scholarly journals Activation of TGF-beta signalling in breast cancer metastatic cells

2008 ◽  
Vol 10 (S2) ◽  
Author(s):  
S Giampieri ◽  
E Sahai
Keyword(s):  
Breast Cancer ◽  
Tgf Beta ◽  
Metastatic Cells

Bioavailability of TGF-Beta in Breast Cancer

2005 ◽  
Author(s):  
Michael Jobling ◽  
Mary H. Barcellos-Hoff ◽  
Joni Mott
Keyword(s):  
Breast Cancer ◽  
Tgf Beta

scholarly journals Discovering novel cancer bio-markers in acquired lapatinib resistance using Bayesian methods

2021 ◽  
Author(s):  
A K M Azad ◽  
Salem A Alyami
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Sampling Methods ◽  
Differential Expression Analysis ◽  
Breast Cancer Cell Lines ◽  
Mcmc Methods ◽  
Tgf Beta ◽  
Exponential Random Graph Models ◽  
Statistical Process ◽  
Dual Inhibitor

Abstract Signalling transduction pathways (STPs) are commonly hijacked by many cancers for their growth and malignancy, but demystifying their underlying mechanisms is difficult. Here, we developed methodologies with a fully Bayesian approach in discovering novel driver bio-markers in aberrant STPs given high-throughput gene expression (GE) data. This project, namely ‘PathTurbEr’ (Pathway Perturbation Driver) uses the GE dataset derived from the lapatinib (an EGFR/HER dual inhibitor) sensitive and resistant samples from breast cancer cell lines (SKBR3). Differential expression analysis revealed 512 differentially expressed genes (DEGs) and their pathway enrichment revealed 13 highly perturbed singalling pathways in lapatinib resistance, including PI3K-AKT, Chemokine, Hippo and TGF-$\beta $ singalling pathways. Next, the aberration in TGF-$\beta $ STP was modelled as a causal Bayesian network (BN) using three MCMC sampling methods, i.e. Neighbourhood sampler (NS) and Hit-and-Run (HAR) sampler that potentially yield robust inference with lower chances of getting stuck at local optima and faster convergence compared to other state-of-art methods. Next, we examined the structural features of the optimal BN as a statistical process that generates the global structure using $p_1$-model, a special class of Exponential Random Graph Models (ERGMs), and MCMC methods for their hyper-parameter sampling. This step enabled key drivers identification that drive the aberration within the perturbed BN structure of STP, and yielded 34, 34 and 23 perturbation driver genes out of 80 constituent genes of three perturbed STP models of TGF-$\beta $ signalling inferred by NS, HAR and MH sampling methods, respectively. Functional-relevance and disease-relevance analyses suggested their significant associations with breast cancer progression/resistance.

scholarly journals Thrombospondin‐4 mediates hyperglycemia‐ and TGF ‐beta‐induced inflammation in breast cancer

2020 ◽  
Author(s):  
Santoshi Muppala ◽  
Roy Xiao ◽  
Jasmine Gajeton ◽  
Irene Krukovets ◽  
Dmitriy Verbovetskiy ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tgf Beta ◽  
Thrombospondin 4

scholarly journals Clinical significance of proliferative potential of occult metastatic cells in bone marrow of patients with breast cancer

2003 ◽  
Vol 89 (3) ◽  
pp. 539-545 ◽  
Author(s):  
J-Y Pierga ◽  
C Bonneton ◽  
H Magdelénat ◽  
A Vincent-Salomon ◽  
C Nos ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Bone Marrow ◽  
Clinical Significance ◽  
Proliferative Potential ◽  
Metastatic Cells

365 Identification of a novel TGF-beta-induced signaling cascade involved in EMT and invasion of breast cancer cells

2004 ◽  
Vol 2 (8) ◽  
pp. 110
Author(s):  
A. Viloria-Petit ◽  
B. Ozdamar ◽  
R. Bose ◽  
H.-R. Wang ◽  
M. Barrios-Rodiles ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Signaling Cascade ◽  
Tgf Beta

scholarly journals Comparison of the effect of rhodium citrate-associated iron oxide nanoparticles on metastatic and non-metastatic breast cancer cells

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Natalia Lemos Chaves ◽  
Danilo Aquino Amorim ◽  
Cláudio Afonso Pinho Lopes ◽  
Irina Estrela-Lopis ◽  
Julia Böttner ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Human Tumor ◽  
Metastatic Breast ◽  
Cytotoxic Action ◽  
Dependent Manner ◽  
Metastatic Cells ◽  
Mcf 7

Abstract Background Nanocarriers have the potential to improve the therapeutic index of currently available drugs by increasing drug efficacy, lowering drug toxicity and achieving steady-state therapeutic levels of drugs over an extended period. The association of maghemite nanoparticles (NPs) with rhodium citrate (forming the complex hereafter referred to as MRC) has the potential to increase the specificity of the cytotoxic action of the latter compound, since this nanocomposite can be guided or transported to a target by the use of an external magnetic field. However, the behavior of these nanoparticles for an extended time of exposure to breast cancer cells has not yet been explored, and nor has MRC cytotoxicity comparison in different cell lines been performed until now. In this work, the effects of MRC NPs on these cells were analyzed for up to 72 h of exposure, and we focused on comparing NPs’ therapeutic effectiveness in different cell lines to elect the most responsive model, while elucidating the underlying action mechanism. Results MRC complexes exhibited broad cytotoxicity on human tumor cells, mainly in the first 24 h. However, while MRC induced cytotoxicity in MDA-MB-231 in a time-dependent manner, progressively decreasing the required dose for significant reduction in cell viability at 48 and 72 h, MCF-7 appears to recover its viability after 48 h of exposure. The recovery of MCF-7 is possibly explained by a resistance mechanism mediated by PGP (P-glycoprotein) proteins, which increase in these cells after MRC treatment. Remaining viable tumor metastatic cells had the migration capacity reduced after treatment with MRC (24 h). Moreover, MRC treatment induced S phase arrest of the cell cycle. Conclusion MRC act at the nucleus, inhibiting DNA synthesis and proliferation and inducing cell death. These effects were verified in both tumor lines, but MDA-MB-231 cells seem to be more responsive to the effects of NPs. In addition, NPs may also disrupt the metastatic activity of remaining cells, by reducing their migratory capacity. Our results suggest that MRC nanoparticles are a promising nanomaterial that can provide a convenient route for tumor targeting and treatment, mainly in metastatic cells.

Different Targeting Strategies for Treating Breast Cancer Bone Metastases

2018 ◽  
Vol 24 (28) ◽  
pp. 3320-3331 ◽  
Author(s):  
Iram Irshad ◽  
Pegah Varamini
Keyword(s):  
Breast Cancer ◽  
Quality Of Life ◽  
Bone Metastasis ◽  
Treatment Options ◽  
Tumor Burden ◽  
Breast Cancer Patients ◽  
Physiological Processes ◽  
Metastatic Cells ◽  
Skeletal Complications

Background: Breast cancer is the most frequently diagnosed malignancy in women worldwide. Breast cancer tends to metastasize to bone. Around 70% of the breast cancer patients eventually develop bone metastasis. After the bone invasion, metastatic cells disrupt the balance between osteoblastic and osteoclastic activities, leading to skeletal complications, characterized by pain and pathological fractures and hence worsening the patient's quality of life. Once tumor invades the bone, it is hard to treat it with, the so-far available treatments options (e.g. bisphosphonates and denosumab). Bone metastasis should be essentially controlled, in cancer treatment and there is a strong need to explore new, more efficient therapeutic targets. This review discusses the bone physiological processes and the recent advances in exploring different pathways involved in bone metastasis. Furthermore, some novel treatment options, which are under preclinical and clinical investigations, are highlighted. Conclusion: A deeper understanding of these metastatic pathways can provide oncology researchers with novel avenues for treating bone metastasis, one of the main challenges to cure breast cancer. The restoration of healthy bone environment will not only improve the patient's quality of life but also reduces the tumor burden.

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