PARP Inhibitors Cancer Review
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A phase II study of nab-paclitaxel in combination with ramucirumab in patients with previously treated advanced gastric cancer

Nanoparticle albumin-bound (nab)-paclitaxel was developed to improve paclitaxel solubility
and does not need premedication to avoid infusion-related reactions associated with
solvent-based (sb)-paclitaxel. We conducted a phase II trial to investigate the efficacy
and safety of nab-paclitaxel plus ramucirumab combination therapy for previously treated
advanced gastric cancer.
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PARP Inhibitors Cancer Review
Poly ADP ribose polymerase (PARP) inhibitors for triple negative breast cancer (TNBC) The Phase III failure of Iniparib to extend OS or PFS in TNBC patients has cast a dark shadow on PARP inhibitors drug class and R&D in one of the most active area in industrial oncology. The most advanced product iniparib (BSI 201, Sanofi Aventis) has shown 30% response rates in Phase I trials and 62% in triple negative breast cancer patients in Phase II trials. Addition of Iniparib to chemotherapy increased overall survival to 12.2 months from 7.7 months on gemcitabine+ carboplatin. A global Phase III trial in squamous NSCLC was initiated in 2010. It has completed enrollment of TNBC patients in Phase III trials. The NDA and MAA is expected to be filed in 1-2 Q 2011. The second product olaparib has shown 40% response rates in extended Phase I trials and completed Phase II studies. Olaparib planned Phase III trials in BRCA1/BRCA2 positive breast cancer was cancelled by Astra Zeneca and focus shifted to Phase III in ovarian cancer patients. Olaparib extended PFS and time to progression by 4 and 4.6 months over placebo. Veliparib from Abbott is the third PARPi to complete Phase II trials in advanced metastatic breast cancer with 37% RR in BRCA positive patients. Tumor cells use PARP pathway to repair DNA damage to proliferate and replicate. A new test to identify defective genes RAD51 assay indicates that PARP inhibitors may benefit 60% of the ovarian cancer patients. Inhibition of PARP offers novel agents for treating tumors with DNA repair defects. PARP inhibitors have the market potential to generate 10-15 billion annual sales with each brand worth $3-5 billion in sales within 5 years after approval and marketing in major markets.
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Wendt Lab Metastatic Breast cancer

Wendt Lab Metastatic Breast cancer | PARP Inhibitors Cancer Review | Scoop.it
Metastatic breast cancer research. Bioluminesent imaging of drug resistant cancer. Wendt lab at the Purdue center for cancer research.Mouse models of breast cancer progression...
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UCLA scientists create a renewable source of cancer-fighting T cells | UCLA Broad Stem Cell Center

UCLA scientists create a renewable source of cancer-fighting T cells | UCLA Broad Stem Cell Center | PARP Inhibitors Cancer Review | Scoop.it
A study by UCLA researchers is the first to demonstrate a technique for coaxing pluripotent stem cells — which can give rise to every cell type in the body and which can be grown indefinitely in the lab — into becoming mature T cells capable of killing tumor cells.
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Breast cancer cells in mice tricked into turning into fat cells | EurekAlert! Science News

Breast cancer cells in mice tricked into turning into fat cells | EurekAlert! Science News | PARP Inhibitors Cancer Review | Scoop.it
As cancer cells respond to cues in their microenvironment, they can enter a highly plastic state in which they are susceptible to transdifferentiation into a different type of cell. Researchers at the University of Basel in Switzerland exploited this critical phase, known as an...
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The Next Wave of Stroma-Targeting Therapy in Pancreatic Cancer

The Next Wave of Stroma-Targeting Therapy in Pancreatic Cancer | PARP Inhibitors Cancer Review | Scoop.it
The stroma of pancreatic ductal adenocarcinoma (PDA) forms a major barrier to therapy and immune surveillance. Elahi-Gedwillo and colleagues demonstrate that halofuginone has potent antifibrotic activity in PDA by directly inhibiting the activation of pancreatic stellate cells, thereby reducing...
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B591, a novel specific pan-PI3K inhibitor, preferentially targets cancer stem cells

B591, a novel specific pan-PI3K inhibitor, preferentially targets cancer stem cells | PARP Inhibitors Cancer Review | Scoop.it
The phosphoinositide 3-kinase (PI3K) signaling pathway is one of the most frequently activated signaling pathways in human cancer, playing a central role in tumorigenesis as well as the maintenance of CSCs. Here, we designed and identified B591, a dihydrobenzofuran-imidazolium salt, as a novel specific pan-PI3K inhibitor with potent inhibitory activity against class I PI3K isoforms, which showed effective inhibition of cellular PI3K/mTOR signaling pathway and robust antitumor activity in a set of cancer cell lines. Notably, compared with bulk tumor cell populations, B591 exhibited more potency in suppressing CSCs survival and inducing CSCs apoptosis, and presence of B591 effectively eliminated paclitaxel-enriched CSCs. B591 diminished self-renewal capacity and decreased the expression of epithelial-mesenchymal transition (EMT) markers of CSCs. In vivo, B591 preferentially decreased CSCs levels in mouse xenograft model of human breast cancer as evidenced especially by remarkable reduction of tumor-initiating ability. Consistent with the preferential targeting of CSCs, B591 effectively inhibited breast tumor metastasis and delayed tumor regrowth following paclitaxel treatment. Taken together, our findings establish B591, a novel PI3K inhibitor, as a strong candidate for clinical evaluation as a CSCs targeting agent.
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Functionalized selenium nanoparticles for targeted delivery of doxorubicin to improve non-small-cell lung cancer therapy

Functionalized selenium nanoparticles for targeted delivery of doxorubicin to improve non-small-cell lung cancer therapy | PARP Inhibitors Cancer Review | Scoop.it
Abstract
Background
Selenium nanoparticles (SeNPs) loaded with chemotherapeutic drugs provided a novel perspective for cancer therapy.

Materials and methods
Here, SeNPs were modified with cyclic peptide (Arg–Gly–Asp–d-Phe–Cys [RGDfC]) to fabricate tumor-targeting delivery carrier RGDfC-SeNPs and, then, doxorubicin (DOX) was loaded to the surface of RGDfC-SeNPs for improving the antitumor efficacy of DOX in non-small-cell lung carcinoma therapy.

Results
The chemical structure characterization of RGDfC-Se@DOX showed that DOX was successfully loaded to the surface of RGDfC-SeNPs to prepare functionalized antitumor drug delivery system RGDfC-Se@DOX. RGDfC-Se@DOX exhibited effective cellular uptake in A549 cells and entered A549 cells mainly by clathrin-mediated endocytosis pathway. Compared to free DOX or Se@DOX at the equivalent dose of DOX, RGDfC-Se@DOX showed greater activity to inhibit A549 cells’ proliferation and migration/invasion and induce A549 cells’ apoptosis. More importantly, compared with passive targeting delivery system Se@DOX, active targeting delivery system RGDfC-Se@DOX exhibited more significant antitumor efficacy in vivo.

Conclusion
Taken together, RGDfC-Se@DOX may be a novel promising drug candidate for the lung carcinoma therapy.

Keywords: nanoscale drug carrier, antitumor, chemotherapy, RGDfC peptide, apoptosis
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Cervical cancer: unequal progress

Cervical cancer: unequal progress | PARP Inhibitors Cancer Review | Scoop.it
Cervical cancer—a disease affecting more than half a million women every year—is now
largely preventable. And yet despite an effective vaccine being available for more
than 13 years, it still caused 270 000 deaths globally in 2015, 90% of which were
in low-income and middle-income countries (LMICs).
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New Cancer Treatment Combination Takes Down Patient-derived Colorectal Cancer Initiating Cells | Stem Cells Portal - Stem Cells Journal Online Community

New Cancer Treatment Combination Takes Down Patient-derived Colorectal Cancer Initiating Cells | Stem Cells Portal - Stem Cells Journal Online Community | PARP Inhibitors Cancer Review | Scoop.it
Researchers show how the inhibition of a DNA repair mediator may represent an exciting means to potentiate chemotherapy in colorectal cancer patients...
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Researchers Develop an Experimental Therapy for Triple-negative Breast Cancer | Cell And Molecular Biology

Researchers Develop an Experimental Therapy for Triple-negative Breast Cancer | Cell And Molecular Biology | PARP Inhibitors Cancer Review | Scoop.it
Between 12 and 17% of all breast cancer cases are triple-negative, a highly aggressive type with few therapeutic options.| Cell And Molecular Biology...
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ARTEMIS clinical trial offers triple-negative patients personalized therapy | MD Anderson Cancer Center

ARTEMIS clinical trial offers triple-negative patients personalized therapy | MD Anderson Cancer Center | PARP Inhibitors Cancer Review | Scoop.it
The ARTEMIS study uses molecular testing of triple-negative breast cancer to guide patients into clinical trials of targeted therapies to fight the deadly subtype of the disease.
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Sex differences in GBM revealed by analysis of patient imaging, transcriptome, and survival data

Sex differences in GBM revealed by analysis of patient imaging, transcriptome, and survival data | PARP Inhibitors Cancer Review | Scoop.it
In recent years, there has been increasing interest in personalized medicine for cancer, considering the unique biology of each tumor and patient to optimize therapeutic approaches. Sex differences play a role in patient outcomes, and Yang et al. determined that in the case of the brain tumor glioblastoma, these go beyond hormonal influences and appear to be intrinsic to the tumor cells themselves. The authors found that the sex of the patient correlates not only with prognosis but also with responses to different treatments, suggesting that it may be an important factor to consider when optimizing the therapeutic regimen for each patient.

Sex differences in the incidence and outcome of human disease are broadly recognized but, in most cases, not sufficiently understood to enable sex-specific approaches to treatment. Glioblastoma (GBM), the most common malignant brain tumor, provides a case in point. Despite well-established differences in incidence and emerging indications of differences in outcome, there are few insights that distinguish male and female GBM at the molecular level or allow specific targeting of these biological differences. Here, using a quantitative imaging–based measure of response, we found that standard therapy is more effective in female compared with male patients with GBM. We then applied a computational algorithm to linked GBM transcriptome and outcome data and identified sex-specific molecular subtypes of GBM in which cell cycle and integrin signaling are the critical determinants of survival for male and female patients, respectively. The clinical relevance of cell cycle and integrin signaling pathway signatures was further established through correlations between gene expression and in vitro chemotherapy sensitivity in a panel of male and female patient-derived GBM cell lines. Together, these results suggest that greater precision in GBM molecular subtyping can be achieved through sex-specific analyses and that improved outcomes for all patients might be accomplished by tailoring treatment to sex differences in molecular mechanisms.
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Pediatric Brain Tumor Foundation - Research

Pediatric Brain Tumor Foundation - Research | PARP Inhibitors Cancer Review | Scoop.it
Research The Pediatric Brain Tumor Foundation is the world’s leading nonprofit dedicated to childhood brain tumor research. Since 1991, we have invested more than $30 million in research and have played a leading role in fostering innovation in the field. The research we fund has paved the way for more focused efforts to understand the cellular and molecular biology of childhood brain tumors. This has opened avenues for the discovery of new diagnostic and treatment approaches. WHAT WE FUND Basic, translational and clinical approaches to pediatric brain tumor research will improve the lives of children. We take this into account when setting research priorities. Find out more about our research funding. >> RESEARCH ADVISORY NETWORK Our research grants are peer-reviewed and must meet high standards of scientific merit. We rely on the expertise of this distinguished group to help us evaluate the best funding opportunities. Meet our scientific advisors. >> RESEARCH FUNDING PROGRAMS We are dedicated to making a difference for children with brain tumors of all types. To help accomplish this mandate while remaining responsive to changes in research, we’ve developed several different funding initiatives. Find out more about our funding programs.  >> FUNDING PARTNERS
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Mechanisms of PARP inhibitor sensitivity and resistance - ScienceDirect

Mechanisms of PARP inhibitor sensitivity and resistance - ScienceDirect | PARP Inhibitors Cancer Review | Scoop.it
Abstract
BRCA1 and BRCA2 deficient tumor cells are sensitive to inhibitors of Poly ADP Ribose Polymerase (PARP1) through the mechanism of synthetic lethality. Several PARP inhibitors, which are oral drugs and generally well tolerated, have now received FDA approval for various ovarian cancer and breast cancer indications. Despite their use in the clinic, PARP inhibitor resistance is common and develops through multiple mechanisms. Broadly speaking, BRCA1/2-deficient tumor cells can become resistant to PARP inhibitors by restoring homologous recombination (HR) repair and/or by stabilizing their replication forks. Here, we review the mechanism of PARP inhibitor resistance.

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Photodynamic therapy for basal cell carcinoma - Collier - 2018 - British Journal of Dermatology - Wiley Online Library

Photodynamic therapy for basal cell carcinoma - Collier - 2018 - British Journal of Dermatology - Wiley Online Library | PARP Inhibitors Cancer Review | Scoop.it
This is the largest systematic review to‐date which compares the treatment of basal cell carcinoma (BCC) with a treatment called photodynamic therapy (PDT) and alternative treatments. PDT is an established treatment option for low‐risk BCC.  PDT involves putting a cream on the skin and leaving it for 3 hours. Then a red light is shone on it; this often causes pain for a few minutes but few other side effects.  At least two treatment sessions are needed.  In our study we only used evidence from high quality studies (Randomised Control Trials) and only looked at studies which included treatments for low‐risk BCC types (superficial and nodular).  The main medical databases were searched to find all suitable studies. The benefits of treatments were compared, using previously‐agreed criteria. The differences between how often treatments would cure (effectiveness), how the area would look after treatment (cosmetic result), and the side‐effects, including pain, were compared at different times. Imiquimod and fluorouracil creams are applied regularly to the BCC over 4‐6 weeks. The creams cause discomfort which increases with time.  The peak pain from PDT was higher than imiquimod and fluorouracil, although the combined discomfort from imiquimod and PDT appeared similar. Cure rates between fluorouracil and PDT were comparable although rates with imiquimod were higher than PDT applied once. The cosmetic result with both creams was similar to PDT. Cryosurgery (freezing with liquid nitrogen) is a convenient quick treatment.  Cure rates were similar to PDT, although the cosmetic results were poorer. Surgical excision, where the tumour is cut out and the skin stitched, showed the highest cure rates. The cosmetic result after PDT was as good or better than other treatments. Our review showed that PDT is an effective treatment for low‐risk BCC, with excellent cosmetic results and safety.
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Briacell advancing Bria-IMT™ Immunotherapy for Advanced Breast Cancer Patients

Briacell advancing Bria-IMT™ Immunotherapy for Advanced Breast Cancer Patients | PARP Inhibitors Cancer Review | Scoop.it

BriaCell Therapeutics (OTC: BCTXF) (TSX.V: BCT), a biotechnology company developing targeted, safe treatments for cancer, is advancing the development of its lead product candidate Bria-IMT™, which has demonstrated positive results in three clinical studies to date. An article discussing the company reads, “Bria-IMT™ works by providing breast cancer antigens and a direct stimulation of the cancer fighting T-cells. This way, the therapy strengthens the body’s ability to fight cancer. Bria-IMT™ has achieved proof of concept in clinical trials, and its safety has also been assessed as excellent. Even in heavily pre-treated advanced breast cancer patients, Bria-IMT™ managed to elicit tumor regression. . . . In the combination study, six patients have been treated with Bria-IMT™ and KEYTRUDA®. In all of the patients, the combination was very well tolerated, and the study is ongoing. 

 

We believe that Bria-IMT™, BriaCell’s lead product candidate, awakens the patient’s immune system to recognize tumor cells as foreign, and hence destroys them. We hypothesize that Bria-IMT™ exerts its action via changing the tumor’s antigen-presentation system {i.e. the system that presents antigen material on the surface of the tumor cell – to be recognized by the T cells of the immune system as either self (i.e., safe) or foreign (i.e., to be destroyed)}. Specifically, Bria-IMT™ may stimulate the dendritic cells, a key component of the antigen-presenting system, to display certain immunogenic (i.e., immune response-generating) protein fragments to T cells, which activates the T Cells to destroy the tumor cells either directly, or by inducing a humoral (antibody-generating) response.

Our preliminary analyses have shown several up-regulated genes in SV-BR-1-GM that encode proteins known to be immunogenic (i.e. immune response-generating).

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TLR Signaling Is Activated in Lymph Node–Resident CLL Cells and Is Only Partially Inhibited by Ibrutinib

TLR Signaling Is Activated in Lymph Node–Resident CLL Cells and Is Only Partially Inhibited by Ibrutinib | PARP Inhibitors Cancer Review | Scoop.it
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Chronic lymphocytic leukemia (CLL) is a malignancy of mature B cells driven by B-cell receptor (BCR) signaling and activated primarily in the lymph node. The Bruton's tyrosine kinase (BTK) inhibitor ibrutinib effectively inhibits BCR-dependent proliferation and survival...
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Characterization of Tumor-Suppressor Gene Inactivation Events in 33 Cancer Types

Characterization of Tumor-Suppressor Gene Inactivation Events in 33 Cancer Types | PARP Inhibitors Cancer Review | Scoop.it
Highlights

A computational framework based on the two-hit model to classify inactivation events

Landscape of tumor-suppressor gene (TSG) inactivation events across cancers

Genetic and functional impact of TSG inactivation events

TSG × cancer inactivation events tend to cluster by TSG function
Summary
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PNAS Plus: Real-time dynamics of mutagenesis reveal the chronology of DNA repair... - Europe PMC Article - Europe PMC

PNAS Plus: Real-time dynamics of mutagenesis reveal the chronology of DNA repair... - Europe PMC Article - Europe PMC | PARP Inhibitors Cancer Review | Scoop.it
A central goal in genetics is to understand how mutation rates are regulated by the genome maintenance system in response to DNA damage or drug treatments. This has been challenging because existing mutation assays only show time and population averages ...
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Cervical cancer

Cervical cancer | PARP Inhibitors Cancer Review | Scoop.it
Each year, more than half a million women are diagnosed with cervical cancer and the
disease results in over 300 000 deaths worldwide. High-risk subtypes of the human
papilloma virus (HPV) are the cause of the disease in most cases.
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JCI - PARP inhibition enhances tumor cell-intrinsic immunity in ERCC1-deficient non-small cell lung cancer

JCI - PARP inhibition enhances tumor cell-intrinsic immunity in ERCC1-deficient non-small cell lung cancer | PARP Inhibitors Cancer Review | Scoop.it
The cyclic GMP-AMP synthase–stimulator of interferon genes (cGAS/STING) pathway detects cytosolic DNA to activate innate immune responses. Poly(ADP-ribose) polymerase inhibitors (PARPi) selectively target cancer cells with DNA repair deficiencies such as those caused by BRCA1 mutations or ERCC1 defects. Using isogenic cell lines and patient-derived samples, we showed that ERCC1-defective non-small cell lung cancer (NSCLC) cells exhibit an enhanced type I interferon transcriptomic signature, and that low ERCC1 expression correlates with increased lymphocytic infiltration. We demonstrated that clinical PARPi, including olaparib and rucaparib, have cell-autonomous immunomodulatory properties in ERCC1-defective NSCLC and BRCA1-defective triple-negative breast cancer (TNBC) cells. Mechanistically, PARPi generated cytoplasmic chromatin fragments with micronuclei characteristics; these were found to activate cGAS/STING, downstream type I interferon signaling and CCL5 secretion. Importantly, these effects were suppressed in PARP1-null TNBC cells, suggesting that this phenotype resulted from an on-target effect of PARPi on PARP1. PARPi also potentiated interferon-γ-induced PD-L1 expression in NSCLC cell lines and in fresh patient tumor cells; this effect was enhanced in ERCC1-deficient contexts. Our data provide the preclinical rationale for using PARPi as immunomodulatory agents in appropriately molecularly-selected populations.
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New Cancer Treatment Combination Takes Down Patient-derived Colorectal Cancer Initiating Cells | Stem Cells Portal - Stem Cells Journal Online Community

New Cancer Treatment Combination Takes Down Patient-derived Colorectal Cancer Initiating Cells | Stem Cells Portal - Stem Cells Journal Online Community | PARP Inhibitors Cancer Review | Scoop.it
Researchers show how the inhibition of a DNA repair mediator may represent an exciting means to potentiate chemotherapy in colorectal cancer patients...
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Rhabdomyosarcoma

Rhabdomyosarcoma | PARP Inhibitors Cancer Review | Scoop.it
Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma in children. This Primer highlights RMS epidemiology and disease mechanisms and presents the state of the art in clinical care, including diagnostics, risk-based disease management and prevention of late treatment effects.
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2018 in Review: New Cancer Drug Approvals

2018 in Review: New Cancer Drug Approvals | PARP Inhibitors Cancer Review | Scoop.it
In 2018, the FDA approved several new drug treatments for different cancer types that American Cancer Society editors believe will make a significant difference.
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Age-related remodelling of oesophageal epithelia by mutated cancer drivers

Age-related remodelling of oesophageal epithelia by mutated cancer drivers | PARP Inhibitors Cancer Review | Scoop.it
Driver-mutated clones emerge multifocally from early childhood and increase their number and size with ageing, and ultimately replace almost the entire oesophageal epithelium in the extremely elderly. Compared with mutations in oesophageal cancer, there is a marked overrepresentation of NOTCH1 and PPM1D mutations in physiologically normal oesophageal epithelia; these mutations can be acquired before late adolescence (as early as early infancy) and significantly increase in number with heavy smoking and drinking. The remodelling of the oesophageal epithelium by driver-mutated clones is an inevitable consequence of normal ageing, which—depending on lifestyle risks—may affect cancer development.
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PARP inhibitors in ovarian cancer - ScienceDirect

PARP inhibitors in ovarian cancer - ScienceDirect | PARP Inhibitors Cancer Review | Scoop.it
Highlights

Ovarian cancer is the most lethal gynecologic malignancy.


PARP inhibitors are effective therapeutic agents by inducing synthetic lethality.


FDA and EMA approved PARP inhibitors in ovarian cancer: olaparib, rucaparib, and niraparib.


Combinations of PARP inhibitors with other agents may overcome resistance mechanisms.


Abstract
Poly-ADP-ribose polymerase inhibitors (PARPis) are the most active and interesting therapies approved for the treatment of epithelial ovarian cancer. They have changed the clinical management of a disease characterized, in almost half of cases, by extreme genetic complexity and alteration of DNA damage repair pathways, particularly homologous recombination (HR) deficiency. In this review, we provide an updated overview of the available results of recent clinical trials on the three Food and Drug Administration and European Medicines Agency approved PARPis in ovarian cancer: olaparib, niraparib, and rucaparib. Furthermore, we anticipate the future perspective of combination regimens with antiangiogenic, immunocheckpoint inhibitors, and other biological agents as strategies to overcome resistance mechanisms, potentiate the therapeutic efficacy, and expand their clinical use in non-HR deficient tumors.
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GPR35 promotes glycolysis, proliferation, and oncogenic signaling by engaging with the sodium potassium pump

GPR35 promotes glycolysis, proliferation, and oncogenic signaling by engaging with the sodium potassium pump | PARP Inhibitors Cancer Review | Scoop.it
Disease-associated polymorphisms can give insight into protein function, particularly for receptors whose ligands are unknown or controversial. Polymorphisms in the G protein–coupled receptor GPR35 are associated with increased risk for certain inflammatory diseases of the bile duct and large intestine that have increased cancer risk. Schneditz et al. found that GPR35 promoted the activity of Na/K-ATPase, a ubiquitous and essential transmembrane pump that sets the membrane potential in cells, in a manner that did not rely on its proposed ligands. A disease-associated variant of GPR35 ind