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Advancing Precision Medicine: Tailoring Personalized Therapies
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2020
Kyle B. Matchett, Niamh Lynam-Lennon, R. William Watson, James A. L. Brown
Dr. Luca Magnani’s group (Imperial College London, London, UK) demonstrated the importance of combining metabolic and mutation profiling in recurrent breast cancer patients. Endocrine therapies represent the gold standard for the treatment of breast cancer as first line treatments following curative surgery. Importantly, these therapies target, directly or indirectly, estrogen receptor alpha (ERα). Aromatase inhibitors (AIs) block estrogen production in various sites of the body, while Tamoxifen directly antagonizes estrogen receptor (ER) activation. Their similar method of action suggested that any resistance mechanisms would likewise be similar. However, recent evidence in metastatic patients revealed AI resistant tumors were particularly enriched for ER mutations, which were demonstrated to confer resistance [23, 24]. Moreover, drug-specific resistance mechanisms were not limited to ER mutations, as cholesterol biosynthesis can directly fuel ER activation via alternative ligands. Examining a cohort of matched primary-metastatic relapses treated uniquely with either Tamoxifen or AIs they observed AI-treated patients had significant amplification of the aromatase gene CYP19A1 and this amplification event was rare in patients treated with Tamoxifen [25]. This highlighted the importance of profiling tumor recurrence, allowing the monitoring of acquired resistance mechanisms and tailoring of treatments.
Advancing Precision Medicine: Tailoring Personalized Therapies
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2019
Kyle B. Matchett, Niamh Lynam-Lennon, R. William Watson, James A. L. Brown
Dr. Luca Magnani’s group (Imperial College London, London, UK) demonstrated the importance of combining metabolic and mutation profiling in recurrent breast cancer patients. Endocrine therapies represent the gold standard for the treatment of breast cancer as first line treatments following curative surgery. Importantly, these therapies target, directly or indirectly, estrogen receptor alpha (ERα). Aromatase inhibitors (AIs) block estrogen production in various sites of the body, while Tamoxifen directly antagonizes estrogen receptor (ER) activation. Their similar method of action suggested that any resistance mechanisms would likewise be similar. However, recent evidence in metastatic patients revealed AI resistant tumors were particularly enriched for ER mutations, which were demonstrated to confer resistance [23, 24]. Moreover, drug-specific resistance mechanisms were not limited to ER mutations, as cholesterol biosynthesis can directly fuel ER activation via alternative ligands. Examining a cohort of matched primary-metastatic relapses treated uniquely with either Tamoxifen or AIs they observed AI-treated patients had significant amplification of the aromatase gene CYP19A1 and this amplification event was rare in patients treated with Tamoxifen [25]. This highlighted the importance of profiling tumor recurrence, allowing the monitoring of acquired resistance mechanisms and tailoring of treatments.
Phenolic Compounds potential health Benefits and toxicity
Published in Quan V. Vuong, Utilisation of Bioactive Compounds from Agricultural and Food Waste, 2017
Deep Jyoti Bhuyan, Amrita Basu
Myricetin has been broadly studied to investigate its anticancer properties and mechanisms of action against different types of cancer (Maggiolini et al. 2005, Lu et al. 2006, Kumamoto et al. 2009, Sun et al. 2012, Devi et al. 2015). For instance, in human colon cancer cells, myricetin induces cell death via BAX/BCL2-dependent pathway (Kim et al. 2014), whereas in the colorectal carcinoma cells, it inhibits MMP2 protein expression and enzyme activity (Ko et al. 2005). It also acts as an agonist for estrogen receptor alpha which leads to inhibition of hormone-dependent MCF7 breast-cancer cell proliferation (Maggiolini et al. 2005). Additionally, myricetin interacts with a number of oncoproteins, such as protein kinase B (PKB) (AKT), Fyn, MEK1, and JAK1–STAT3 (Janus kinase–signal transducer and activator of transcription 3), and reduces the neoplastic transformation of cancer cells (Kumamoto et al. 2009, Sun et al. 2012, Devi et al. 2015). Lu et al. (2006) showed that the plant flavonoids—quercetin and myricetin, inhibit thioredoxin reductase (TrxR) (which is overexpressed in many aggressive tumors) that induces cell death.
Folic acid engineered sulforaphane loaded microbeads for targeting breast cancer
Published in Journal of Biomaterials Science, Polymer Edition, 2023
Zafar Khan, Abdulsalam Alhalmi, Neha Tyagi, Wasi Uzzaman Khan, Afsana Sheikh, Mohammed A. S. Abourehab, Kanchan Kohli, Prashant Kesharwani
Sulforaphane (SFN) or 1-isothiocyanato-4-(methanesulfinyl) butane is a sulphur-rich compound having powerful anti-carcinogen activity and antioxidant properties. It is mostly present in cruciferous vegetables like broccoli, Brussels sprouts, cauliflower, cabbage, and other cruciferous vegetables [19–21]. The mechanism by which it exhibits chemo-preventive or chemotherapeutic effects includes modulation of phase 1 and phase 2 xenobiotic-metabolizing enzymes as well as direct inhibition of carcinogen binding to DNA. As a result, it reduces the mutation rate by inhibiting DNA adduct formation. Sulforaphane has been found to promote apoptosis, toxifies potential carcinogens, suppress cell cycle progression, and inhibit angiogenesis of human breast cancer cells. It inhibits the expression of estrogen receptor alpha in breast cancer cells [22–25]. Designing a novel pharmaceutical formulation necessitates a systematic and frenetic plane including assets (manpower, time, and money) as well as number of experimental runs. We have previously developed SFN decorated gold nanoparticle and investigated its effect on tumor selectivity and tumor reduction efficiency. The developed preparation revealed enhanced distribution, significant cell reducing effect and increased retention at the site of tumor [26]. Another study reported the synergistic effect of selenium nanoparticle in conjugation to SFN, wherein high tumor accumulation and improved anti-cancer effect was reported [27].
Impact of occupational cadmium exposure on bone in sewage workers
Published in International Journal of Occupational and Environmental Health, 2018
Mona M Taha, Heba Mahdy-Abdallah, Eman M Shahy, Khadiga S Ibrahim, Safaa Elserougy
Accumulating evidence suggested that estrogen seems to play a major role in male bone metabolism [16]. Estrogen effect was mediated by estrogen receptor (estrogen receptor alpha [ER-α]), which represents a member of steroid hormone receptor family. It functions as an important part of the hormone–receptor complex that promotes specific target genes expression [17]. Genetic alterations in multiple genes can account for this genetic component and ER-α gene represents one of the various potential candidates. Kim et al. [17] recorded that ER-α gene polymorphism is associated with osteoporosis development in Korean vegetarian men. Polymorphism of the ER-α gene found on intron 1 may affect gene expression and/or interindividual susceptibility in the estrogen hormone through its regulatory action in mRNA transcription. Other possibility was due to that this polymorphism might be associated with unidentified polymorphisms that is responsible for the quality or function of the protein encoded by the ER-α gene [18].