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      Recent advances of therapeutic targets based on the molecular signature in breast cancer: genetic mutations and implications for current treatment paradigms

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          Abstract

          Breast cancer is the most common malignancy in women all over the world. Genetic background of women contributes to her risk of having breast cancer. Certain inherited DNA mutations can dramatically increase the risk of developing certain cancers and are responsible for many of the cancers that run in some families. Regarding the widespread multigene panels, whole exome sequencing is capable of providing the evaluation of genetic function mutations for development novel strategy in clinical trials. Targeting the mutant proteins involved in breast cancer can be an effective therapeutic approach for developing novel drugs. This systematic review discusses gene mutations linked to breast cancer, focusing on signaling pathways that are being targeted with investigational therapeutic strategies, where clinical trials could be potentially initiated in the future are being highlighted.

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          AMP-activated/SNF1 protein kinases: conserved guardians of cellular energy.

          D Hardie (2007)
          The SNF1/AMP-activated protein kinase (AMPK) family maintains the balance between ATP production and consumption in all eukaryotic cells. The kinases are heterotrimers that comprise a catalytic subunit and regulatory subunits that sense cellular energy levels. When energy status is compromised, the system activates catabolic pathways and switches off protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. Surprisingly, recent results indicate that the AMPK system is also important in functions that go beyond the regulation of energy homeostasis, such as the maintenance of cell polarity in epithelial cells.
          Article 0 comments Cited 624 times – based on 0 reviews     Review now
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            Impact of mutant p53 functional properties on TP53 mutation patterns and tumor phenotype: lessons from recent developments in the IARC TP53 database.

            Audrey Petitjean, Ewy Mathe, Shunsuke Kato … (2007)
            The tumor suppressor gene TP53 is frequently mutated in human cancers. More than 75% of all mutations are missense substitutions that have been extensively analyzed in various yeast and human cell assays. The International Agency for Research on Cancer (IARC) TP53 database (www-p53.iarc.fr) compiles all genetic variations that have been reported in TP53. Here, we present recent database developments that include new annotations on the functional properties of mutant proteins, and we perform a systematic analysis of the database to determine the functional properties that contribute to the occurrence of mutational "hotspots" in different cancer types and to the phenotype of tumors. This analysis showed that loss of transactivation capacity is a key factor for the selection of missense mutations, and that difference in mutation frequencies is closely related to nucleotide substitution rates along TP53 coding sequence. An interesting new finding is that in patients with an inherited missense mutation, the age at onset of tumors was related to the functional severity of the mutation, mutations with total loss of transactivation activity being associated with earlier cancer onset compared to mutations that retain partial transactivation capacity. Furthermore, 80% of the most common mutants show a capacity to exert dominant-negative effect (DNE) over wild-type p53, compared to only 45% of the less frequent mutants studied, suggesting that DNE may play a role in shaping mutation patterns. These results provide new insights into the factors that shape mutation patterns and influence mutation phenotype, which may have clinical interest.
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              A genome-wide association study identifies alleles in FGFR2 associated with risk of sporadic postmenopausal breast cancer.

              David Hunter, Peter Kraft, Kevin B. Jacobs … (2007)
              We conducted a genome-wide association study (GWAS) of breast cancer by genotyping 528,173 SNPs in 1,145 postmenopausal women of European ancestry with invasive breast cancer and 1,142 controls. We identified four SNPs in intron 2 of FGFR2 (which encodes a receptor tyrosine kinase and is amplified or overexpressed in some breast cancers) that were highly associated with breast cancer and confirmed this association in 1,776 affected individuals and 2,072 controls from three additional studies. Across the four studies, the association with all four SNPs was highly statistically significant (P(trend) for the most strongly associated SNP (rs1219648) = 1.1 x 10(-10); population attributable risk = 16%). Four SNPs at other loci most strongly associated with breast cancer in the initial GWAS were not associated in the replication studies. Our summary results from the GWAS are available online in a form that should speed the identification of additional risk loci.
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                Author and article information

                Contributors
                Zeinab Safarpour Lima: safarpourlima.z@iums.ac.ir
                Mostafa Ghadamzadeh: ghadamzadeh.m@iums.ac.ir
                Farzad Tahmasebi Arashloo: farzad.tahmaseby@yahoo.com
                Ghazaleh Amjad: amjad.gh@iums.ac.ir
                Mohammad Reza Ebadi: MRE5MD@yahoo.com
                Ladan Younesi: 00989124966317 , younesi.l@iums.ac.ir
                Journal
                Journal ID (nlm-ta): J Hematol Oncol
                Journal ID (iso-abbrev): J Hematol Oncol
                Title: Journal of Hematology & Oncology
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1756-8722
                Publication date (Electronic): 11 April 2019
                Publication date PMC-release: 11 April 2019
                Publication date Collection: 2019
                Volume: 12
                Electronic Location Identifier: 38
                Affiliations
                [1 ]ISNI 0000 0004 4911 7066, GRID grid.411746.1, Shahid Akbar Abadi Clinical Research Development Unit (ShCRDU), , Iran University of Medical Sciences (IUMS), ; Tehran, Iran
                [2 ]ISNI 0000 0004 4911 7066, GRID grid.411746.1, Departement of Radiology, , Hasheminejad Kidney Centre (HKC), Iran University of Medical Sciences, ; Tehran, Iran
                [3 ]ISNI 0000 0001 2092 9755, GRID grid.412105.3, Clinical Research Unit, , Afzalipour Hospital, Kerman University of Medical Sciences, ; Kerman, Iran
                [4 ]ISNI 0000 0004 4911 7066, GRID grid.411746.1, Shohadaye Haft-e-tir Hospital, Iran University of Medical Sciences (IUMS), ; Tehran, Iran
                Article
                Publisher ID: 725
                DOI: 10.1186/s13045-019-0725-6
                PMC ID: 6460547
                PubMed ID: 30975222
                SO-VID: 5f2a337f-5bf3-4d80-8c22-0648bab2bb4c
                Copyright © © The Author(s). 2019
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 14 January 2019
                Date accepted : 27 March 2019
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: breast,new drug,chromosome,molecular patterns,mutations
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: breast, new drug, chromosome, molecular patterns, mutations

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