13975-Kelley, Mark
Faculty

Mark R. Kelley, PHD

Betty and Earl Herr Professor of Pediatric Oncology Research

Bio

My work has focused on translational research in DNA damage and repair, specifically, to determine how those activities can be exploited therapeutically to treat cancers and protect normal cells from oxidative and DNA base damage. Since 1993, I have focused specifically on the enzyme apurinic/apyrimidinic endonuclease 1/ Redox effector factor-1 (APE1/Ref-1)—mechanistically as well as a therapeutic target in cancers and other diseases that manifest cancer-like properties. APE1/Ref-1 is unique to the Base Excision Repair Pathway (BER), with dual repair and redox signaling functions that are crucial to cellular viability. My work has been the first to tease apart those functions, not only to fully characterize them, but to also determine how to manipulate each function individually for therapeutic benefit. In doing the latter, I discovered and have been developing a redox-specific inhibitor of Ref-1, as well as second-generation analogs that are under further investigation. This original work was the impetus for becoming Chief Scientific Founder and Officer of Apexian Pharmaceutical, an integrated drug development company that’s leveraging the APE1/Ref-1 target platform to produce new therapeutics for some of the deadliest and hardest-to-treat cancers. Apexian recently submitted and received a treatment IND (IND125360) for a new drug that targets Ref-1; its potential indications include ovarian, colon, pancreatic cancer, leukemias as well as other adult and pediatric cancers. APX3330 is completing a phase 1 clinical trial for safety and recommended Phase II dose (RP2D) in cancer patients (NCT03375086). I am also exploring APE1/Ref-1 and BER for mechanistic and therapeutic opportunities in chemotherapy-induced peripheral neuropathy (CIPN) and other diseases. In broader terms, all the academic chairs I’ve held and the program leader and director positions I currently hold are dedicated to fast-tracking collaboration and translational research to find more effective cancer treatments. In my Associate Director positions, I also help equip the next generation of researchers by training and mentoring junior faculty, postdoctorates, fellows, MD students and others. My expertise in Ref-1 functions, drug development, such as taking APX3330 to clinical trials and development of second generation compounds, as well as years of studies centering on Ref-1 and its role as a node in cancer cells will augment this application.

I serve on numerous consulting/scientific boards of several biotechnology companies and have and still serves on various NIH/NCI study sections and Cancer Center review panels. I was chair of the Cancer Etiology Study Section at NIH and reviews for numerous international agencies. I am a member of American Association for the Advancement of Science, American Association for Cancer Research, Society for Pediatric Research, and American Society of Clinical Oncology. I also serve on the editorial board of Frontiers in Bioscience, Journal of Pharmacology and Experimental Therapeutics, Mutation Research; Molecular and Fundamental Mechanisms (Assoc Editor) and Current Molecular Pharmacology.

1993–1998        Associate Professor of Pediatrics, Section of Pediatric Endocrinology and Dept. of Biochemistry and Molecular Biology, Indiana University School of Medicine (IUSM)

1995– 2017      Associate Director, Wells Center for Pediatric Research, IUSM

1997–present   Professor of Pediatrics and Dept. of Biochemistry and Molecular Biology, IUSM

2001–2006        Program Leader, Experimental and Developmental Therapeutics Research, IUSCC, IUSM

2002–2006        Chemical Pathology Study Section Member & Cancer Etiology Study Section Member

2004–2006        Cancer Etiology Study Section Chairperson

2008–2012        NCI-F Manpower and Training: T32 Training grant and K99/R00 Career development Awards

2001–2008        Jonathan and Jennifer Simmons Professor of Pediatrics, Dept. of Pediatrics, IUSM

2002–present   Professor, Dept. of Pharmacology and Toxicology, Indiana University School of Medicine

2005–present   Associate Director of Basic Science Research, Indiana University Simon Cancer Center

2006–present   Chair, IU Simon Cancer Center Translational Research Acceleration Collaboration (ITRAC)

2008–present   Director, Program in Pediatric Molecular Oncology and Experimental Therapeutics, IUSM

2008–present   Betty and Earl Herr Chair in Pediatric Oncology Research

2008–present   Chief Scientific Founder and Officer, Apexian Pharmaceuticals, Indianapolis, IN

2012–2016        Co-Director, Chemical Biology and Drug Discovery Initiative, IU Simon Cancer Center

2012–2016        NCI-F Grant Review SEP: Cancer Health Disparities/Diversity in Basic Cancer Research

2013–2016        Chair, NCI Omnibus Special Emphasis Panel: drug discovery reviews

2017—present  Member, Basic Mechanisms of Cancer Therapeutics (BMCT) Study Section, NIH

2004-- 2018      75 NIH study section review panels over 14 years.

Key Publications

 

Ref-1/APE1 inhibition with novel small molecules blocks ocular neovascularization. Sardar Pasha SPB, Sishtla K, Sulaiman RS, Park B, Shetty T, Shah F, Fishel ML, Wikel JH, Kelley MR, Corson TW. J Pharmacol Exp Ther. 2018 Aug 3. PMID:30076264

APX3330 Promotes Neurorestorative Effects after Stroke in Type One Diabetic Rats.  Yan T, Venkat P, Chopp M, Zacharek A, Yu P, Ning R, Qiao X, Kelley MR, Chen J. Aging Dis. 2018 Jun 1;9(3):453-466. 2018. PMID:29896433

 APE1/Ref-1 redox-specific inhibition decreases survivin protein levels and induces cell cycle arrest in prostate cancer cells. McIlwain DW, Fishel ML, Boos A, Kelley MR, Jerde TJ.  Oncotarget. 2017 Dec 13;9(13):10962-10977. 2018 Feb 16. PMID:29541389

APE1/Ref-1 knockdown in pancreatic ductal adenocarcinoma: Characterizing gene expression changes and identifying novel pathways using single-cell RNA sequencing. Shah F, Goossens E, Atallah NM, Grimard M, Kelley MR, Fishel ML. Mol Oncol. 2017 Sep 18. doi: 10.1002/1878-0261.12138. PMID:28922540

Exploiting the Ref-1-APE1 node in cancer signaling and other diseases: from bench to clinic. Shah F, Logsdon D, Messmann RA, Fehrenbacher JC, Fishel ML, Kelley MR. NPJ Precis Oncol. 2017;1. Epub 2017 Jun 8. PMID:28825044

Ref-1/APE1 as a Transcriptional Regulator and Novel Therapeutic Target in Pediatric T-cell Leukemia. Ding J, Fishel ML, Reed AM, McAdams E, Czader MB, Cardoso AA, Kelley MR. Mol Cancer Ther. 2017 Jul;16(7):1401-1411. Epub 2017 Apr 26. MID:28446640

Challenges and opportunities identifying therapeutic targets for chemotherapy-induced peripheral neuropathy resulting from oxidative DNA damage.  Kelley MR, Fehrenbacher JC. Neural Regen Res. 2017 Jan;12(1):72-74. PMID:28250749

Regulation of HIF1α under Hypoxia by APE1/Ref-1 Impacts CA9 Expression: Dual Targeting in Patient-Derived 3D Pancreatic Cancer Models. Logsdon DP, Grimard M, Luo M, Shahda S, Jiang Y, Tong Y, Yu Z, Zyromski N, Schipani E, Carta F, Supuran CT, Korc M, Ivan M, Kelley MR, Fishel ML.  Mol Cancer Ther. 2016 Nov;15(11):2722-2732. Epub 2016 Aug 17. PMID:  27535970

Identification and Characterization of New Chemical Entities Targeting Apurinic/Apyrimidinic Endonuclease 1 for the Prevention of Chemotherapy-Induced Peripheral Neuropathy. Kelley MR, Wikel JH, Guo C, Pollok KE, Bailey BJ, Wireman R, Fishel ML, Vasko MR. J Pharmacol Exp Ther. 2016 Nov;359(2):300-309. Epub 2016 Sep 8. PMID:27608656 

Titles & Appointments

  • Betty and Earl Herr Professor of Pediatric Oncology Research
  • Professor of Pediatrics
  • Professor of Biochemistry & Molecular Biology
  • Professor of Pharmacology & Toxicology
  • Professor of Ophthalmology
  • Education
    1987 FEL The Rockefeller University
    1987 FEL The Rockefeller University
    1984 PhD Louisiana State University (Baton Rouge)
    1984 PHD Louisiana State University
    1984 PHD Louisiana State University
    1981 MS Louisiana State University (Baton Rouge)
    1981 MS Louisiana State University
    1981 MS Louisiana State University
    1979 BA Depauw University
    1979 BA DePauw University
    1979 BA DePauw University
  • Research

    Since joining the Department of Pediatrics at the IU School of Medicine, Dr. Kelley's work has focused on translational research in DNA damage and repair, specifically, to determine how those activities can be exploited therapeutically to treat cancers and protect normal cells from oxidative and DNA base damage. DNA’s integrity faces threats from both endogenous agents (intracellular oxidation, alkylation, and ROS) and exogenous agents, including environmental mutagens and anticancer therapeutics. Since 1993, he has focused specifically on the enzyme apurinic/apyrimidinic endonuclease 1/ Redox effector factor-1 (APE1/Ref-1)—mechanistically as well as a therapeutic target in cancers and other diseases that manifest cancer-like properties (such as neoangiogenesis). APE1/Ref-1 is unique to the Base Excision Repair Pathway (BER), with dual repair and redox signaling functions that are crucial to cellular viability. Dr. Kelley has been the first to tease apart those functions, not only to fully characterize them, but to also determine how to manipulate each function individually for therapeutic benefit. In doing the latter, he discovered and has been developing a redox-specific inhibitor of Ref-1, as well as second-generation analogs that are under further investigation. This original work was the impetus for him becoming Chief Scientific Founder and Officer of Apexian Pharmaceuticals, an integrated drug development company that is leveraging the APE1/Ref-1 target platform to produce new therapeutics for some of the deadliest and hardest-to-treat cancers. Apexian recently received a treatment IND (IND125360) for a new drug that targets Ref-1; its potential indications include colon, pancreatic ovarian, leukemias as well as other adult and pediatric cancers. He is also exploring APE1/Ref-1 and BER for mechanistic and therapeutic opportunities in chemotherapy-induced peripheral neuropathy (CIPN). Anti-CIPN indication is also included in the APX3330 IND. In broader terms, all the academic chairs he has held and the program leader and director positions he currently holds are dedicated to fast-tracking collaboration and translational research to find more effective cancer treatments. In his Associate Director positions, he also helps equip the next generation of researchers by training and mentoring junior faculty, postdoctorates, fellows, MD students and others.    

    All of the discoveries during my career have culminated in 20 patents and over 177 articles in peer reviewed journals as well as 31 review articles/book chapters, attesting to my contributions to the field of DNA repair and redox signaling.

    A brief overview of my research includes:

    1.   Comprehensive molecular characterization of the APE1/Ref-1 enzyme and its functions

    The Base Excision Repair (BER) pathway is the body’s main defense in repairing oxidative damage to DNA. The most singular BER protein that has no “backup” or equivalent is APE1/Ref-1. Its dual name alludes to its unique dual functions as an AP endonuclease and as a redox effector factor (the “Ref” part of its name). Since 1987, I have studied BER extensively and was the first to fully characterize APE1/Ref-1’s translational and clinical relevance and differentiate its functions using chemical molecules (findings published in 1995, 2001, and more recently). While the fully folded protein performs its endonuclease function a locally unfolded configuration of the protein performs redox activities at its amino terminus. Unlike other redox proteins, APE1/Ref-1’s cysteine residues are buried. Also, unlike other redox proteins that require two cysteine residues, APE1/Ref-1 requires three to perform its complex redox functions (published in 2012 and 2013). My efforts in these areas have given me an unprecedented advantage in developing a new class of therapeutics that can selectively modify one function or the other (detailed further in Contribution 4).

    ·       Kelley, M.R., Cheng, L., Foster, R., Tritt, R., Broshears, J., & Koch, M. (2001). Elevated and altered expression of the multifunctional DNA base excision repair and redox enzyme Ape1/ref-1 in prostate cancer. Clin Cancer Res, 7(4), 824-830. PMID: 11309329

    ·       Su, D., Delaplane, S., Luo, M., Rempel, D., Vu, B., Kelley, M. R., Gross, M. L., & Georgiadis, M. (2011). Interactions of APE1with a redox inhibitor: Evidence for an alternate conformation of the enzyme. Biochemistry, 50(1), 82-92. PMCID: PMC3070192

    ·       Luo, M., Zhang, J., He. H., Su, D., Chen, Q., Gross, M., Kelley, M. R., & Georgiadis, M. (2012).  Characterization of the Redox Activity and Disulfide Bond Formation in Apurinic / Apyrimidinic Endonuclease. Biochemistry, 51(2), 695-705. PMCID: PMC3293223

    ·       Zhang, J., Luo, M., Marascot, D., Logsdon, D., LaFavers, K. A., Chen, Q., Reed, A., Kelley, M. R., Gross, M. L., & Georgiadis, M. M. (2013). Inhibition of Apurinic/apyrimidinic endonuclease I’s redox activity revisited. Biochemistry, 52(17), 2955-66. PMCID: PMC3706204

    2. Discoveries that APE1/Ref-1’s redox activities help maintain the DNA-binding capability of numerous transcription factors (Fos, Jun, HIF-1α, PAX, NF-kB, STAT3, as well as p53), and the therapeutic value of modulating that redox activity

    APE1/Ref-1 is a master regulator of oxidative stress; and, as such, its redox activity maintains many transcription factors by keeping them in their active (reduced) state. Many of those factors are involved in cell growth, progression, proliferation, apoptosis, angiogenesis, and inflammation. I have shown that upregulation of APE1 occurs in many solid cancers (GBM, neuroblastoma, ovarian, etc), contributing to therapeutic resistance. This is especially true with pancreatic cancer (PDAC). Inhibition of APE1’s redox activity blocks their proliferation and migration: by (1) decreasing the transcription activity of NF-κB, AP-1, HIF-1α and STAT3— key factors involved survival, invasion, and metastasis—and by (2) cell cycle arrest at G2 and increased p53-induced apoptosis. More details of those discoveries are listed in Contribution 5. Another recent finding is that APE1 inhibition also activates nuclear factor erythroid-related factor 2 (NRF2) in a dose-dependent fashion, regardless of whether abnormally high ROS are present or not. This has therapeutic implications for stimulating the NRF2 pathway to treat diseases caused by oxidative stress.

    ·       Jiang, Y., Zhou, S., Sandusky, G. E., Kelley, M. R., & Fishel, M. L. (2010). Reduced expression of DNA repair and redox signaling protein APE1/Ref-1 impairs human pancreatic cancer cell survival, proliferation, and cell cycle progression. Cancer Invest, 28(9): 885-895. PMCID: PMC2966714

    ·       Fishel, M. L, Jiang, Y., Rajeshkumar, N. V., Scandura, G., Sinn, A. L, He, Y., Shen, C., Jones, D. R., Pollok, K. E., Ivan, M., Maitra, A., & Kelley, M. R. (2011). Impact of APE1/Ref-1 Redox Inhibition on Pancreatic Tumor Growth. Mol Cancer Ther, 10(9), 1698-708. PMCID: PMC3170439

    ·       Kelley, M. R., Georgiadis, M. M., & Fishel, M. L. (2012). APE1/Ref-1 Role in Redox Signaling: Translational Applications of Targeting the Redox Function of the DNA Repair/Redox Protein APE1/Ref-1. Current Mol Pharmacol, 5(1), 36-53. PMCID: PMC3319314.

    ·       Fishel, M. L., Devlin, C. M., Jiang, Y., Luo, M., He, Y., Yu, Z., Tong, Y., Lipking, K. P., Maitra, A., Rejeshkumar, N. V., Wu, X., Scandura, G., Kelley, M. R., & Ivan, M. (2015). Apurinic/Apyrimidinic Endonuclease/Redox Factor-1 (APE1/Ref-1) redox function negatively regulates NRF2. J Biol Chem, 290(5), 3057-68. PMCID: PMC4317024

    3. Anti-angiogenesis and anti-inflammatory therapeutics in cancer and non-cancer systems and impact on tumor microenvironment

    I was the first to demonstrate a new role of APE1 with its involvement in angiogenesis and show that inhibition of APE1’s redox function abrogates that role. This discovery holds great promise for treating any condition characterized by abnormal neovascularization, including cancers and many diseases of the eye (AMD, diabetic retinopathy, ROP). Regarding the latter, APE1 is highly expressed in the retina, choroid, and retinal pigment epithelium. Using mouse models we demonstrated that APE1’s redox activity is required for cellular proliferation, migration, and tube formation. My lab was the first to show that redox-specific APE1 inhibition regulates RPEs’ response to oxidative stress and accumulation of intracellular ROS, while reducing a broad panel of stress- and toxicity-responsive transcription factors that are otherwise upregulated in retinal disease. APE1 inhibition could augment the results of today’s most advanced anti-angiogenic treatments, including anti-VEGF therapy. Additionally, I’ve shown that APE1 inhibition suppresses inflammatory response in activated human macrophages—downregulating TNF-α, IL-6, IL-12, and other molecules and inhibiting transcription of AP-1 and NF-κB. Thus, APE1 inhibition holds promise as a novel therapeutic strategy for inhibiting tumor-associated macrophages and impacting the tumor-microenvironment as well as tumor-immunotherapy.

    ·       Luo, M., Delaplane, S., Jiang, A., Reed, A., He, Y., Fishel, M., Nyland II, R., Borch, R. F., Qiao, X., Georgiadis, M. M., & Kelley, M. R. (2008). Role of the multifunctional DNA repair and redox signaling protein Ape1/Ref-1 in cancer and endothelial cells: Small molecule inhibition of Ape1’s redox function. Antiox Redox Signal, 10(11), 1853-1867. PMCID: PMC2587278

    ·       Jedinak, A., Dudhgaonkara, S., Kelley, M. R., & Sliva, D. (2011). Apurinic/apyrimidinic endonuclease 1 regulates inflammatory response in macrophages. Anticancer Res, 31(2), 379-85. PMCID: PMC3256557

    ·       Jiang, A., Gao, H., Kelley, M. R., & Qiao, X. (2011). Inhibition of APE1/Ref-1 Redox Activity with APX3330 Blocks Retinal Angiogenesis In Vitro and In Vivo. Vision Res, 51, 93-100. PMCID: PMC3010438

    ·       Li, Y., Liu, X., Zhou, T., Kelley, M. R., Edwards, P., Gao, H., & Qiao, X. (2014). Inhibition of APE1/Ref-1 redox activity rescues human retinal pigment epithelial cells from oxidative stress and reduces choroidal neovascularization. Redox Biol, 21(2), 485-494. PMCID: PMC3949093

     

    4. Studies relating to DNA damage and repair of neuronal cells resulting in chemotherapy induced peripheral neuropathy (CIPN)

    A perennial problem in treating cancer with platinating agents, microtubule stabilizers, and ionizing radiation is the development of cancer-induced peripheral neuropathy (CIPN). The nerves’ high metabolic activity and high gene transcription rates make them very susceptible to DNA damage. Anticancer agents not only cause damage by forming adducts, but also by producing ROS. My lab was the first to identify that the repair function of APE1 contributes to the survival of nondividing post-mitotic cells following oxidative DNA damage. I further showed that overexpression of the repair function of APE1 can protect hippocampal and DRG neurons after irradiation and can attenuate CIPN after administration of platinating agents. Serendipitously, inhibition of APE1’s redox function enhances APE1’s repair function in this milieu. Currently no effective treatments exist for CIPN; therefore my lab’s discoveries hold promise for a breakthrough therapy that could significantly improve patients’ quality of life after anticancer treatment both for prevention and reversal of CIPN.

    ·       Vasko, M. R., Guo, C., Thompson, E. L., & Kelley, M. R. (2011). The repair function of the multifunctional DNA repair/redox protein APE1 is neuroprotective after ionizing radiation. DNA Repair, 10(9), 942-952. PMCID: PMC3162094

    ·       Kelley, M. R., Jiang, Y. Guo, C., Reed, A., Meng, H., & Vasko, M. R. (2014). Role of the DNA base excision repair protein, APE1 in cisplatin, oxaliplatin, or carboplatin induced sensory neuropathy. PloS One, 9(9), e106485. PMID: 25188410

    ·       Kim H-S, Guo C, Thompson EL, Jiang Y, Kelley MR, Vasko MR, Lee S-H. (2015) APE1, the DNA base excision repair protein, regulates the removal of platinum adducts in sensory neuronal cultures by NER. Mutation Research Sept 2015: 779:96-104. PMCID: PMC4554977

    ·       M.R. Kelley, J.H. Wikel, C. Guo, K.E. Pollok, B.J. Bailey, R. Wireman, M.L. Fishel, and M.R. Vasko. (2016) Identification and Characterization of new chemical entities targeting apurinic/apyrimidinic endonuclease 1 for the prevention of chemotherapy-induced peripheral neuropathy. J Pharmacol Exp Ther. 2016 Sept 8. pii: jpet.116.235283 (epub ahead of print). PMCID: PMC5074487

     

    5. Identification and development of small-molecule inhibitors of both APE1/Ref-1’s redox signaling and DNA repair functions, including development of APX3330 for Phase 1/2 trials in cancer

    Others’ research efforts to inhibit APE1 yielded topoisomerase poisons or nonspecific BER inhibitors—not true APE1 inhibitors. My group was the first to isolate and develop true APE1 inhibitors, and further was able to selectively block just the endonuclease or redox function of APE1. A lead compound is ready for early clinical trials, and preclinical testing is underway for 2nd-generation compounds. Additionally, my lab recently showed, for the first time, that APE1’s redox function directly regulates STAT3 transcriptional activity and DNA binding; and, that APE1 inhibition synergistically works with STAT 3 blockage to inhibit the proliferation and viability of human PDAC cells. This has the potential to be a breakthrough technology in this difficult-to-treat cancer. APE1 redox inhibition also holds promise as a potential treatment for inflammatory-based liver diseases, as well as taxane resistant prostate cancer and in situations where anti-angiogenic agents are used (anti-VEGF or anti-VEGF-R) to enhance the effectiveness of those agents.

    ·       Bapat, A., Glass, L. S., Luo, M., Fishel, M. L., Long, E. C., Georgiadis, M. M., & Kelley, M. R. (2010). Novel small-molecule inhibitor of apurinic/apyrimidinic endonuclease 1 blocks proliferation and reduces viability of glioblastoma cells. J Pharmacol Exp Ther, 334(3), 988-98. PMCID: PMC2939666

    ·       Kelley, M. R., Luo, M., Reed, A., Su, D., Delaplane, S., Borch, R. F., Nyland II RL, Gross, M. L., & Georgiadis, M. (2011). Functional analysis of new and novel analogs of E3330 that block the redox signaling activity of the multifunctional AP endonuclease/redox signaling enzyme APE1/Ref-1. Antiox Redox Signal, 14(8), 1387-1401. PMCID: PMC3061197

    ·       Cardoso, A. A., Jiang, Y., Luo, M., Reed, A. R., He, Y., Kelley, M. R., & Fishel, M. L. (2012). APE1/Ref-1 Regulates STAT3 Transcriptional Activity and APE1/Ref-1-STAT3 Dual-Targeting Effectively Inhibits Pancreatic Cancer Cell Survival. PloS One, 7(10): e47462. PMCID: PMC3477158

    ·       Fishel ML, Devlin CM, Jiang Y, Luo M, He Y, Yu Zhangsheng, Tong Y, Lipking KP, Maitra A, Rejeshkumar NV, Wu X, Scandura G, Kelley M.R., Ivan M. (2015) Apurinic/Apyrimidinic Endonuclease/Redox Factor-1 (APE1/Ref-1) redox function negatively regulates NRF2. J Biol Chem. 2015 Jan 30;290(5):3057-68. PMCID: PMC4317024

  • Professional Organizations
    American Association for Cancer Research
    American Association for the Advancement of Science
    American Society of Clinical Oncology
    Education Board Member, American Health Council 2017 -
    Society for Pediatric Research
  • Clinical Interests

    Dr. Kelley discovered and has been developing a redox-specific inhibitor of Ref-1, as well as second-generation analogs that are under further investigation. This original work was the impetus for him becoming Chief Scientific Founder and Officer of Apexian Pharmaceuticals, an integrated drug development company that’s leveraging the APE1/Ref-1 target platform to produce new therapeutics for some of the deadliest and hardest-to-treat cancers. Apexian recently received a treatment IND (IND125360) for a new drug that targets Ref-1; its potential indications include colon, pancreatic, ovarian, leukemias as well as other adult and pediatric cancers. He is also exploring APE1/Ref-1 and BER for mechanistic and therapeutic opportunities in chemotherapy-induced peripheral neuropathy (CIPN). Anti-CIPN indication is also included in the APX3330 IND. The phase I trial with APX3330 is concluding in the early fall of 2018 and phase II trials are being planned.

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