Intraperitoneal chemotherapy for advanced epithelial ovarian malignancy: Lessons learned

Bunting, Michael W; Chan, Warren S. W.; Brand, Alison; Blomfield, Penelope

doi:10.1111/j.1479-828x.2009.01080.x

Cited by 5 publications

(3 citation statements)

References 22 publications

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“…Loss of 53BP1 in cavin3 HeLa KO cells could revert the PARP sensitivity of these cells to WT cell levels as demonstrated in clonogenic survival and cell viability assays (orange dots, Figure 8—figure supplement 2A–C ). These findings agree with several studies demonstrating that homologous recombination DNA repair is partially restored in BRCA1-deficient cells following 53BP1 loss ( Bouwman et al, 2010 ; Bunting et al, 2009 ; Cao et al, 2009 ; Turner et al, 2007 ; Yang et al, 2017 ).…”

Section: Resultssupporting

confidence: 93%

“…Recent reports have linked 53BP1 loss to PARP inhibitor resistance, presumably, as loss of 53BP1 partially restores homologous recombination repair in BRCA1-deficient cells ( Bouwman et al, 2010 ; Bunting et al, 2009 ; Cao et al, 2009 ; Turner et al, 2007 ; Yang et al, 2017 ). This restoration is made possible because homologous recombination and non-homologous end-joining repair pathways compete to repair DNA breaks during DNA replication.…”

Section: Resultsmentioning

confidence: 99%

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Cavin3 released from caveolae interacts with BRCA1 to regulate the cellular stress response

McMahon

Stroud

Gambin

et al. 2021

eLife

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Caveolae-associated protein 3 (cavin3) is inactivated in most cancers. We characterized how cavin3 affects the cellular proteome using genome-edited cells together with label-free quantitative proteomics. These studies revealed a prominent role for cavin3 in DNA repair, with BRCA1 and BRCA1 A-complex components being downregulated on cavin3 deletion. Cellular and cell-free expression assays revealed a direct interaction between BRCA1 and cavin3 that occurs when cavin3 is released from caveolae that are disassembled in response to UV and mechanical stress. Overexpression and RNAi-depletion revealed that cavin3 sensitized various cancer cells to UV-induced apoptosis. Supporting a role in DNA repair, cavin3-deficient cells were sensitive to PARP inhibition, where concomitant depletion of 53BP1 restored BRCA1-dependent sensitivity to PARP inhibition. We conclude that cavin3 functions together with BRCA1 in multiple cancer-related pathways. The loss of cavin3 function may provide tumor cell survival by attenuating apoptotic sensitivity and hindering DNA repair under chronic stress conditions.

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Section: Resultssupporting

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Cavin3 released from caveolae interacts with BRCA1 to regulate the cellular stress response

McMahon

Stroud

Gambin

et al. 2021

eLife

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“…Like in GOG 172, however, catheter-related complications were frequent (18 patients, 47%) and were the most frequent cause of early discontinuation of treatment (8 patients, 21%) despite our efforts to prevent catheter-related complications through education and training workshops prior to opening the study. Rates of catheter-related complications should improve as centers gain more experience in administering IP chemotherapy [26,27]. …”

Section: Discussionmentioning

confidence: 99%

Feasibility, acceptability and preferences for intraperitoneal chemotherapy with paclitaxel and cisplatin after optimal debulking surgery for ovarian and related cancers: an ANZGOG study

et al. 2013

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ObjectiveIntraperitoneal (IP) chemotherapy in women with optimally debulked stage III ovarian cancer has been reported to prolong overall survival, but has not been widely adopted due to concerns about its toxicity, inconvenience and acceptability to patients. The purposes of this study were to determine the regimen's feasibility, adverse events, catheter-related complications, progression-free survival, health-related quality of life (HRQL), and patients' preferences for IP versus intravenous (IV) chemotherapy.MethodsWe conducted a single arm, multi-center study of IP chemotherapy with IV paclitaxel 135 mg/m2 (D1) over 3 hours, IP cisplatin 75 mg/m2 (D2), and IP paclitaxel 60 mg/m2 (D8) for 6 cycles in women with optimally debulked stage III ovarian or related cancers.ResultsThirty-eight eligible patients were recruited from 12 sites between July 2007 and December 2009. Seventy-one percent (n=27) completed at least 4 cycles and 63% (n=24) completed all 6 cycles. Grade 3 or 4 adverse events included nausea (n=2), vomiting (n=2), abdominal pain (n=2), and diarrhea (n=1), but not febrile neutropenia, neurotoxicity, or nephropathy. There were no treatment-related deaths. Catheter-related complications were the most frequent cause of early discontinuation of treatment (16 patients, 21%). Apart from neurotoxicity HRQL which worsened over time, HRQL was stable or improved with time. Most patients (≥50%) judged moderate benefits (e.g., an extra 6 months survival time or a 5% improvement in survival rates) necessary to make IP chemotherapy worthwhile.ConclusionIP chemotherapy was feasible, tolerable, and most participants considered moderate survival benefits sufficient to warrant the adverse effects and inconvenience.

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The intracellular uptake of CD95 modified paclitaxel-loaded poly(lactic-co-glycolic acid) microparticles

Ateh¹,

Leinster²,

Lambert³

et al. 2011

Biomaterials

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Intraperitoneal chemotherapy for advanced epithelial ovarian malignancy: Lessons learned

Abstract: This study demonstrates the feasibility and practicality of and lessons learned from initial experiences with IP chemotherapy for ovarian cancer in Australia.

Cited by 5 publications

References 22 publications

Cavin3 released from caveolae interacts with BRCA1 to regulate the cellular stress response

Cavin3 released from caveolae interacts with BRCA1 to regulate the cellular stress response

Feasibility, acceptability and preferences for intraperitoneal chemotherapy with paclitaxel and cisplatin after optimal debulking surgery for ovarian and related cancers: an ANZGOG study

The intracellular uptake of CD95 modified paclitaxel-loaded poly(lactic-co-glycolic acid) microparticles

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