PARP Inhibitors Cancer Review
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Current perspective: Osimertinib-induced QT prolongation: new drugs with new side-effects need careful patient monitoring

Current perspective: Osimertinib-induced QT prolongation: new drugs with new side-effects need careful patient monitoring | PARP Inhibitors Cancer Review | Scoop.it
An increasing number of tyrosine kinase inhibitors (TKIs) are available for the treatment
of non–small cell lung cancer (NSCLC). QT prolongation is one of the known, but relatively
rare, adverse events of several TKIs (e.g. osimertinib, crizotinib, ceritinib). Screening
for QT prolongation in (high risk) patients is advised for these TKIs. When a QT prolongation
develops, the physician is challenged with the question whether to (permanently) discontinue
the TKI. In this perspective, we report on a patient who developed a grade III QT
prolongation during osimertinib (a third-generation epidermal growth factor receptor
[EGFR]-TKI) treatment.
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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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Neratinib is effective in breast tumors bearing both amplification and mutation of ERBB2 (HER2)

Neratinib is effective in breast tumors bearing both amplification and mutation of ERBB2 (HER2) | PARP Inhibitors Cancer Review | Scoop.it
Breast cancers with amplification or mutation in the epidermal growth factor receptor (EGFR) family member HER2 are usually treated with targeted inhibitors, but resistance is common. Amplification and mutation of HER2 are generally considered mutually exclusive occurrences in treatment-naïve patients. However, Cocco et al . discovered a small proportion of treatment-naïve and, more often, previously treated patients with metastatic breast cancer in which HER2 amplification and mutation were coincident. It is not yet clear why, but these co-amplified/mutant cells were resistant to currently approved HER2-specific and HER2/EGFR-specific inhibitors but were sensitive to the new pan-EGFR inhibitor neratinib. Neratinib, which inhibits EGFR and HER2, as well as HER3 and HER4, was more effective at blocking the activity of the EGFR pathway and other receptor tyrosine kinases, common modes of resistance in HER2-driven tumors. Patients and mice bearing their tumor cells showed improved survival and even tumor regression on neratinib, suggesting that this may be a treatment option for certain breast cancer patients.

Mutations in ERBB2 , the gene encoding epidermal growth factor receptor (EGFR) family member HER2, are common in and drive the growth of “HER2-negative” (not ERBB2 amplified) tumors but are rare in “HER2-positive” ( ERBB2 amplified) breast cancer. We analyzed DNA-sequencing data from HER2-positive patients and used cell lines and a patient-derived xenograft model to test the consequence of HER2 mutations on the efficacy of anti-HER2 agents such as trastuzumab, lapatinib, and neratinib, an irreversible pan-EGFR inhibitor. HER2 mutations were present in ~7% of HER2-positive tumors, all of which were metastatic but not all were previously treated. Compared to HER2 amplification alone, in both patients and cultured cell lines, the co-occurrence of HER2 mutation and amplification was associated with poor response to trastuzumab and lapatinib, the standard-of-care anti-HER2 agents. In mice, xenografts established from a patient whose HER2-positive tumor acquired a D769Y mutation in HER2 after progression on trastuzumab-based therapy were resistant to trastuzumab or lapatinib but were sensitive to neratinib. Clinical data revealed that six heavily pretreated patients with tumors bearing coincident HER2 amplification and mutation subsequently exhibited a statistically significant response to neratinib monotherapy. Thus, these findings indicate that coincident HER2 mutation reduces the efficacy of therapies commonly used to treat HER2-positive breast cancer, particularly in metastatic and previously HER2 inhibitor–treated patients, as well as potentially in patients scheduled for first-line treatment. Therefore, we propose that clinical studies testing the efficacy of neratinib are warranted selectively in breast cancer patients whose tumors carry both amplification and mutation of ERBB2 /HER2.
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IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity

IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity | PARP Inhibitors Cancer Review | Scoop.it
In human and mouse models of ovarian cancer, endoplasmic reticulum stress and the activation of the IRE1α–XBP1 pathway decreases the metabolic fitness of T cells and limits their anti-tumour functions.
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Resistance to therapy and tumor relapse attributed to specific cancer cell population

Resistance to therapy and tumor relapse attributed to specific cancer cell population | PARP Inhibitors Cancer Review | Scoop.it
Resistance to therapy is a major problem in cancer patients, as resistant cells are at the root of tumour relapse and are associated with high morbidity and mortality. A better understanding of the mechanisms associated with ...
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A slow-cycling LGR5 tumour population mediates basal cell carcinoma relapse after therapy

A slow-cycling LGR5 tumour population mediates basal cell carcinoma relapse after therapy | PARP Inhibitors Cancer Review | Scoop.it
Treatment of basal cell carcinoma with Smoothened inhibitors leaves a small population of quiescent cells that can drive relapse but can be eliminated by additional treatment with a Wnt signalling inhibitor.
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Checkpoint blockade therapy resistance in Hodgkin's lymphoma

CORRESPONDENCE| VOLUME 392, ISSUE 10154, P1194-1196, OCTOBER 06, 2018 Checkpoint blockade therapy resistance in Hodgkin's lymphoma Published:October 06, 2018DOI:https://doi.org/10.1016/S0140-6736(18)31867-1 About 50 years ago, the enigma of Hodgkin's lymphoma was depicted as the Hodgkin maze in two editorials in The Lancet.1,  2 The uncertainties of the time were expressed through two questions: “Infection or neoplasm?” and “One entity or two (or more)?”.2 Subsequently, advances in cell biology and molecular pathology provided answers to these questions. Substantial evidence now indicates that classical Hodgkin's lymphoma is a distinct neoplastic entity, with heterogeneous pathological features, which might be associated with Epstein-Barr virus infection. Cases with intermediate features between classical Hodgkin's lymphoma and diffuse large B-cell lymphomas have been recognised. Typically, rare Hodgkin and Reed-Sternberg (HRS) cells are surrounded by immune and inflammatory cells, including T helper 2 cells and T regulatory cells.3 HRS cells express programmed cell death ligand (PD-L) 1 and 2, which bind programmed cell death 1 (PD-1), a receptor expressed by T cells (figure). Binding activates the PD-1 signal transduction pathway, which inactivates tumour-specific T cells. The PD-L1–PD-1 pathway, therefore, functions as a checkpoint that regulates T cell-mediated immune responses. Through this mechanism, HRS cells escape immune surveillance and thereby evade immune destruction. Checkpoint-inhibiting antibodies showed promising results in the treatment of relapsed or chemotherapy-refractive classical Hodgkin's lymphoma, with durable clinical responses in heavily pretreated patients, although their tumours developed immune resistance.3 The mechanisms of resistance to checkpoint-inhibiting antibodies have been partially identified in solid tumours,4 but remain largely unknown in classical Hodgkin's lymphoma. These uncertainties mean that we are again in the Hodgkin maze, because of the disease's enigmatic tangle that includes inflammatory responses to HRS cells and Epstein-Barr virus, the aberrant phenotype of HRS cells, deregulated oncogenic pathways, immune escape, and tumor–host interface crosstalk (figure). We can learn about the mechanisms of resistance to checkpoint blockade in classical Hodgkin's lymphoma from progress in solid tumours. For example, a preclinical study showed that resistance correlated with infiltration of the tumour by immunosuppressive myeloid cells.4 Therefore, to understand resistance to checkpoint blockade in classical Hodgkin's lymphoma, we should study the inflammatory and immune cells in the tumour microenvironment and the immunomodulatory proteins these cells express. This research is now possible using multiplexing immunofluorescence and immunohistochemistry, and digital image analysis.5 Such research should reveal how to overcome drug resistance in classical Hodgkin's lymphoma through rational combinations of checkpoint inhibitors and cellular immunotherapy. We thank Valerie Matarese for precious collaboration and editing of the manuscript. We declare no competing interests. References The Lancet The Hodgkin maze. Lancet. 1969; 294: 728-730 The Lancet Further in the Hodgkin maze. Lancet. 1971; 297: 1053-1054 Carbone A Gloghini A Castagna L Santoro A Carlo-Stella C Primary refractory and early-relapsed Hodgkin's lymphoma: strategies for therapeutic targeting based on the tumour microenvironment. J Pathol. 2015; 237: 4-13 View in Article De Henau O Rausch M Winkler D et al. Overcoming resistance to checkpoint blockade therapy by targeting PI3Kγ in myeloid cells. Nature. 2016; 539: 443-447 View in Article Carey CD Gusenleitner D Lipschitz M et al. Topological analysis reveals a PD-L1-associated microenvironmental niche for Reed-Sternberg cells in Hodgkin lymphoma. Blood. 2017; 130: 2420-2430 View in Article Article Info Publication History Published: 06 October 2018 IDENTIFICATION DOI: 10.1016/S0140-6736(18)31867-1 Copyright © 2018 Elsevier Ltd. All rights reserved. ScienceDirect Access this article on ScienceDirect
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Methylation of all BRCA1 copies predicts response to the PARP inhibitor rucaparib in ovarian carcinoma

Methylation of all BRCA1 copies predicts response to the PARP inhibitor rucaparib in ovarian carcinoma | PARP Inhibitors Cancer Review | Scoop.it
Accurately identifying patients with high-grade serous ovarian carcinoma (HGSOC) who respond to poly(ADP-ribose) polymerase inhibitor (PARPi) therapy is of great clinical importance. Here we show that quantitative BRCA1 methylation analysis provides new insight into PARPi response in preclinical models and ovarian cancer patients. The response of 12 HGSOC patient-derived xenografts (PDX) to the PARPi rucaparib was assessed, with variable dose-dependent responses observed in chemo-naive BRCA1/2-mutated PDX, and no responses in PDX lacking DNA repair pathway defects. Among BRCA1-methylated PDX, silencing of all BRCA1 copies predicts rucaparib response, whilst heterozygous methylation is associated with resistance. Analysis of 21 BRCA1-methylated platinum-sensitive recurrent HGSOC (ARIEL2 Part 1 trial) confirmed that homozygous or hemizygous BRCA1 methylation predicts rucaparib clinical response, and that methylation loss can occur after exposure to chemotherapy. Accordingly, quantitative BRCA1 methylation analysis in a pre-treatment biopsy could allow identification of patients most likely to benefit, and facilitate tailoring of PARPi therapy.
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An aggressive cancer’s road to conquest : Research Highlights

An aggressive cancer’s road to conquest : Research Highlights | PARP Inhibitors Cancer Review | Scoop.it
The type of lung cell that spawns a particularly deadly form of cancer helps to determine how it spreads.
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FDA Approves Moxetumomab Pasudotox-tdfk for the Treatment of HCL - The ASCO Post

FDA Approves Moxetumomab Pasudotox-tdfk for the Treatment of HCL - The ASCO Post | PARP Inhibitors Cancer Review | Scoop.it
FDA Approves Moxetumomab Pasudotox-tdfk for the Treatment of Hairy Cell Leukemia By The ASCO Post September 25, 2018 ON SEPTEMBER 13, 2018, the U.S. Food and Drug Administration (FDA) approved moxetumomab pasudotox-tdfk (Lumoxiti) injection for intravenous use for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who have received at least two prior systemic therapies, including treatment with a purine nucleoside analog. Moxetumomab pasudotox-tdfk is a CD22-directed cytotoxin and is the first of this type of treatment for patients with HCL. Richard Pazdur, MD “[Moxetumomab pasudotox-tdfk] fills an unmet need for patients with hairy cell leukemia whose disease has progressed after trying other FDA-approved therapies,” said Richard Pazdur, MD, Director of the FDA’s Oncology Center of Excellence and Acting Director of the Office of Hematology and Oncology Products in the FDA’s Center for Drug Evaluation and Research. “This therapy is the result of important research conducted by the National Cancer Institute that led to the development and clinical trials of this new type of treatment for patients with this rare blood cancer.” The efficacy of moxetumomab pasudotox-tdfk was assessed in Study 1053, a single-arm, open-label clinical trial of 80 patients who had received prior treatment for HCL with at least two systemic therapies, including a purine nucleoside analog. The trial measured durable complete response, defined as maintenance of hematologic remission for more than 180 days after achievement of a complete response. Thirty percent of patients in the trial achieved a durable complete response, and the overall response rate was 75%. The recommended dose of moxetumomab pasudotox-tdfk is 0.04 mg/kg administered as a 30-minute intravenous infusion on days 1, 3, and 5 of each 28-day cycle for a maximum of 6 cycles or until occurrence of disease progression or unacceptable toxicity. Safety Profile COMMON SIDE effects of moxetumomab pasudotox-tdfk include infusion-related reactions, edema, nausea, fatigue, headache, pyrexia, constipation, anemia, and diarrhea. The prescribing information for moxetumomab pasudotox-tdfk includes a boxed warning about the risk of developing capillary leak syndrome. The boxed warning also notes the risk of hemolytic uremic syndrome, a condition caused by the abnormal destruction of red blood cells. Patients should be made aware of the importance of maintaining adequate fluid intake, and blood chemistry values should be monitored frequently. Other serious warnings include decreased renal function, infusion-related reactions, and electrolyte abnormalities. Women who are breastfeeding should not be given moxetumomab pasudotox-tdfk. ■
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Cancers | A Novel Role for the Interleukin-1 Receptor Axis in Resistance to Anti-EGFR Therapy

Cancers | A Novel Role for the Interleukin-1 Receptor Axis in Resistance to Anti-EGFR Therapy | PARP Inhibitors Cancer Review | Scoop.it
Cetuximab (CTX) is a monoclonal antibody targeting the epidermal growth factor receptor (EGFR), commonly used to treat patients with metastatic colorectal cancer (mCRC). Unfortunately, objective remissions occur only in a minority of patients and are of short duration, with a population of cells...
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C/EBPδ links IL-6 and HIF-1 signaling to promote breast cancer stem cell-associated phenotypes

C/EBPδ links IL-6 and HIF-1 signaling to promote breast cancer stem cell-associated phenotypes | PARP Inhibitors Cancer Review | Scoop.it

STAT3 signaling is activated preferentially in tumor-initiating cells in claudin-low models of human breast cancer. Stem Cells [...] Prolyl-isomerase Pin1 controls normal and cancer stem cells of the breast. EMBO Mol Med. 2014;6:99–1

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Breaking down the epidemiology of brain cancer

Breaking down the epidemiology of brain cancer | PARP Inhibitors Cancer Review | Scoop.it
Brain cancer comprises only 2% of cancers, but is notoriously difficult to treat. Understanding the location of such tumours, as well as the underlying genetics, will help to tackle this devastating disease.
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Gallbladder Cancer | Gastroenterology | JAMA | JAMA Network

Gallbladder Cancer | Gastroenterology | JAMA | JAMA Network | PARP Inhibitors Cancer Review | Scoop.it
This JAMA Patient Page describes the symptoms, diagnosis, and treatment of gallbladder cancer.
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Classification and Personalized Prognosis in Myeloproliferative Neoplasms | NEJM

Abstract
BACKGROUND
Myeloproliferative neoplasms, such as polycythemia vera, essential thrombocythemia, and myelofibrosis, are chronic hematologic cancers with varied progression rates. The genomic characterization of patients with myeloproliferative neoplasms offers the potential for personalized diagnosis, risk stratification, and treatment.

METHODS
We sequenced coding exons from 69 myeloid cancer genes in patients with myeloproliferative neoplasms, comprehensively annotating driver mutations and copy-number changes. We developed a genomic classification for myeloproliferative neoplasms and multistage prognostic models for predicting outcomes in individual patients. Classification and prognostic models were validated in an external cohort.

RESULTS
A total of 2035 patients were included in the analysis. A total of 33 genes had driver mutations in at least 5 patients, with mutations in JAK2, CALR, or MPL being the sole abnormality in 45% of the patients. The numbers of driver mutations increased with age and advanced disease. Driver mutations, germline polymorphisms, and demographic variables independently predicted whether patients received a diagnosis of essential thrombocythemia as compared with polycythemia vera or a diagnosis of chronic-phase disease as compared with myelofibrosis. We defined eight genomic subgroups that showed distinct clinical phenotypes, including blood counts, risk of leukemic transformation, and event-free survival. Integrating 63 clinical and genomic variables, we created prognostic models capable of generating personally tailored predictions of clinical outcomes in patients with chronic-phase myeloproliferative neoplasms and myelofibrosis. The predicted and observed outcomes correlated well in internal cross-validation of a training cohort and in an independent external cohort. Even within individual categories of existing prognostic schemas, our models substantially improved predictive accuracy.

CONCLUSIONS
Comprehensive genomic characterization identified distinct genetic subgroups and provided a classification of myeloproliferative neoplasms on the basis of causal biologic mechanisms. Integration of genomic data with clinical variables enabled the personalized predictions of patients’ outcomes and may support the treatment of patients with myeloproliferative neoplasms. (Funded by the Wellcome Trust and others.)
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Leukemia inhibitory factor functions in parallel with interleukin-6 to promote ovarian cancer growth

Leukemia inhibitory factor functions in parallel with interleukin-6 to promote ovarian cancer growth | PARP Inhibitors Cancer Review | Scoop.it
Brief Communication...
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IL-8-induced O -GlcNAc modification via GLUT3 and GFAT regulates cancer stem cell-like properties in colon and lung cancer cells

IL-8-induced O -GlcNAc modification via GLUT3 and GFAT regulates cancer stem cell-like properties in colon and lung cancer cells | PARP Inhibitors Cancer Review | Scoop.it
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SWI/SNF catalytic subunits’ switch drives resistance to EZH2 inhibitors in ARID1A -mutated cells

SWI/SNF catalytic subunits’ switch drives resistance to EZH2 inhibitors in ARID1A -mutated cells | PARP Inhibitors Cancer Review | Scoop.it
The mechanism of resistance to EZH2 inhibitors in cancers with inactivating SWI/SNF mutations is unknown. Here, the authors demonstrate that the switch of the SWI/SNF catalytic subunits from SMARCA4 to SMARCA2 drives resistance to EZH2 inhibitors in ARID1A-mutated ovarian cancer cells.
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Cancer origins—genetics rules the day

Cancer origins—genetics rules the day | PARP Inhibitors Cancer Review | Scoop.it
Summary
A major goal of cancer research is to identify central molecular and cellular mechanisms underlying the development of tumors and their response to treatment, with the aim of uncovering key vulnerabilities. Early events in the development of cancer may inform such vulnerabilities (1), but early tumors are much more difficult to observe and study in patients than established tumors. Indeed, one of the hardest issues to resolve in early tumor development is the relative contributions of the oncogenic driver mutations and the nonpathogenic gene networks expressed in a precancerous cell. On page 91 of this issue, Park et al. (2) investigate the mechanisms of development of neuro endocrine cancer in the lung and the prostate using human epithelial cells in culture. They find that these neuroendocrine tumors can arise from non-neuroendocrine epithelial cells, which converge upon reprogramming toward a neuroendocrine fate via a common and specific combination of genetic factors.

http://www.sciencemag.org/about/science-licenses-journal-article-reuse
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Analysis of cell proliferation and tissue remodelling uncovers a KLF4 activity score associated with poor prognosis in colorectal cancer

Analysis of cell proliferation and tissue remodelling uncovers a KLF4 activity score associated with poor prognosis in colorectal cancer | PARP Inhibitors Cancer Review | Scoop.it
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Adaptive Biotechnologies’ ClonoSEQ assay receives FDA approval to test for MRD in ALL or MM patients

Adaptive Biotechnologies’ ClonoSEQ assay receives FDA approval to test for MRD in ALL or MM patients | PARP Inhibitors Cancer Review | Scoop.it
The Food and Drug Administration approves Adaptive Biotechnologies’ ClonoSEQ assay for use in testing for minimal residual disease in patients with acute lymphoblastic leukemia or multiple myeloma.
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FDA Approves Dacomitinib for Metastatic NSCLC | ESMO

FDA Approves Dacomitinib for Metastatic NSCLC | ESMO | PARP Inhibitors Cancer Review | Scoop.it
It is approved for first-line treatment of patients with tumours with EGFR exon 19 deletion or exon 21 L858R substitution mutations as detected by an FDA-approved test...
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Pfizer Snatches FDA Approval For Rare Front-Line Lung Cancer Indication - Pfizer Inc. (NYSE:PFE)

Pfizer Snatches FDA Approval For Rare Front-Line Lung Cancer Indication - Pfizer Inc. (NYSE:PFE) | PARP Inhibitors Cancer Review | Scoop.it
Pfizer receives FDA approval for Vizimpro which treats a rare form of lung cancer.With the latest FDA approval for Vizimpro, Pfizer now has two drugs that targ...
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Dipeptide γ‑secretase inhibitor treatment enhances the anti‑tumor effects of cisplatin against gastric cancer by suppressing cancer stem cell properties

Dipeptide γ‑secretase inhibitor treatment enhances the anti‑tumor effects of cisplatin against gastric cancer by suppressing cancer stem cell properties | PARP Inhibitors Cancer Review | Scoop.it
The γ‑secretase inhibitor blocks Notch activity by preventing its cleavage at the cell surface. In the present study, the effect of the γ‑secretase inhibitor on the viability of gastric cancer cells when administered in combination with cisplatin was investigated, with particular focus on CD44highLgr‑5high cancer cells. The four gastric cancer cell lines, MKN45, MKN74, SC‑6‑JCK and SH‑10‑TC, were used for the experiments. In the MTT assay, treatment with 25 µM dipeptide γ‑secretase inhibitor (DAPT) alone did not affect cell proliferation in any of the four cell lines. Gastric cancer cells subjected to combination treatment with DAPT and cisplatin exhibited decreased viability when compared with those treated with cisplatin alone. Flow cytometry was performed to evaluate the expression of cluster of differentiation (CD)‑44 and leucine‑rich repeat‑containing G‑protein coupled receptor 5 (Lgr‑5), two cancer stem cell markers in gastric cancers. Treatment with cisplatin alone significantly increased the proportion of CD44highLgr‑5high cells. However, the addition of DAPT to cisplatin reduced the CD44highLgr‑5high fraction, suggesting that DAPT reduced the number of gastric cancer cells. In conclusion, the present study demonstrated the synergistic effects of DAPT in combination with cisplatin by decreasing the survival of gastric cancer cells. In addition, combination treatment with DAPT reduced the number of CD44highLgr‑5high cells, which are thought to exhibit cancer stem cell properties. These results highlight the therapeutic potential of DAPT in gastric cancer treatment.
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Novocure’s Tumor Treating Fields: Innovative brain cancer therapy with survival and safety benefits

Novocure’s Tumor Treating Fields: Innovative brain cancer therapy with survival and safety benefits | PARP Inhibitors Cancer Review | Scoop.it
Novocure milestones in brain cancer treatment. Novocure was founded in 2000 with a patient-forward approach that remains the centre of its corporate mission. The timeline highlights more than 18 years of preclinical and clinical research with many significant milestones, establishing Novocure as an innovator in oncology and dedicated to improving the lives of people with brain cancer. Optune® is a non-invasive portable device that delivers alternating electric fields to dividing cancer cells. The NovoTAL™ system is a software programme that optimizes transducer array layouts for an individual patient based on head size and tumour location. GBM, glioblastoma multiforme; NCCN, National Comprehensive Cancer Network.
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Targeting the Residual Leukemia Cells after Chemotherapy

One of the biggest challenges in treating acute myeloid leukemia (AML) is relapse
of aggressive disease after treatment. In this issue of Cancer Cell, Boyd et al. characterize
a molecularly distinct population of chemotherapy-induced transient leukemic regenerating
cells (LRCs), which can be exploited to prevent AML recurrence.
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Science snaps: how nappy technology is helping us see cancer more clearly

Science snaps: how nappy technology is helping us see cancer more clearly | PARP Inhibitors Cancer Review | Scoop.it
In this Science Snaps blog post, find out how scientists have adapted the technology found in babies' nappies to take sharper images of cancer cells.
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