or obstetricians and oncologists than breast cancer during pregnancy alone. Because metastatic breast cancer BIBF1120 Vargatef still may be considered to be incurable, quality of life aspects for the mother become more relevant.Although we now know that this tumor responded well to treatment, this was not clear from the beginning, and the tumor biology was considered to be highly aggressive, as evidenced by the development of such a large tumor in a short period of time, the lack of steroid receptors, low tumor grading, lymph node and distant metastases and HER 2/neu overexpression. This is in agreement with a previous study, which showed that cases of pregnancy associated breast cancer have poorer prognostic factors, such as HER 2/neu overexpression and negative hormone receptors.
3 Because administration of trastuzumab has generally resulted in higher response rates in HER 2/ neu overexpressing tumors in patients with HER 2/ neu overexpression outside of pregnancy, it was decided to combine vinorelbine with trastuzumab in order to ensure effective treatment while maintaining a good quality of life for the pregnant woman. Although chemotherapy was found to be associated with low birth weight, prematurity and complications after birth, such as respiratory distress,4 6 as shown in this case report, chemotherapy and treatment with bisphosphonates did not lead to problems for the fetus in the third trimester, and chemotherapy can be considered to be a safe treatment option. Earlier reported experiences with vinorelbine in the second and third trimester indicate no grade 3 4 side effects and, with the exception of anemia, no malformation of the offspring.
5,7 The choice of trastuzumab, which may be used for tumor cases coupled with HER 2/neushowed that mitotic inhibitors, such as vinca alkaloids and nocodazole, effectively caused ROS generation by increasing mitochondrial accumulation in lung adenocarcinoma cells. Aberrant ROS mediated prolonged JNK activation induces DNA damage and Mcl 1 downregulation followed by mitochondrial dysfunction, caspase activation, and cell apoptosis. The signaling axis of the apoptotic pathway is not required for vinca alkaloids and nocodazole induced prometaphase arrest but is unusually activated following mitotic arrest.
Consistent with a current study that has shown VNR induces ROS mediated endothelial cell injury, we further provide the molecular mechanisms for ROS generation and ROS regulated apoptotic signals in vinca alkaloid treated lung adenocarcinoma cells. For anticancer therapy, vinca alkaloid induced G2/M phase arrest was an indistinct concept for decades. However, in this study, immunostaining using an MPM2 antibody, which has been used to detect mitosis specific and cell cycle controlled phosphoproteins such as DNA topoisomerase IIa and IIb, we showed a specific prometaphase arrest caused by vinca alkaloids and nocodazole. Vinca alkaloids bind to the vinca binding domain in the b subunit of tubulin dimmers and then depolymerize microtubules by the destruction of mitotic spindles at high concentrations or block mitosis without depolymerization at low concentrations. We showed evidence of mitotic prometaphase arrest due to the lack of a tubulin rearrangement and the presence of lamin A/C degradation. Notably, mitotic arr
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