2018
DOI: 10.1055/s-0044-101614
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Update Breast Cancer 2018 (Part 2) – Advanced Breast Cancer, Quality of Life and Prevention

Abstract: The treatment of metastatic breast cancer has become more complicated due to increasing numbers of new therapies which need to be tested. Therapies are now being developed to treat special clinical or molecular subgroups. Even though intrinsic molecular subtypes play a major role, more and more new therapies for subgroups and histological subtypes are being developed, such as the use of PARP inhibitors to treat patients with BRCA mutations (breast and ovarian cancer). Supportive therapies are also evolving, al… Show more

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Cited by 24 publications
(20 citation statements)
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“…Systemic treatment for TNBC has been restricted mainly to conventional chemotherapy in the past [ 8 10 , 14 , 17 ], but new targeted therapies such as immune-checkpoint inhibitors [ 18 ] and poly-adenosine diphosphate ribose polymerase (PARP) inhibitors [ 19 , 20 ] have been under investigation in clinical trials, which are suitable for subgroups of TNBC patients with a germline BRCA1/2 mutation or a homologous recombination deficiency (HRD) in the tumor [ 7 , 14 , 21 , 22 ]. Interestingly, TNBC is associated with an increased deoxyribonucleic acid (DNA)-repair defect in the tumor cells, which is caused either by germline mutations in genes such as BRCA1/2, PALB2, and others [ 23 , 24 ] or by a somatic HRD, which can be exploited by systemic therapies [ 21 ].…”
Section: Introductionmentioning
confidence: 99%
“…Systemic treatment for TNBC has been restricted mainly to conventional chemotherapy in the past [ 8 10 , 14 , 17 ], but new targeted therapies such as immune-checkpoint inhibitors [ 18 ] and poly-adenosine diphosphate ribose polymerase (PARP) inhibitors [ 19 , 20 ] have been under investigation in clinical trials, which are suitable for subgroups of TNBC patients with a germline BRCA1/2 mutation or a homologous recombination deficiency (HRD) in the tumor [ 7 , 14 , 21 , 22 ]. Interestingly, TNBC is associated with an increased deoxyribonucleic acid (DNA)-repair defect in the tumor cells, which is caused either by germline mutations in genes such as BRCA1/2, PALB2, and others [ 23 , 24 ] or by a somatic HRD, which can be exploited by systemic therapies [ 21 ].…”
Section: Introductionmentioning
confidence: 99%
“…A trial examining denosumab as a chemopreventive drug in BRCA1 mutation carriers independently of pregnancy is currently ongoing 39 . Additional information about the molecular mechanisms involved in the way in which pregnancy influences breast tissue may therefore be useful for breast cancer prevention 1,34,40 . Identifying women who are at increased risk for breast cancer after pregnancy 4 may help address this specific risk during that time period.…”
Section: Discussionmentioning
confidence: 99%
“…Nevertheless, about half of the BC patients discontinue this kind of therapy . Considering that there are novel substances interfering with endocrine‐related pathways like the phosphatidylinositol 3 kinase–akt murine thymoma viral oncogene–mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway or the cyclin‐dependent kinase 4/6 (CDK4/6) cell cycle pathway, combination therapies with AIs—not only for the metastatic but increasingly also for the primary BC patient—are gaining ground . This development in turn requires more than ever—especially against the backdrop of the cost–benefit ratio of novel drugs—patients’ adherence with AIs as a basis for an appropriate ET.…”
Section: Discussionmentioning
confidence: 99%