Abstract:Breast cancer is becoming one of the main lethal carcinomas in the recent era, and its occurrence rate is increasing day by day. There are different breast cancer biomarkers, and their overexpression takes place in the metastasis of cancer cells. The most prevalent breast cancer biomarker is the human epidermal growth factor receptor2 (HER2). As this biomarker is overexpressed in malignant breast tissues, it has become the main focus in targeted therapies to fight breast cancer. There is a cascade of mechanism… Show more
“…Hence, RTK overexpression, ligand overexpression, and gain-of-function mutations in an RTK gene are all mechanisms for pathologic, elevated RTK signaling [7]. Indeed, EGFR and ERBB2 have been validated as targets for therapeutic intervention in numerous types of tumors; monoclonal antibodies and small molecular tyrosine kinase inhibitors have been approved to treat tumors dependent on these receptors [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]. It appears that ERBB3, particularly ERBB3-ERBB2 heterodimers, also drives various human tumors [24,25].…”
Metastatic skin cutaneous melanomas remain a significant clinical problem. In particular, those melanomas that do not contain a gain-of-function BRAF allele remain challenging to treat because of the paucity of targets for therapeutic intervention. Thus, here we investigate the role of the ERBB4 receptor tyrosine kinase in skin cutaneous melanomas that contain wild-type BRAF alleles (“BRAF WT melanomas”). We have performed in silico analyses of a public repository (The Cancer Genome Atlas - TCGA) of skin cutaneous melanoma gene expression and mutation data (TCGA-SKCM data set). These analyses demonstrate that ERBB4 overexpression strongly correlates with RAS gene or NF1 mutations that stimulate RAS signaling. Thus, these results have led us to hypothesize that elevated ERBB4 signaling promotes PI3K signaling, which cooperates with elevated RAS signaling to drive BRAF WT melanomas. We have tested this hypothesis using commercially available BRAF WT melanoma cell lines. Overexpression of wild-type ERBB4 stimulates clonogenic proliferation of the MEL-JUSO, MEWO, and IPC-298 BRAF WT melanoma cell lines. Moreover, overexpression of a dominant-negative ERBB4 (K751M) mutant inhibits clonogenic proliferation of the MEL-JUSO and MEWO cell lines. We discuss how these results may impact strategies for treating metastatic BRAF WT skin cutaneous melanomas.
“…Hence, RTK overexpression, ligand overexpression, and gain-of-function mutations in an RTK gene are all mechanisms for pathologic, elevated RTK signaling [7]. Indeed, EGFR and ERBB2 have been validated as targets for therapeutic intervention in numerous types of tumors; monoclonal antibodies and small molecular tyrosine kinase inhibitors have been approved to treat tumors dependent on these receptors [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]. It appears that ERBB3, particularly ERBB3-ERBB2 heterodimers, also drives various human tumors [24,25].…”
Metastatic skin cutaneous melanomas remain a significant clinical problem. In particular, those melanomas that do not contain a gain-of-function BRAF allele remain challenging to treat because of the paucity of targets for therapeutic intervention. Thus, here we investigate the role of the ERBB4 receptor tyrosine kinase in skin cutaneous melanomas that contain wild-type BRAF alleles (“BRAF WT melanomas”). We have performed in silico analyses of a public repository (The Cancer Genome Atlas - TCGA) of skin cutaneous melanoma gene expression and mutation data (TCGA-SKCM data set). These analyses demonstrate that ERBB4 overexpression strongly correlates with RAS gene or NF1 mutations that stimulate RAS signaling. Thus, these results have led us to hypothesize that elevated ERBB4 signaling promotes PI3K signaling, which cooperates with elevated RAS signaling to drive BRAF WT melanomas. We have tested this hypothesis using commercially available BRAF WT melanoma cell lines. Overexpression of wild-type ERBB4 stimulates clonogenic proliferation of the MEL-JUSO, MEWO, and IPC-298 BRAF WT melanoma cell lines. Moreover, overexpression of a dominant-negative ERBB4 (K751M) mutant inhibits clonogenic proliferation of the MEL-JUSO and MEWO cell lines. We discuss how these results may impact strategies for treating metastatic BRAF WT skin cutaneous melanomas.
“…The aforementioned QDs appear to be the best alternative for screening cell receptors. To generate effective fluorescence probes, the surface of QDs must be changed utilising various biological substances [ 27 ]. Figure 2 Various Nanotechnology based tools utilized in treatment of cancer.…”
“…BC is classified into three main tumor subtypes rooted in enhancement in expression of either progesterone receptor (PR) or estrogen receptor (ER), and/or epidermal growth factor receptor 2 (ERBB2) gene mutation [ 10 , 11 , 12 , 13 , 14 ]. Each type of cancer has a unique risk factor and treatment available [ 15 , 16 ].…”
Breast cancer (BC) is a highly metastatic multifactorial disease with various histological and molecular subtypes. Due to recent advancements, the mortality rate in BC has improved over the past five decades. Detection and treatment of many cancers are now possible due to the application of nanomedicine in clinical practice. Nanomedicine products such as Doxil® and Abraxane® have already been extensively used for BC adjuvant therapy with favorable clinical outcomes. However, these products were designed initially for generic anticancer purposes and not specifically for BC treatment. With a better understanding of the molecular biology of BC, several novel and promising nanotherapeutic strategies and devices have been developed in recent years. In this context, multi-functionalized nanostructures are becoming potential carriers for enhanced chemotherapy in BC patients. To design these nanostructures, a wide range of materials, such as proteins, lipids, polymers, and hybrid materials, can be used and tailored for specific purposes against BC. Selective targeting of BC cells results in the activation of programmed cell death in BC cells and can be considered a promising strategy for managing triple-negative BC. Currently, conventional BC screening methods such as mammography, digital breast tomosynthesis (DBT), ultrasonography, and magnetic resonance imaging (MRI) are either costly or expose the user to hazardous radiation that could harm them. Therefore, there is a need for such analytical techniques for detecting BC that are highly selective and sensitive, have a very low detection limit, are durable, biocompatible, and reproducible. In detecting BC biomarkers, nanostructures are used alone or in conjunction with numerous molecules. This review intends to highlight the recent advances in nanomedicine in BC treatment and diagnosis, emphasizing the targeting of BC cells that overexpress receptors of epidermal growth factors. Researchers may gain insight from these strategies to design and develop more tailored nanomedicine for BC to achieve further improvements in cancer specificity, antitumorigenic effects, anti-metastasis effects, and drug resistance reversal effects.
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