Clinical Oncology

[Treatment of the relapsed epithelial ovarian cancer ]

BOÉR Katalin

SEPTEMBER 10, 2017

Clinical Oncology - 2017;4(03)

[Ovarian cancer remains the most lethal gynaecological cancer and most patients present with advanced FIGO stage disease. Despite optimal upfront surgery and the administration of front-line paclitaxel-carboplatin chemotherapy, approximately two-third of ovarian cancer patients will relapse in the fi rst 3 years. In the last years, the goal in the treatment of ovarian cancer has shifted to maintenance therapy, trying to extend the progression free intervals of the patients. Remarkable advances in the knowledge of molecular biology of relapses led to the introduction the combination of antiangiogenic agent bevacizumab and chemotherapy, which showed to be effective in all phases of the disease, in fi rst-line therapy, as maintenance therapy, and in platinum-sensitive and platinum-resistant recurrence as well. Very recently, a new maintenance therapy, olaparib monotherapy has been introduced into clinical practice to treat platinum-sensitive, relapsed, high-grade serous ovarian cancer. Despite progresses in this therapy, are still some areas of controversy on how to manage epithelial ovarian cancer relapses. The aim of this manuscript is to give an overview on the management of relapsed ovarian cancer in the context of new available therapeutic modalities.]

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[Immunosuppressive therapies, which were used in the past few years, have been causing different kinds of immunosuppression. In case of impaired cellular immunity, there is an increased risk of having the reactivation of latent viral infections. Certain viral infections or viral reactivations can be life threatening for patients with malignant diseases. Mild viral infections during chemotherapy can also disadvance the tumor therapy, which could affect the chance of recovery in a negative way. This is the reason, why the possibility of carrying viral infections or viral reactivations should be taken into consideration even in patients with solid tumor. Due to this, risk adaptive prevention strategies, and in certain cases, early antiviral therapies are needed.]

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[The renal cell cancer is among the ten most frequent cancers in developed countries. Its inci dence rate continuously increased until recently. On the other hand, survival parameters of renal cell cancer patients considerably improved in the last decade due to early diagnosis and developments in the treatment of irresectable disease. Huge progress had been made in understanding of the biological background of this chemo- and radiotherapy resistant disease, leading to the introduction of drugs in fi rst and further line treatment acting on VEGF and mTOR signal transduction pathways. Simultaneously, the era of widespread cytokine treatments had been ended. Recent studies had ensured the introduction of several drugs with new mechanism of action (MET, AXL; FGFR, PD-1 inhibition) into the therapy; these new advances completely changed the treatment landscape of RCC further improving progression free and overall survival. In this publication a review of data regarding the targeted treatment of clear cell renal cancer will be provided and as of our recent knowledge therapeutic positions of different drugs used will be discussed.]

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[In most cases, the targeted therapy is able to produce clinical response, but after a certain interval it turns to be ineffective due to secondary resistance against the therapy. One of the most demanding challenge in treatment of cancer is to prevent or inhibit such resistance, which could have several forms, e.g. appearance of new driver activating mutations in the treated tumor, clon(s) existed in minority with different mutations (targets) can grow and replace the temporarely sensitive tumor cells (on the basis of tumor heterogeneity); another pathway takes over the role in cancer progression, etc. Such problems are very common in the RAS-RAF-MEK-ERK pathway. These are very important proteins to collect extracellular signals in order to regular different cell functions, especially proliferation. With activating mutations make the RAS-pathway independent from the normal .regulation. To inhibit the consequence of the mutations is largely still an unsolved problem, with few exceptions (e.g. inhibition of BRAF mutations). Theoretically, the inhibition of the next steps of the pathway, MEK and ERK, may stop the pathologically activated signals, partly due to their inhibition, and party to effi ciently decrease the feedback inside the pathway. This review discusses aspects of this possibilities, especially to overcome resistance and prolong the effectiveness of therapy.]

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