanocomposite in inducing apoptosis in cancer cells. The integrated targeted dual image-guided phototherapy offered by this composite substantially enhances the precision and efficacy of cancer therapy, achieving an impressive photothermal efficiency of ~33.8%. Our findings demonstrate the utility of the anti-EGFR-MPB nanocomposite for both invitro and invivo photoacoustic image-guided PTT and PDT. The optimal treatment strategy for triple-negative breast cancer is found to be the use of 250 μg/ml of nanocomposite irradiated with 1.0 W/cm2 808-nm laser for 7 min.

Synergistic effect of the sphingosine kinase inhibitor safingol in combination with 2'-nitroflavone in breast cancer.

Sphingosine kinase-1 (SPHK1), the enzyme that catalyzes the synthesis of the pro-oncogenic molecule sphingosine-1-phosphate, is commonly upregulated in breast cancer cells and has been linked with poor prognosis and progression by promoting cell transformation, proliferation, angiogenesis, and metastasis. Therefore, SPHK1-targeting drugs have been proposed for breast cancer treatment, with better antitumor results when they are combined with chemotherapy. Previously, we demonstrated that the synthetic flavonoid 2'-nitroflavone (2'NF) exerted a potent and selective antiproliferative effect in murine HER2-positive LM3 mammary tumor cells. As we found that these cells overexpress SPHK1, we decided to explore the antitumor action of the combination of SPHK inhibitors (safingol or SKI-II) with 2'NF. In vitro assays showed that the combination induced a synergistic antiproliferative effect in LM3 cells. Similar results were obtained when human HER2-positive MDA-MB-453 breast cancer cells were treated with the combination of 2'NF/safingol. We also found that safingol potentiated the 2'NF apoptotic effect in both cell lines. The synergistic antitumor effect was confirmed in vivo in an LM3 syngeneic breast cancer model. Moreover, western blot analysis of tumor lysates revealed that combined treatment increased PARP cleavage and Bax protein levels and decreased anti-apoptotic Bcl-xL and Bcl-2 protein levels. Additionally, mice treated with both compounds showed no histopathological effects on different organ tissues. In summary, these findings suggest that the combination safingol/2'NF can be proposed as a potential therapeutic strategy for HER2-positive breast cancer treatment. KEY MESSAGES: The combination safingol/2'-nitroflavone exerts a synergic antitumor action in vitro. Safingol potentiates 2'-nitroflavone apoptotic effect in breast cancer cells. Safingol enhances the 2'-nitroflavone antitumor activity in vivo in breast cancer.

Review on the application of ginsenosides and their pharmaceutical preparations in the treatment of breast cancer

Ginsenosides, as the main active ingredients of ginseng, have shown great potential in the treatment of breast cancer. Studies have found that many types of ginsenosides, such as PPD ginsenosides Rh2, Rg3, CK and PPT ginsenosides Rg1, Rg2, have inhibitory effects on breast cancer cells. These components can effectively inhibit the development of breast cancer by directly inhibiting the proliferation of cancer cells, inducing apoptosis, enhancing the anticancer ability of NK cells, and remodeling the tumor microenvironment. In addition, the liposome and nanoparticle drug delivery system synthesized by ginsenoside showed great advantages in the application of drug formulations, providing a new strategy for the targeted transportation of antitumor drugs and improving the tumor killing ability. These research results not only provide a new strategy for breast cancer treatment, but also expand the application prospect of ginsenosides in cancer treatment. In the future, with the in-depth research, ginsenosides and their pharmaceutical preparations are expected to play a greater role in the treatment of breast cancer and bring more hope to patients.

Integration of transcriptomics and machine learning for insights into breast cancer: exploring lipid metabolism and immune interactions.

Breast cancer (BRCA) represents a substantial global health challenge marked by inadequate early detection rates. The complex interplay between the tumor immune microenvironment and fatty acid metabolism in BRCA requires further investigation to elucidate the specific role of lipid metabolism in this disease. We systematically integrated nine machine learning algorithms into 184 unique combinations to develop a consensus model for lipid metabolism-related prognostic genes (LMPGS). Additionally, transcriptomics analysis provided a comprehensive understanding of this prognostic signature. Using the ESTIMATE method, we evaluated immune infiltration among different risk subgroups and assessed their responsiveness to immunotherapy. Tailored treatments were screened for specific risk subgroups. Finally, we verified the expression of key genes through in vitro experiments. We identified 259 differentially expressed genes (DEGs) related to lipid metabolism through analysis of the cancer genome atlas program (TCGA) database. Subsequently, via univariate Cox regression analysis and C-index analysis, we developed an optimal machine learning algorithm to construct a 21-gene LMPGS model. We used optimal cutoff values to divide the lipid metabolism prognostic gene scores into two groups according to high and low scores. Our study revealed distinct biological functions and mutation landscapes between high-scoring and low-scoring patients. The low-scoring group presented a greater immune score, whereas the high-scoring group presented enhanced responses to both immunotherapy and chemotherapy drugs. Single-cell analysis highlighted significant upregulation of CPNE3 in epithelial cells. Moreover, by employing molecular docking, we identified niclosamide as a potential targeted therapeutic drug. Finally, our experiments demonstrated high expression of MTMR9 and CPNE3 in BRCA and their significant correlation with prognosis. By employing bioinformatics and diverse machine learning algorithms, we successfully identified genes associated with lipid metabolism in BRCA and uncovered potential therapeutic agents, thereby offering novel insights into the mechanisms and treatment strategies for BRCA.

The Influence of Microbiota on Breast Cancer: A Review

Breast cancer remains one of the leading causes of death among women worldwide, and recent research highlights its growing connection to alterations in the microbiota. This review delves into the intricate relationship between microbiotas and breast cancer, exploring its presence in healthy breast tissue, its changes during cancer progression, and its considerable impact on both the tumor microenvironment (TME) and the tumor immune microenvironment (TIME). We extensively analyze how the microbiota influences cancer growth, invasion, metastasis, resistance to drugs, and the evasion of the immune system, with a special focus on its effects on the TIME. Furthermore, we investigate distinct microbial profiles associated with the four primary molecular subtypes of breast cancer, examining how the microbiota in tumor tissues compares with that in adjacent normal tissues. Emerging studies suggest that microbiotas could serve as valuable diagnostic and prognostic biomarkers, as well as targets for therapy. This review emphasizes the urgent need for further research to improve strategies for breast cancer prevention, diagnosis, and treatment. By offering a detailed examination of the microbiota’s critical role in breast cancer, this review aims to foster the development of novel microbiota-based approaches for managing the disease.

Bacterial Living Therapeutics with Engineered Protein Secretion Circuits to Eliminate Breast Cancer Cells.

Cancer therapy can be limited by potential side effects, and bacteria-based living cancer therapeutics have gained scientific interest in recent years. However, the full potential of bacteria as therapeutics has yet to be explored due to engineering challenges. In this study, we present a bacterial device designed to specifically target and eliminate breast cancer cells. We have engineered Escherichia coli (E. coli) to bind to HER2 receptors on breast cancer cells while also secreting a toxin, HlyE, which is a pore-forming protein. The binding of E. coli to HER2 is facilitated by a nanobody expressed on the bacteria's surface via the Ag43 autotransporter protein system. Our findings demonstrate that the nanobody efficiently binds to HER2+ cells in vitro, and we have utilized the YebF secretion tag to secrete HlyE and kill the target cancer cells. Overall, our results highlight the potential of our engineered bacteria as an innovative strategy for breast cancer treatment.

TNBC-DX genomic test in early-stage triple-negative breast cancer treated with neoadjuvant taxane-based therapy

Identification of biomarkers to optimize treatment strategies for early-stage triple-negative breast cancer (TNBC) is crucial. This study presents the development and validation of TNBC-DX, a novel test aimed at predicting both short- and long-term outcomes in early-stage TNBC. The objective of this study was to evaluate the association between TNBC-DX and efficacy outcomes [pathologic complete response (pCR), distant disease-free survival (DDFS) or event-free survival (EFS), and overall survival (OS)] in the validation cohorts. Information from 1259 patients with early-stage TNBC (SCAN-B, CALGB-40603, and BrighTNess) was used to establish the TNBC-DX scores. Independent validation of TNBC-DX was carried out in three studies: (i) WSG-ADAPT-TN; (ii) MMJ-CAR-2014-01; and (iii) NeoPACT, including 527 patients with stage I-III TNBC undergoing neoadjuvant chemotherapy. In WSG-ADAPT-TN, patients were randomized to receive nab-paclitaxel plus gemcitabine or carboplatin. In MMJ-CAR-2014-01, patients received carboplatin plus docetaxel. In NeoPACT, patients received carboplatin plus docetaxel and pembrolizumab. TNBC-DX test was created incorporating the 10-gene Core Immune Gene module, the 4-gene tumor cell proliferation signature, tumor size, and nodal staging. In the two independent validation cohorts without pembrolizumab, the TNBC-DX pCR score was significantly associated with pCR after adjustment for clinicopathological variables and treatment regimen [odds ratio per 10-unit increment 1.34, 95% confidence interval (CI) 1.20-1.52, P < 0.001]. pCR rates for the TNBC-DX pCR-high, pCR-medium, and pCR-low categories were 56.3%, 53.6%, and 22.5% respectively (odds ratio for pCR-high versus pCR-low 3.48, 95% CI 1.72-7.15, P < 0.001). Inaddition, the TNBC-DX risk score was significantly associated with DDFS [hazard ratio (HR) high-risk versus low-risk 0.24, 95% CI 0.15-0.41, P < 0.001] and OS (HR 0.19, 95% CI 0.11-0.35, P < 0.001). In the validation cohort with pembrolizumab, the TNBC-DX scores were significantly associated with pCR, EFS, and OS. TNBC-DX predicts pCR to neoadjuvant taxane-carboplatin in stage I-III TNBC and helps to forecast the patient's long-term survival in the absence of neoadjuvant anthracycline-cyclophosphamide, and independent of pembrolizumab use.

231 (PB219): Optimizing treatment strategies for HER2-positive breast and gastric cancer: preclinical evaluation of disitamab vedotin, trastuzumab emtansine, trastuzumab deruxtecan, and their combinations therapies in mouse models

231 (PB219): Optimizing treatment strategies for HER2-positive breast and gastric cancer: preclinical evaluation of disitamab vedotin, trastuzumab emtansine, trastuzumab deruxtecan, and their combinations therapies in mouse models

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Background: Dyslipidaemia has been proposed as a potential risk factor for breast cancer. This study aimed to evaluate the association between serum lipid profiles and breast cancer among women, comparing lipid levels between breast cancer patients and healthy controls. Methods: A hospital-based cross-sectional observational study was conducted at SMS Medical College and Hospital, Jaipur, from ethics committee approval until June 2024. The study included 100 breast cancer patients and 100 matched healthy controls. Inclusion criteria were individuals aged 18 years or older with informed consent, while exclusion criteria included critically ill patients, those with malignancies other than breast cancer, and those on lipid-lowering therapy. The lipid profile was assessed according to the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) guidelines. Data collection involved clinical examination, anthropometric measurements, and biochemical analysis of serum lipid levels. Results: The mean age of participants was 48.5 years for the Case Group and 45.92 years for the Control Group. Serum lipid profiles showed significantly higher levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL), and triglycerides (TG) in breast cancer patients compared to controls, with TC at 197 ± 42.2 mg/dl vs. 174.06 ± 38.46 mg/dl, LDL at 152.65 ± 32.57 mg/dl vs. 121.09 ± 24.56 mg/dl, and TG at 162.12 ± 15.64 mg/dl vs. 138.23 ± 22.99 mg/dl. High-density lipoprotein cholesterol (HDL) was significantly lower in breast cancer patients (36.0 ± 16.60 mg/dl vs. 50.60 ± 17.64 mg/dl). Subgroup analysis by age showed similar trends across different age groups. No significant differences were observed between premenopausal and postmenopausal women in lipid levels. Conclusion: Elevated serum lipid levels, particularly TC, LDL, and TG, are associated with breast cancer. Monitoring and managing lipid levels may offer potential benefits in breast cancer prevention and treatment strategies.

Recent progress and applications of single-cell sequencing technology in breast cancer.

Single-cell RNA sequencing (scRNA-seq) technology enables the precise analysis of individual cell transcripts with high sensitivity and throughput. When integrated with multiomics technologies, scRNA-seq significantly enhances the understanding of cellular diversity, particularly within the tumor microenvironment. Similarly, single-cell DNA sequencing has emerged as a powerful tool in cancer research, offering unparalleled insights into the genetic heterogeneity and evolution of tumors. In the context of breast cancer, this technology holds substantial promise for decoding the intricate genomic landscape that drives disease progression, treatment resistance, and metastasis. By unraveling the complexities of tumor biology at a granular level, single-cell DNA sequencing provides a pathway to advancing our comprehension of breast cancer and improving patient outcomes through personalized therapeutic interventions. As single-cell sequencing technology continues to evolve and integrate into clinical practice, its application is poised to revolutionize the diagnosis, prognosis, and treatment strategies for breast cancer. This review explores the potential of single-cell sequencing technology to deepen our understanding of breast cancer, highlighting key approaches, recent advancements, and the role of the tumor microenvironment in disease plasticity. Additionally, the review discusses the impact of single-cell sequencing in paving the way for the development of personalized therapies.