Factors of the ovarian cancer resistance to combined chemotherapy with platinum preparations

1996 ◽  
Vol 122 (6) ◽  
pp. 1213-1216 ◽  
Author(s):  
A. G. Blyumenberg ◽  
L. B. Gorbacheva ◽  
V. A. Gorbunova ◽  
V. P. Kozachenko ◽  
V. Z. Lankin
Keyword(s):  
Ovarian Cancer ◽  
Combined Chemotherapy ◽  
Cancer Resistance ◽  
Platinum Preparations

scholarly journals Combined chemotherapy and allogeneic human Vγ9Vδ2 T lymphocyte-immunotherapies efficiently control the development of human epithelial ovarian cancer cells in vivo

2019 ◽  
Vol 8 (11) ◽  
pp. e1649971 ◽  
Author(s):  
Noémie Joalland ◽  
Laura Lafrance ◽  
Thibauld Oullier ◽  
Séverine Marionneau-Lambot ◽  
Delphine Loussouarn ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cancer Cells ◽  
T Lymphocyte ◽  
Ovarian Cancer Cells ◽  
Combined Chemotherapy

Fuel on the fire: Contribution of thrombocytosis to ovarian cancer resistance to taxane-based chemotherapy.

2012 ◽  
Vol 125 ◽  
pp. S36
Author(s):  
J. Bottsford-Miller ◽  
R. Stone ◽  
A. Nick ◽  
B. Zand ◽  
C. Pecot ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Resistance

scholarly journals Regulation and pharmacological targeting of RAD51 in cancer

NAR Cancer ◽  
2020 ◽  
Vol 2 (3) ◽  
Author(s):  
McKenzie K Grundy ◽  
Ronald J Buckanovich ◽  
Kara A Bernstein
Keyword(s):  
Ovarian Cancer ◽  
Dna Damage ◽  
Homologous Recombination ◽  
Patient Outcomes ◽  
Cancer Biology ◽  
Cancer Resistance ◽  
Breast And Ovarian Cancer ◽  
Resistance To Therapy ◽  
Damage Repair

Abstract Regulation of homologous recombination (HR) is central for cancer prevention. However, too little HR can increase cancer incidence, whereas too much HR can drive cancer resistance to therapy. Importantly, therapeutics targeting HR deficiency have demonstrated a profound efficacy in the clinic improving patient outcomes, particularly for breast and ovarian cancer. RAD51 is central to DNA damage repair in the HR pathway. As such, understanding the function and regulation of RAD51 is essential for cancer biology. This review will focus on the role of RAD51 in cancer and beyond and how modulation of its function can be exploited as a cancer therapeutic.

scholarly journals STAT3 regulated miR-216a promotes ovarian cancer proliferation and cisplatin resistance

2018 ◽  
Vol 38 (4) ◽  
Author(s):  
Pengfei Jin ◽  
Yanjun Liu ◽  
Ruijuan Wang
Keyword(s):  
Ovarian Cancer ◽  
Colony Formation ◽  
Cisplatin Resistance ◽  
Soft Agar ◽  
Luciferase Assay ◽  
Ovarian Cancer Cells ◽  
Cancer Resistance ◽  
Cancer Proliferation ◽  
Bioinformatics Analyses ◽  
Potential Strategy

Cisplatin is the first-line treatment for ovarian cancer. However, the clinical outcome of cisplatin treatment in ovarian cancer is hindered by cancer resistance. Here we aim to explore the role and mechanism of miR-216a in the cisplatin resistance of ovarian cancer. The effects of miR-216a overexpression and inhibition on ovarian cell proliferation, colony formation, and cisplatin resistance were investigated by MTT assay and soft agar colony formation assay. Bioinformatics analyses using TargetScan and rVista, qPCR, and luciferase assay were also used to explore and verify downstream effectors and regulators of miR-216a. Proliferation, colony formation, and cisplatin resistance of ovarian cancer cells are promoted by miR-216a overexpression but inhibited by miR-216a inhibition. PTEN is a direct target of miR-216a and PTEN expression antagonizes the tumor-promoting function of miR-216a. STAT3 is a regulator of miR-216a, and PTEN is also regulated by STAT3. miR-216a up-regulation is associated with cisplatin resistance in ovarian cancer and this effect is mediated by PTEN. STAT3 is a regulator of miR-216a. Strategies that inhibit miR-216a is a potential strategy for overcoming the cisplatin resistance in ovarian cancer.

scholarly journals HE4 Levels in Ovarian Cancer-Resistant Menopausal Women

2019 ◽  
pp. 224-227
Author(s):  
Wiwi Irawan ◽  
Syahrul Rauf ◽  
Nasrudin A. Mappaware ◽  
St. Maisuri T. Chalid
Keyword(s):  
Ovarian Cancer ◽  
Cancer Patients ◽  
Clinical Symptoms ◽  
Menopausal Status ◽  
Ultrasound Image ◽  
Cancer Resistance ◽  
Menopausal Women ◽  
Chemiluminescent Microparticle Immunoassay ◽  
Resistant Group ◽  
The Mean

Abstract Objective: To analyse the predictive value of HE4 in ovarian cancer patients according to their resistance and menopausal status Methods: Thirteen premenopausal and twenty-five menopausal ovarian cancer patients were measured for HE4 levels measured using automated chemiluminescent microparticle immunoassay ARCHITECT HE4. Patients categorized into resistant and non-resistant after six cycles of chemotherapy in addition to their clinical symptoms and ultrasound image of cancer. Results: The mean HE4 levels were higher in the resistant group compared with a non-resistant group (274.97 pmol/l vs 128.83 pmol/l; p=0.015). Five menopausal resistant women with HE4 levels >140 pmol/l compared with two women in the non-resistant group. In the pre-menopause group, eight resistant women with HE level >70 pmol/l whereas four women in the non-resistant group. HE levels in menopausal and premenopausal for both ovarian cancers resistant and non-resistant were not significantly different (p>0.05). Conclusion: HE4 levels in resistant ovarian cancer patients are higher compared with non-resistant but do not predict ovarian cancer resistance based on patient menopausal status. Keywords: HE4, ovarian cancer, resistance.   Abstak Tujuan: Untuk menganalisis nilai prediktif HE4 pada pasien kanker ovarium berdasarkan resistensi dan status menopausenya Metode: Dilakukan pengukuran kadar HE4 menggunakan metode microparticle immunoassay ARCHITECT HE4 terhadap pasien kanker ovarium terdiri dari 13 perempuan premenopausal dan 25 perempuan menopause. Pasien dikategorikan menjadi resisten dan tidak resisten setelah 6 siklus kemoterapi selain gejala klinis dan gambar USG. Hasil: Rerata kadar HE4 rata-rata lebih tinggi pada kelompok yang resisten dibandingkan dengan kelompok yang tidak resisten (274,97 pmol/l vs 128,83 pmol/l; p=0,015). Terdapat 5 perempuan menopause yang resisten kanker ovarium dan 2 perempuan dalam kelompok yang tidak resisten dengan kadar HE4 >140 pmol/l. Pada kelompok premenopause, 8 perempuan yang resisten dengan tingkat HE >70 pmol/l sedangkan 4 perempuan dalam kelompok tidak resisten. Kadar HE dalam menopause dan premenopause untuk kedua kanker ovarium resisten dan tidak resisten tidak berbeda secara signifikan (p>0,05). Kesimpulan: Kadar HE4 pada pasien kanker ovarium lebih tinggi daripada tidak resisten tetapi tidak memprediksi resistensi kanker ovarium berdasarkan status menopause pasien. Kata kunci : HE4, kanker ovarium, resistensi .

scholarly journals FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Carlos J Diaz Osterman ◽  
Duygu Ozmadenci ◽  
Elizabeth G Kleinschmidt ◽  
Kristin N Taylor ◽  
Allison M Barrie ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Chemotherapy Resistance ◽  
Gene Copy Number ◽  
Gene Copy ◽  
Platinum Resistance ◽  
Cancer Resistance ◽  
Copy Number Alterations ◽  
Neo Adjuvant Chemotherapy ◽  
Platinum Chemotherapy ◽  
Repair Genes

Gene copy number alterations, tumor cell stemness, and the development of platinum chemotherapy resistance contribute to high-grade serous ovarian cancer (HGSOC) recurrence. Stem phenotypes involving Wnt-β-catenin, aldehyde dehydrogenase activities, intrinsic platinum resistance, and tumorsphere formation are here associated with spontaneous gains in Kras, Myc and FAK (KMF) genes in a new aggressive murine model of ovarian cancer. Adhesion-independent FAK signaling sustained KMF and human tumorsphere proliferation as well as resistance to cisplatin cytotoxicity. Platinum-resistant tumorspheres can acquire a dependence on FAK for growth. Accordingly, increased FAK tyrosine phosphorylation was observed within HGSOC patient tumors surviving neo-adjuvant chemotherapy. Combining a FAK inhibitor with platinum overcame chemoresistance and triggered cell apoptosis. FAK transcriptomic analyses across knockout and reconstituted cells identified 135 targets, elevated in HGSOC, that were regulated by FAK activity and β-catenin including Myc, pluripotency and DNA repair genes. These studies reveal an oncogenic FAK signaling role supporting chemoresistance.

scholarly journals FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy

2019 ◽  
Author(s):  
Carlos J. Díaz Osterman ◽  
Duygu Ozmadenci ◽  
Elizabeth G. Kleinschmidt ◽  
Kristin N. Taylor ◽  
Allison M. Barrie ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Gene Copy ◽  
Platinum Resistance ◽  
List Type ◽  
High Grade ◽  
Cancer Resistance ◽  
Platinum Chemotherapy

AbstractGene copy number changes, cancer stem cell (CSC) increases, and platinum chemotherapy resistance contribute to poor prognosis in patients with recurrent high grade serous ovarian cancer (HGSOC). CSC phenotypes involving Wnt-β-catenin and aldehyde dehydrogenase activities, platinum resistance, and tumor initiating frequency are here associated with spontaneous genetic gains, including genes encodingKRAS,MYCandFAK, in a new murine model of ovarian cancer (KMF). Noncanonical FAK signaling was sufficient to sustain human and KMF tumorsphere proliferation, CSC survival, and platinum resistance. Increased FAK tyrosine phosphorylation occurred in HGSOC patient tumors surviving neo-adjuvant platinum and paclitaxel chemotherapy and platinum resistant tumorspheres acquired FAK dependence for growth. Importantly, combining a pharmacologic FAK inhibitor with platinum overcame chemoresistance and triggered apoptosisin vitroandin vivo. Knockout, rescue, genomic and transcriptomic analyses collectively identified more than 400 genes regulated along a FAK/β-catenin/Myc axis impacting stemness and DNA repair in HGSOC, with 66 genes gained in a majority of Cancer Genome Atlas samples. Together, these results support combinatorial testing of FAK inhibitors for the treatment of recurrent ovarian cancer.Graphical SummaryKey PointsHigh grade serous ovarian carcinoma tumors containPTK2(FAK) 8q24.3 gains associated with prognostic differences.KMF, a new murine ovarian cancer model withK-Ras,Myc, andFAK gene gains and intrinsic platinum resistance.FAK activation in tumors surviving platinum chemotherapy promotes cancer stem cell survival.FAK facilitates a β-catenin-Myc signaling axis controlling gene expression supporting platinum resistance.FAK activity is essential for KMF tumor growth and is a targetable cellular adaptation of platinum resistance.

scholarly journals The Serum Level of Vascular Endothelial Growth Factor (VEGF) is Declined after Paclitaxel-Carboplatin Combined Chemotherapy Treatment on Epithelial Ovarian Cancer

2016 ◽  
Author(s):  
Amelia Abdullah
Keyword(s):  
Ovarian Cancer ◽  
Cell Differentiation ◽  
Serum Level ◽  
Epithelial Ovarian Cancer ◽  
Early Stage ◽  
Clinical Staging ◽  
Teaching Hospitals ◽  
Advanced Stage ◽  
Combined Chemotherapy ◽  
Differentiated Cells

Objective: To assess the effect of Paclitaxel-Carboplatin combination on epithelial ovarian cancer by studying the changes in VEGF serum levels after receiving 3 series of chemotherapy. Methods: This was a cohort study conducted at several teaching hospitals in Obstetrics and Gynecology Department of the Faculty of Medicine, Hasanuddin University from April 2011 to March 2012. The subjects were patients with ovarian cancer who met the inclusion criteria and had undergone surgery. The clinical staging was determined with 2009 FIGO criteria. They went through histopathology examination to determine the histological type and cell differentiation of the lesion. They also went through combined chemotherapy of Paclitaxel and Carboplatin. The data were analyzed with paired t-test. Results: The study reveals that out of 30 cases of ovarian cancer who received a combination chemotherapy, most were < 45 years of age (53.33%), nulliparous (46.7%), serosum type (53.3%), with moderate differentiation (36.7%), and in advanced stage (73.3%). The VEGF serum level after 3 series of chemotherapy was lower than before (the average value: 294.67 vs 572.77 ng/ml). There was a significant change in VEGF serum level after receiving chemotherapy (p=0.000). The VEGF serum level of advanced-stage and early stage epithelial ovarian cancer after chemotherapy decreases significantly (p=0.000 and p=0.011). The advanced-stage cases showed more responses to chemotherapy than the early-stage did. There was a tendency that adenocarcinoma serosum type was more responsive to the therapy than mucinosum type (p=0.000 vs 0.003). Conclusion: There is no difference in VEGF serum level based on cell differentiation but there is a tendency that well and moderate differentiated cells have a greater change than the poor differentiated cells (p=0.003, p=0.003 vs p=0.019). [Indones J Obstet Gynecol 2012; 36-3: 135-9] Keywords: carboplatin, epithelial ovarian cancer, paclitaxel, VEGF

Sign in / Sign up

Export Citation Format

Share Document