Background/Aim: Trastuzumab and tamoxifen are two of the most widely prescribed anti-cancer drugs for breast cancer (BC). To date, few studies have explored the impact of anticancer drugs on metabolic pathways in BC. Metabolomics is an emerging technology that can identify new biomarkers for tracking therapy response and novel therapeutic targets. Materials and Methods: We employed ultra-high-performance liquid chromatography-quadrupole time of flight mass spectrometry (UHPLC-QTOF-MS) to investigate changes in MCF-7 and SkBr3 cell lines treated with either tamoxifen, trastuzumab or a combination of both. The Bruker Human Metabolome Database (HMDB) metabolite library was used to match spectra and the MetaboScape software to assign each feature with a putative metabolite name or molecular formula for metabolite annotation. Results: A total of 98 metabolites were found to significantly differ in abundance in MCF-7 and SkBr3 treated cells. Moreover, the metabolic profile of the combination medication is similar to that of tamoxifen alone, according to functional enrichment analysis. Conclusion: Tamoxifen/trastuzumab treatment had a significant effect on pathways essential for the control of energy-production, which have previously been linked to cancer progression, and aggressivenessCancer is considered the second leading cause of death after heart disease with the number of cases estimated to grow to over 13.1 million by 2030 (1). Worldwide, breast cancer (BC) is the second leading cause of cancer-related death, after lung cancer, among women (2-5). This cancer type is recognized as a heterogeneous and multifaceted disease with a varied range of pathological, clinical, and molecular characteristics. BC is hormone-responsive and classified into three subtypes based on specific estrogen (E), progesterone (P), and human epidermal growth factor molecular biomarkers. The main hormones involved in the regulation of tumor growth or regression and cellular function are estrogen and progesterone. After malignant transformation, because the mammary glands contain unique receptor sites, the cells may maintain all or some of the normal complement of receptor sites (6-9). With respect to the retained receptor sites, breast tumors are classified as one of the estrogen-or progesterone-positive or -negative receptor (ER-/PRpositive/-negative) subtypes. Experimental breast tumor models demonstrate evidence of PR estrogen regulation, indicating that PR is present in approximately 59% of ERpositive metastatic tumors (10,11). Clinical studies have shown that women with hormone receptor-positive tumors have successfully survived therapy with adjuvant hormone and/or chemotherapy regimens (12, 13). Human epidermal growth factor receptor (HER2) is a third molecular target that belongs to the transmembrane receptor tyrosine kinase family. It plays an essential role in the mediation of growth and progression of breast cancer cells (14). Worldwide, approximately 20% of BC overexpress the HER2 receptor 79 This article is freely accessible onli...

Skin cancer, including malignant melanoma (MM) and keratinocyte carcinoma (KC), historically named non-melanoma skin cancers (NMSC), represents the most common type of cancer among the white skin population. Despite decades of clinical research, the incidence rate of melanoma is increasing globally. Therefore, a better understanding of disease pathogenesis and resistance mechanisms is considered vital to accomplish early diagnosis and satisfactory control. The “Omics” field has recently gained attention, as it can help in identifying and exploring metabolites and metabolic pathways that assist cancer cells in proliferation, which can be further utilized to improve the diagnosis and treatment of skin cancer. Although skin tissues contain diverse metabolic enzymes, it remains challenging to fully characterize these metabolites. Metabolomics is a powerful omics technique that allows us to measure and compare a vast array of metabolites in a biological sample. This technology enables us to study the dermal metabolic effects and get a clear explanation of the pathogenesis of skin diseases. The purpose of this literature review is to illustrate how metabolomics technology can be used to evaluate the metabolic profile of human skin cancer, using a variety of analytical platforms including gas chromatography-mass spectrometry (GC-MS), liquid chromatography-mass spectrometry (LC-MS), and nuclear magnetic resonance (NMR). Data collection has not been based on any analytical method.

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The use of poly(lactide‐co‐glycolide) (PLGA) nanoparticles (NPs) as carriers for chemotherapeutic drugs is regarded as an actively targeted nano‐therapy for the specific delivery of anti‐cancer drugs to target cells. However, the exact mechanism by which PLGA NPs boost anticancer cytotoxicity at the molecular level remains largely unclear. This study employed different molecular approaches to define the response of carcinoma FaDu cells to different types of treatment, specifically: paclitaxel (PTX) alone, drug free PLGA NPs, and PTX‐loaded PTX‐PLGA NPs. Functional cell assays revealed that PTX‐PLGA NPs treated cells had a higher level of apoptosis than PTX alone, whereas the complementary, UHPLC‐MS/MS (TIMS‐TOF) based multi‐omics analyses revealed that PTX‐PLGA NPs treatment resulted in increased abundance of proteins associated with tubulin, as well as metabolites such as 5‐thymidylic acid, PC(18:1(9Z)/18:1(9Z0), vitamin D, and sphinganine among others. The multi‐omics analyses revealed new insights about the molecular mechanisms underlying the action of novel anticancer NP therapies. In particular, PTX‐loaded NPs appeared to exacerbate specific changes induced by both PLGA‐NPs and PTX as a free drug. Hence, the PTX‐PLGA NPs’ molecular mode of action, seen in greater detail, depends on this synergy that ultimately accelerates the apoptotic process, resulting in cancer cell death.