scholarly journals Diallyl disulfide and diallyl trisulfide in garlic as novel therapeutic agents to overcome drug resistance in breast cancer

2021 ◽  
Author(s):  
RamaRao Malla ◽  
Rakshmitha Marni ◽  
Anindita Chakraborty ◽  
Mohammad Amjad Kamal
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Therapeutic Agents ◽  
Diallyl Disulfide ◽  
Diallyl Trisulfide ◽  
Novel Therapeutic

scholarly journals CBP/β-Catenin/FOXM1 Is a Novel Therapeutic Target in Triple Negative Breast Cancer

Cancers ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 525 ◽  
Author(s):  
Alexander Ring ◽  
Cu Nguyen ◽  
Goar Smbatyan ◽  
Debu Tripathy ◽  
Min Yu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Drug Resistance ◽  
Triple Negative Breast Cancer ◽  
Therapeutic Target ◽  
Triple Negative ◽  
Creb Binding Protein ◽  
Novel Therapeutic

Background: Triple negative breast cancers (TNBCs) are an aggressive BC subtype, characterized by high rates of drug resistance and a high proportion of cancer stem cells (CSC). CSCs are thought to be responsible for tumor initiation and drug resistance. cAMP-response element-binding (CREB) binding protein (CREBBP or CBP) has been implicated in CSC biology and may provide a novel therapeutic target in TNBC. Methods: RNA Seq pre- and post treatment with the CBP-binding small molecule ICG-001 was used to characterize CBP-driven gene expression in TNBC cells. In vitro and in vivo TNBC models were used to determine the therapeutic effect of CBP inhibition via ICG-001. Tissue microarrays (TMAs) were used to investigate the potential of CBP and associated proteins as biomarkers in TNBC. Results: The CBP/ß-catenin/FOXM1 transcriptional complex drives gene expression in TNBC and is associated with increased CSC numbers, drug resistance and poor survival outcome. Targeting of CBP/β-catenin/FOXM1 with ICG-001 eliminated CSCs and sensitized TNBC tumors to chemotherapy. Immunohistochemistry of TMAs demonstrated a significant correlation between FOXM1 expression and TNBC subtype. Conclusion: CBP/β-catenin/FOXM1 transcriptional activity plays an important role in TNBC drug resistance and CSC phenotype. CBP/β-catenin/FOXM1 provides a molecular target for precision therapy in triple negative breast cancer and could form a rationale for potential clinical trials.

scholarly journals Targeted Therapy in Multiple Myeloma

2005 ◽  
Vol 12 (2) ◽  
pp. 91-104 ◽  
Author(s):  
Wee Joo Chng ◽  
Lee Gong Lau ◽  
Noorainun Yusof ◽  
Benjamin M. F. Mow
Keyword(s):  
Multiple Myeloma ◽  
Drug Resistance ◽  
Clinical Trials ◽  
Intracellular Signaling ◽  
Resistance Mechanism ◽  
Growth Factor Receptor ◽  
Therapeutic Agents ◽  
Farnesyltransferase Inhibitors ◽  
Antisense Gene ◽  
Novel Therapeutic

Background: Multiple myeloma (MM) is an incurable malignancy. Recent insights into its biology has allowed the use of novel therapies targeting not only the deregulated intracellular signaling in MM cells but also its interaction with the bone marrow microenvironment that confers drug resistance, growth, and survival advantage to the malignant cells. Methods: We review and summarize the recent advances in our knowledge of myeloma biology as well as the mechanism of action and clinical efficacy for novel therapeutic agents in clinical trials. Results: Several novel therapeutic agents are currently in clinical trials. Thalidomide is already established for both initial and salvage treatment. Bortezomib is being tested alone and in combination with conventional chemotherapy in various settings. Other agents are less effective in producing response but have been able to stabilize disease in patients with relapsed and/or refractory disease, such as arsenic trioxide, farnesyltransferase inhibitors, 2-methoxyestradiol, and vascular endothelial growth factor receptor inhibitors. Insights into drug resistance mechanism have also led to the development of novel agents that sensitize myeloma cells to chemotherapy (Bcl-2 antisense). Gene expression studies have in many instances identified pathways other than the intended target of the drug and have provided insights into the therapeutic mechanisms. Conclusions: In the future, patients with MM will have more therapeutic options available than ever before. The challenge will be to identify patient subgroups that will benefit most from the different therapies and then determine how these biologically based therapies could be combined and incorporated into the overall management of patients.

scholarly journals BET inhibitors as novel therapeutic agents in breast cancer

Oncotarget ◽  
2017 ◽  
Vol 8 (41) ◽  
pp. 71285-71291 ◽  
Author(s):  
Alberto Ocaña ◽  
Cristina Nieto-Jiménez ◽  
Atanasio Pandiella
Keyword(s):  
Breast Cancer ◽  
Therapeutic Agents ◽  
Bet Inhibitors ◽  
Novel Therapeutic

scholarly journals Role of Novel Therapeutic Agents in Modulating Invadopodia Formation in Metastatic Breast Cancer

2020 ◽  
Vol 49 (6) ◽  
pp. 1351-1358
Author(s):  
Siti Nor Aini Harun ◽  
Nurul Akmaryanti Abdullah ◽  
Noraina Muhamad Zakuan ◽  
Hafizah Abdul Hamid ◽  
Muhammad Zulfadli Mehat ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Metastatic Breast ◽  
Therapeutic Agents ◽  
Invadopodia Formation ◽  
Novel Therapeutic

Coumarin Hybrids: Promising Scaffolds in the Treatment of Breast Cancer

2019 ◽  
Vol 19 (17) ◽  
pp. 1443-1458 ◽  
Author(s):  
Rohit Bhatia ◽  
Ravindra K. Rawal
Keyword(s):  
Breast Cancer ◽  
Lung Cancer ◽  
Therapeutic Agents ◽  
Toxicity Profile ◽  
Biological Targets ◽  
Organ Systems ◽  
Hybrid Molecules ◽  
Cause Of Deaths ◽  
Low Toxicity ◽  
Diverse Mode

: Breast cancer is the most common invasive cancer in women, and the second main cause of deaths in women, after lung cancer. There is continuous advancement in the development of therapeutic agents against breast cancer in recent years and it is still in progress. Development of hybrid molecules by combining different pharmacophores to obtain significant biological activity is an excellent approach. Coupling of coumarin scaffold with other distinct motifs has led to the design of newer compounds against breast cancer. These distinct pharmacophores possess a diverse mode of action as well as selectivity. It has been reported in the literature that coumarin hybrids possess significant potency against breast cancer by binding to various biological targets which are associated with breast cancer. Due to low toxicity profile on various organ systems, coumarin hybrids have nowadays attracted the keen attention of researchers to explore their therapeutic ability against breast cancer. Reported coumarin hybrids include coupling with isoxazole, thiazole, monastrol, chalcone, triazole, sulphonamide, triphenylethylene, benzimidazole, pyran, imidazole, stilbene, oestrogen, phenylsulphonylfuroxan, etc. In the present review, a description of various coumarin hybrid molecules has been presented along with their structural-activity relationships.

Clinical applications of circulating tumor DNA in monitoring breast cancer drug resistance

2020 ◽  
Vol 16 (34) ◽  
pp. 2863-2878
Author(s):  
Yang Liu ◽  
Qian Du ◽  
Dan Sun ◽  
Ruiying Han ◽  
Mengmeng Teng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Digital Pcr ◽  
Circulating Tumor Dna ◽  
Resistance Mechanisms ◽  
Clinical Applications ◽  
Current Status ◽  
Cancer Drug ◽  
Genomic Alteration ◽  
Tumor Dna

Breast cancer is one of the leading causes of cancer-related deaths in women worldwide. Unfortunately, treatments often fail because of the development of drug resistance, the underlying mechanisms of which remain unclear. Circulating tumor DNA (ctDNA) is free DNA released into the blood by necrosis, apoptosis or direct secretion by tumor cells. In contrast to repeated, highly invasive tumor biopsies, ctDNA reflects all molecular alterations of tumors dynamically and captures both spatial and temporal tumor heterogeneity. Highly sensitive technologies, including personalized digital PCR and deep sequencing, make it possible to monitor response to therapies, predict drug resistance and tailor treatment regimens by identifying the genomic alteration profile of ctDNA, thereby achieving precision medicine. This review focuses on the current status of ctDNA biology, the technologies used to detect ctDNA and the potential clinical applications of identifying drug resistance mechanisms by detecting tumor-specific genomic alterations in breast cancer.

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