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Open research questions in PARP inhibition in cancer therapy

283 gap statements mined from PARP inhibition in cancer therapy papers in our 7.9M-paper local library, which holds 1,500 papers on the topic — drawn mostly from each paper's own stated research gap, future-work, challenge and limitation notes, and its abstract. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one.

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What the literature leaves open

  • There is a need to investigate the antiproliferative and antitumor activity of NOV202 and olaparib in preclinical prostate cancer models. The study aims to address the gap in understanding the combination of NOV202 and olaparib in reducing tumor growth in prostate cancer xenografts.

    Combination of PARP inhibitor olaparib and a vascular disrupting agent reduces tumor growth in a preclinical model of prostate cancer · 2026 · DOI

  • The development of resistance to PARP inhibitors is a significant challenge in ovarian cancer treatment. There is a need for novel therapeutic strategies that can enhance PARPi sensitivity and overcome resistance mechanisms. The molecular mechanisms underlying gukulenin A's activity are not well understood.

    Marine Sponge-Derived Gukulenin A Sensitizes Ovarian Cancer Cells to PARP Inhibition via Ferroptosis Induction · 2025 · DOI

  • Pharmacokinetic and dosing data remain insufficient for patients with severe kidney impairment (CrCl <30 mL/min) or kidney failure.

    Germline PALB2-mutated triple negative breast cancer treated with Olaparib in a kidney transplant patient · 2026 · DOI

  • Nevertheless, several challenges remain, such as Talazoparib resistance due to restoration of the homologous recombination (HR) pathway in tumor cells and karonudib side effects that have not been fully explored in early clinical studies.

    Mechanisms, Limitations, and Prospects of PARP Inhibitor Talazoparib and MTH1 Inhibitor Karonudib for Malignant Tumor Therapy · 2026 · DOI

  • Future research should focus on nanoparticle drug delivery systems of Talazoparib and karonudib and their corresponding combination therapy to overcome drug resistance and further enhance their effectiveness in future cancer treatment.

    Mechanisms, Limitations, and Prospects of PARP Inhibitor Talazoparib and MTH1 Inhibitor Karonudib for Malignant Tumor Therapy · 2026 · DOI

  • The lack of understanding of the specificity and recognition of ADPr-Ub. The need to develop tools to study ADPr-Ub and determine its phenotypic consequences in cellular systems.

    Specificity and recognition of the ADP-ribosyl-ubiquitin modification in the DNA damage response · 2026 · DOI

  • The need to investigate the effect of PARP1 deficiency on amyloid pathology, neurodegeneration, and cognitive decline.

    PARP1 deficiency mitigates amyloid pathology, neurodegeneration, and cognitive decline in a familial Alzheimer’s disease model · 2026 · DOI

  • There is a need for real-world data on the effectiveness and tolerability of PARPi maintenance therapy in ovarian cancer patients. Prior studies have primarily focused on clinical trial populations, which may not reflect the diversity of real-world patients.

    Poly(ADP-ribose) polymerase inhibitor maintenance therapy in ovarian cancer: a single-center retrospective study · 2026 · DOI

  • The structural basis for SLFN5's biologic activity remains unclear. The specific SLFN5 domains and structural motifs required for SLFN5's transcriptional regulatory activity are poorly defined.

    SLFN5 restrains type I interferon responses and promotes glioblastoma via its N-terminal Schlafen core domain · 2026 · DOI

  • Schlafen 5 (SLFN5) is an important regulator of Type I interferon (IFN-I) signaling and tumorigenesis, yet the structural basis for its biologic activity remains unclear.

    SLFN5 restrains type I interferon responses and promotes glioblastoma via its N-terminal Schlafen core domain · 2026 · DOI

  • These findings indicate that targeting XBP1 in conjunction with Que treatment may represent a promising therapeutic strategy for breast cancer, warranting further investigation through 3D culture systems and in vivo models.

    XBP1 gene silencing augments quercetin-induced apoptosis and anti-metastatic activity in breast cancer cell lines · 2026 · DOI

  • The study faces challenges in terms of the limited sample size. The study faces challenges in terms of the complexity of HRD prediction methods.

    Comprehensive comparison of homologous recombination deficiency predictors in early-stage triple-negative breast cancer · 2026 · DOI

  • The study is based on a retrospective cohort with long-term follow-up. No patient received adjuvant therapy including platinum-based agents or PARP inhibitors. The study has a limited sample size of 235 patients.

    Comprehensive comparison of homologous recombination deficiency predictors in early-stage triple-negative breast cancer · 2026 · DOI

  • ConclusionsOur findings establish that NFV synergizes with CDDP in killing Pt-resistant ovarian cancer cells by promoting a caspase-8-dependent apoptotic-to-secondary pyroptotic response, supporting further investigation of NFV as a potential drug to be repurposed to increase the efficacy of Pt-based therapy.

    The combination of nelfinavir and cisplatin drives lytic cell death through a caspase-8/caspase-3/GSDME axis in platinum-resistant ovarian cancer cells · 2026 · DOI

  • Although we previously reported that RPRD1B exerts a dual oncogenic function in gastric cancer—promoting tumor progression by regulating fatty acid metabolism and interacting with Aurora B to accelerate cell cycle progression—its specific role in mediating 5-FU chemoresistance in this malignancy remains poorly understood.

    Targeting RPRD1B overcomes chemoresistance in gastric cancer by suppressing the TOPBP1-mediated DNA damage repair pathway · 2026 · DOI

  • Investigate the combination of olaparib and NOV202 in other preclinical models of prostate cancer. Examine the long-term effects of the combination treatment. Compare the efficacy of the combination treatment with other PARP inhibitors.

    Combination of PARP inhibitor olaparib and a vascular disrupting agent reduces tumor growth in a preclinical model of prostate cancer · 2026 · DOI

  • The study is retrospective in nature. The sample size may be limited. The study only included patients with primary high-grade serous ovarian carcinoma.

    Comparison of survival outcomes of Olaparib or Olaparib combine with Bevacizumab in patients with primary high-grade serous ovarian carcinoma · 2026 · DOI

  • The advancement of chemotherapy in breast cancer is moving toward personalization rather than abandonment. Chemotherapy will likely remain essential for many patients, but its delivery is becoming more selective, adaptive, and biologically integrated.

    Breast cancer chemotherapy in transition: predictive markers, resistance mechanisms, and new treatment approaches · 2026 · DOI

  • Further investigation into the specific lipid peroxidation pathways targeted by GUA and OLA, - Investigation into how ERK inhibition contributes to mitochondrial dysfunction and increased ROS…

    Marine Sponge-Derived Gukulenin A Sensitizes Ovarian Cancer Cells to PARP Inhibition via Ferroptosis Induction · 2025 · DOI

  • Further investigation of the anti-cancer activity of substituted 2-aminothiophenes - The development of new PARP-1 inhibitors using in silico design and docking…

    IN-SILICO DRUG DESIGN AND SYNTHESIS OF NOVEL 2- AMINOTHIOPHENE AS ANTI-CANCER AGENTS · 2026 · DOI

  • Further investigation of the role of DTX2 in ADPr-Ub production at sites of DNA damage. The development of new tools to study ADPr-Ub and its recognition by proteins.

    Specificity and recognition of the ADP-ribosyl-ubiquitin modification in the DNA damage response · 2026 · DOI

  • Further investigation of the role of PARP1 in Aβ pathology. Development of therapeutic strategies targeting PARP1 for AD.

    PARP1 deficiency mitigates amyloid pathology, neurodegeneration, and cognitive decline in a familial Alzheimer’s disease model · 2026 · DOI

  • Further investigation of the miR-221-5p/RAD18/RAD51 axis in ovarian cancer - Exploration of the therapeutic potential of miR-221-5p restoration in ovarian cancer - Investigation of the role of the miR-221-5p/RAD18/RAD51 axis in other…

    The miR-221-5p/RAD18/RAD51 axis regulates DNA damage tolerance and homologous recombination to drive platinum resistance in ovarian cancer. · 2026 · DOI

  • The underlying epigenetic mechanisms driving platinum resistance in ovarian cancer are poorly understood - The role of the miR-221-5p/RAD18/RAD51 axis in ovarian cancer…

    The miR-221-5p/RAD18/RAD51 axis regulates DNA damage tolerance and homologous recombination to drive platinum resistance in ovarian cancer. · 2026 · DOI

  • Acquired resistance often originates from preexisting heterogeneity within the tumor and is further shaped by continuous diversification during therapy, enabling certain subclones to survive therapeutic pressure and eventually emerge as dominate resistant phenotypes.461 Primary early-stage tumors and advanced metastatic lesions also exhibit marked differences in tumor heterogeneity, drug resistance, and TME…

    Cancer drug response and resistance: molecular mechanisms and combating strategies · 2026 · DOI

Most-cited papers in PARP inhibition in cancer therapy

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Open questions raised by papers listed on this page include: (1) There is a need to investigate the antiproliferative and antitumor activity of NOV202 and olaparib in preclinical prostate cancer models (“Combination of PARP inhibitor olaparib and a vascular disrupting agent reduces…”, 2026); (2) Several challenges remain, such as Talazoparib resistance due to restoration of the homologous recombination (HR) pathway in tumor cells and karonudib side effects that have not been fully explored in early clinical studies (“Mechanisms, Limitations, and Prospects of PARP Inhibitor Talazoparib and MTH1…”, 2026); (3) The lack of understanding of the specificity and recognition of ADPr-Ub (“Specificity and recognition of the ADP-ribosyl-ubiquitin modification in the…”, 2026); (4) There is a need for real-world data on the effectiveness and tolerability of PARPi maintenance therapy in ovarian cancer patients (“Poly(ADP-ribose) polymerase inhibitor maintenance therapy in ovarian cancer: a…”, 2026); (5) The structural basis for SLFN5's biologic activity remains unclear (“SLFN5 restrains type I interferon responses and promotes glioblastoma via its…”, 2026). 283 gap statements have been mined from PARP inhibition in cancer therapy papers in our 7.9M-paper local library, which holds 1,500 papers on the topic; the gaps come from whichever of those papers state one. They are mostly the research gaps the authors state and the papers' abstracts, plus future-work, limitations and challenges passages. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one, so you can read the original claim in context.

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