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Antiangiogenic therapy in ovarian cancer – for whom and when?

100%

Bilgetekin I., Cetin B., Ozet A.

Current Gynecologic Oncology

2017

vol. 15

issue 1

78-85

Tumor angiogenesis appears to be an important process in epithelial ovarian cancer development. Bevacizumab is a monoclonal antibody that can neutralize vascular endothelial growth factor, a promoter of the initiation phase of angiogenesis. First-line chemotherapy in combination with bevacizumab followed by maintenance bevacizumab demonstrated efficacy over chemotherapy alone in two phase III trials (Gynecologic Oncology Group, GOG 218 and ICON7); however, absolute progression-free survival benefit remains modest, with no demonstrated impact on overall survival. The addition of molecularly targeted agents to the treatment of women with recurrent and platinum-sensitive disease has been recently reported in the OCEANS study, which evaluated the benefit of adding bevacizumab to carboplatin and gemcitabine in women with platinum-sensitive recurrent disease. Bevacizumab-based therapy also extended progressionfree survival from 8 to 12 months. However, overall survival was not different between the two arms. In the Gynecologic Oncology Group 213 (GOG 213) trial, women with platinum-sensitive recurrent epithelial ovarian cancer were randomly assigned to medical treatment (carboplatin plus paclitaxel with or without bevacizumab). A significant improvement in progression-free survival (14 versus 10 months, respectively) was observed. A trend towards a significant improvement in overall survival, which was not statistically significant, was reported. In November 14, 2014, based on AURELIA findings, the Food and Drug Administration approved bevacizumab in combination with paclitaxel, pegylated liposomal doxorubicin, or topotecan, for the treatment of patients with platinum-resistant recurrent epithelial ovarian cancer. Ovarian cancer is a primary cancer against which these new agents are being tested. This review will describe the role of angiogenesis inhibitors in epithelial ovarian cancer.

Angiogeneza nowotworowa wydaje się istotnym procesem w rozwoju raka jajnika. Bewacyzumab jest przeciwciałem monoklonalnym zdolnym do neutralizacji naczyniowo-śródbłonkowego czynnika wzrostu, promotora początkowej fazy angiogenezy. W dwóch badaniach klinicznych III fazy (Gynecologic Oncology Group – GOG 218 oraz ICON7) wykazano skuteczność chemioterapii pierwszego rzutu w skojarzeniu z bewacyzumabem i następowym leczeniem podtrzymującym bewacyzumabem w porównaniu z samą chemioterapią, jednak bezwzględne korzyści czasu wolnego bez progresji pozostają niewielkie, bez wpływu na przeżycie całkowite. W badaniu OCEANS oceniono korzyści wynikające z włączenia bewacyzumabu do terapii karboplatyną i gemcytabiną u kobiet z nawrotowym rakiem jajnika wrażliwym na platynę. Leczenie oparte na bewacyzumabie wydłużyło czas przeżycia bez progresji choroby z 8 do 12 miesięcy. Nie stwierdzono różnicy w odniesieniu do przeżycia całkowitego między dwiema grupami pacjentek. W badaniu klinicznym GOG 213 (Gynecologic Oncology Group 213) kobietom z nawrotowym rakiem jajnika wrażliwym na platynę losowo przypisywano rodzaj leczenia (karboplatynę plus paklitaksel z lub bez bewacyzumabu). Zaobserwowano istotną poprawę w zakresie przeżycia bez progresji choroby (odpowiednio 14 i 10 miesięcy). Odnotowano tendencję do poprawy w zakresie przeżycia ogólnego, jednak bez istotności statystycznej. W oparciu o wyniki badania AURELIA 14 listopada 2014 roku Agencja Żywności i Leków zatwierdziła bewacizumab w skojarzeniu z paklitakselem, pegylowaną liposomalną doksorubicyną lub topotekanem w leczeniu chorych z wrażliwym na platynę nawrotowym rakiem jajnika. Rak jajnika jest pierwszym nowotworem, wobec którego badane są te leki. W niniejszej pracy opisano rolę inhibitorów angiogenezy w nabłonkowym raku jajnika.

Cardiotoxicity of antiangiogenic drugs: causes and mechanisms

88%

Tomaszewska B., Muzolf M., Grabysa R., Bodnar L.

OncoReview

2021

vol. 11

issue 1

12-18

Therapy with angiogenesis inhibitors is undoubtedly an advancement in cancer treatment; however, it is associated with a risk of developing cardiotoxicity, which most often manifests in myocardial contractile dysfunction or an increased risk of thromboembolic events. Heart failure is observed in 2–4% of patients treated with bevacizumab and in 3–8% of patients on antiangiogenic tyrosine kinase inhibitors. The proposed pathomechanisms underlying the impairment in systolic function during antiangiogenic drug treatment include mitochondrial dysfunction, a secondary reduction in cardiomyocyte ATP production and redox imbalance, which may contribute to pathological states known as “free radical diseases”. Additionally, therapy with angiogenesis inhibitors may also cause cardiac oxidative stress. The risk factors for cardiac complications include arterial hypertension, which is a known “class effect” of this class of drugs, as well as a number of other factors such as age, comorbidities, prior radiotherapy and baseline left ventricular ejection fraction. The cardiovascular diseases are still the first cause of death in the world. The more effective oncological treatment becomes, the more often comorbidities occur. This fact seems to demand interdisciplinary approach from investigators and practitioners. This article presents the current state of knowledge on the molecular mechanisms of cardiotoxicity of antiangiogenic drugs used in routine clinical practice.

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1 Current Gynecologic Oncology

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1 Bodnar L.

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1 Grabysa R.

1 Muzolf M.

1 Ozet A.

1 Tomaszewska B.

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Antiangiogenic therapy in ovarian cancer – for whom and when?

Cardiotoxicity of antiangiogenic drugs: causes and mechanisms