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509 results on '"Issa, Jean-Pierre J."'

5. Guadecitabine vs treatment choice in newly diagnosed acute myeloid leukemia: a global phase 3 randomized study

Author

Fenaux, Pierre, Gobbi, Marco, Kropf, Patricia L., Issa, Jean-Pierre J., Roboz, Gail J., Mayer, Jiri, Krauter, Jürgen, Robak, Tadeusz, Kantarjian, Hagop, Novak, Jan, Jedrzejczak, Wieslaw. W., Thomas, Xavier, Ojeda-Uribe, Mario, Miyazaki, Yasushi, Min, Yoo Hong, Yeh, Su-Peng, Brandwein, Joseph, Gercheva-Kyuchukova, Liana, Demeter, Judit, Griffiths, Elizabeth, Yee, Karen, Döhner, Konstanze, Hao, Yong, Keer, Harold, Azab, Mohammad, and Döhner, Hartmut

Published
2023
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8. Evolution of DNA methylome from precancerous lesions to invasive lung adenocarcinomas

Author

Hu, Xin, Estecio, Marcos R., Chen, Runzhe, Reuben, Alexandre, Wang, Linghua, Fujimoto, Junya, Carrot-Zhang, Jian, McGranahan, Nicholas, Ying, Lisha, Fukuoka, Junya, Chow, Chi-Wan, Pham, Hoa H. N., Godoy, Myrna C. B., Carter, Brett W., Behrens, Carmen, Zhang, Jianhua, Antonoff, Mara B., Sepesi, Boris, Lu, Yue, Pass, Harvey I., Kadara, Humam, Scheet, Paul, Vaporciyan, Ara A., Heymach, John V., Wistuba, Ignacio I., Lee, J. Jack, Futreal, P. Andrew, Su, Dan, Issa, Jean-Pierre J., and Zhang, Jianjun

Published
2021
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10. Guadecitabine (SGI-110) in patients with intermediate or high-risk myelodysplastic syndromes: phase 2 results from a multicentre, open-label, randomised, phase 1/2 trial

Author

Garcia-Manero, Guillermo, Roboz, Gail, Walsh, Katherine, Kantarjian, Hagop, Ritchie, Ellen, Kropf, Patricia, O'Connell, Casey, Tibes, Raoul, Lunin, Scott, Rosenblat, Todd, Yee, Karen, Stock, Wendy, Griffiths, Elizabeth, Mace, Joseph, Podoltsev, Nikolai, Berdeja, Jesus, Jabbour, Elias, Issa, Jean-Pierre J, Hao, Yong, Keer, Harold N, Azab, Mohammad, and Savona, Michael R

Published
2019
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12. Targeting CDK9 Reactivates Epigenetically Silenced Genes in Cancer

Author

Zhang, Hanghang, Pandey, Somnath, Travers, Meghan, Sun, Hongxing, Morton, George, Madzo, Jozef, Chung, Woonbok, Khowsathit, Jittasak, Perez-Leal, Oscar, Barrero, Carlos A., Merali, Carmen, Okamoto, Yasuyuki, Sato, Takahiro, Pan, Joshua, Garriga, Judit, Bhanu, Natarajan V., Simithy, Johayra, Patel, Bela, Huang, Jian, Raynal, Noël J.-M., Garcia, Benjamin A., Jacobson, Marlene A., Kadoch, Cigall, Merali, Salim, Zhang, Yi, Childers, Wayne, Abou-Gharbia, Magid, Karanicolas, John, Baylin, Stephen B., Zahnow, Cynthia A., Jelinek, Jaroslav, Graña, Xavier, and Issa, Jean-Pierre J.

Published
2018
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14. Epigenetic Inactivation of CHFR in Human Tumors

Author

Toyota, Minoru, Sasaki, Yasushi, Satoh, Ayumi, Ogi, Kazuhiro, Kikuchi, Takefumi, Suzuki, Hiromu, Mita, Hiroaki, Tanaka, Nobuyuki, Itoh, Fumio, Issa, Jean-Pierre J., Jair, Kam-Wing, Schuebel, Kornel E., Imai, Kohzoh, and Tokino, Takashi

Published
2003

15. Guadecitabine (SGI-110) in treatment-naive patients with acute myeloid leukaemia: phase 2 results from a multicentre, randomised, phase 1/2 trial

Author

Kantarjian, Hagop M, Roboz, Gail J, Kropf, Patricia L, Yee, Karen W L, O'Connell, Casey L, Tibes, Raoul, Walsh, Katherine J, Podoltsev, Nikolai A, Griffiths, Elizabeth A, Jabbour, Elias, Garcia-Manero, Guillermo, Rizzieri, David, Stock, Wendy, Savona, Michael R, Rosenblat, Todd L, Berdeja, Jesus G, Ravandi, Farhad, Rock, Edwin P, Hao, Yong, Azab, Mohammad, and Issa, Jean-Pierre J

Published
2017
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25. DNA methylation aging clocks: challenges and recommendations

Author

Bell, Christopher G., Lowe, Robert, Adams, Peter D., Baccarelli, Andrea A., Beck, Stephan, Bell, Jordana T., Christensen, Brock C., Gladyshev, Vadim N., Heijmans, Bastiaan T., Horvath, Steve, Ideker, Trey, Issa, Jean-Pierre J., Kelsey, Karl T., Marioni, Riccardo E., Reik, Wolf, Relton, Caroline L., Schalkwyk, Leonard C., Teschendorff, Andrew E., Wagner, Wolfgang, Zhang, Kang, and Rakyan, Vardhman K.

Published
2019
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27. Postmortem toxicology findings from the Camden Opioid Research Initiative.

Author

Kusic, Dara M., Heil, Jessica, Zajic, Stefan, Brangan, Andrew, Dairo, Oluseun, Heil, Stacey, Feigin, Gerald, Kacinko, Sherri, Buono, Russell J., Ferraro, Thomas N., Rafeq, Rachel, Haroz, Rachel, Baston, Kaitlan, Bodofsky, Elliot, Sabia, Michael, Salzman, Matthew, Resch, Alissa, Madzo, Jozef, Scheinfeldt, Laura B., and Issa, Jean-Pierre J.

Subjects
OPIOID abuse, OPIOID epidemic, SUBSTANCE abuse, OPIOIDS, TOXICOLOGY, DEAD
Abstract

The United States continues to be impacted by decades of an opioid misuse epidemic, worsened by the COVID-19 pandemic and by the growing prevalence of highly potent synthetic opioids (HPSO) such as fentanyl. In instances of a toxicity event, first-response administration of reversal medications such as naloxone can be insufficient to fully counteract the effects of HPSO, particularly when there is co-occurring substance use. In an effort to characterize and study this multi-faceted problem, the Camden Opioid Research Initiative (CORI) has been formed. The CORI study has collected and analyzed post-mortem toxicology data from 42 cases of decedents who expired from opioid-related toxicity in the South New Jersey region to characterize substance use profiles. Co-occurring substance use, whether by intent or through possible contamination of the illicit opioid supply, is pervasive among deaths due to opioid toxicity, and evidence of medication-assisted treatment is scarce. Nearly all (98%) of the toxicology cases show the presence of the HPSO, fentanyl, and very few (7%) results detected evidence of medication-assisted treatment for opioid use disorder, such as buprenorphine or methadone, at the time of death. The opioid toxicity reversal drug, naloxone, was detected in 19% of cases, but 100% of cases expressed one or more stimulants, and sedatives including xylazine were detected in 48% of cases. These results showing complex substance use profiles indicate that efforts at mitigating the opioid misuse epidemic must address the complications presented by co-occurring stimulant and other substance use, and reduce barriers to and stigmas of seeking effective medication-assisted treatments. [ABSTRACT FROM AUTHOR]

Published
2023
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28. Safety and tolerability of guadecitabine (SGI-110) in patients with myelodysplastic syndrome and acute myeloid leukaemia: a multicentre, randomised, dose-escalation phase 1 study

Author

Issa, Jean-Pierre J, Roboz, Gail, Rizzieri, David, Jabbour, Elias, Stock, Wendy, O'Connell, Casey, Yee, Karen, Tibes, Raoul, Griffiths, Elizabeth A, Walsh, Katherine, Daver, Naval, Chung, Woonbok, Naim, Sue, Taverna, Pietro, Oganesian, Aram, Hao, Yong, Lowder, James N, Azab, Mohammad, and Kantarjian, Hagop

Published
2015
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29. Epigenome-wide study identifies epigenetic outliers in normal mucosa of colorectal cancer patients

Author

Ghosh, Jayashri, Schultz, Bryant M., Chan, Joe, Wultsch, Claudia, Singh, Rajveer, Shureiqi, Imad, Chow, Stephanie, Doymaz, Ahmet, Varriano, Sophia, Driscoll, Melissa, Muse, Jennifer, Kleiman, Frida E., Krampis, Konstantinos, Issa, Jean-Pierre J., and Sapienza, Carmen

Subjects
Epigenome, RNA, Ribosomal, 16S, Humans, Dysbiosis, DNA Methylation, Intestinal Mucosa, Colorectal Neoplasms, Article, Epigenesis, Genetic
Abstract

Nongenetic predisposition to colorectal cancer continues to be difficult to measure precisely, hampering efforts in targeted prevention and screening. Epigenetic changes in the normal mucosa of patients with colorectal cancer can serve as a tool in predicting colorectal cancer outcomes. We identified epigenetic changes affecting the normal mucosa of patients with colorectal cancer. DNA methylation profiling on normal colon mucosa from 77 patients with colorectal cancer and 68 controls identified a distinct subgroup of normally-appearing mucosa with markedly disrupted DNA methylation at a large number of CpGs, termed as "Outlier Methylation Phenotype" (OMP) and are present in 15 of 77 patients with cancer versus 0 of 68 controls (P0.001). Similar findings were also seen in publicly available datasets. Comparison of normal colon mucosa transcription profiles of patients with OMP cancer with those of patients with non-OMP cancer indicates genes whose promoters are hypermethylated in the OMP patients are also transcriptionally downregulated, and that many of the genes most affected are involved in interactions between epithelial cells, the mucus layer, and the microbiome. Analysis of 16S rRNA profiles suggests that normal colon mucosa of OMPs are enriched in bacterial genera associated with colorectal cancer risk, advanced tumor stage, chronic intestinal inflammation, malignant transformation, nosocomial infections, and KRAS mutations. In conclusion, our study identifies an epigenetically distinct OMP group in the normal mucosa of patients with colorectal cancer that is characterized by a disrupted methylome, altered gene expression, and microbial dysbiosis. Prospective studies are needed to determine whether OMP could serve as a biomarker for an elevated epigenetic risk for colorectal cancer development.Our study identifies an epigenetically distinct OMP group in the normal mucosa of patients with colorectal cancer that is characterized by a disrupted methylome, altered gene expression, and microbial dysbiosis. Identification of OMPs in healthy controls and patients with colorectal cancer will lead to prevention and better prognosis, respectively.

Published
2022

32. Dose, schedule, safety, and efficacy of guadecitabine in relapsed or refractory acute myeloid leukemia

Author

Roboz, Gail J., Kantarjian, Hagop M., Yee, Karen W. L., Kropf, Patricia L., OʼConnell, Casey L., Griffiths, Elizabeth A., Stock, Wendy, Daver, Naval G., Jabbour, Elias, Ritchie, Ellen K., Walsh, Katherine J., Rizzieri, David, Lunin, Scott D., Curio, Tania, Chung, Woonbok, Hao, Yong, Lowder, James N., Azab, Mohammad, and Issa, Jean‐Pierre J.

Published
2018
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35. Prospective comparison of outcomes with azacitidine and decitabine in patients with AML ineligible for intensive chemotherapy

Author

Zeidan, Amer M., Fenaux, Pierre, Gobbi, Marco, Mayer, Jiří, Roboz, Gail J., Krauter, Jürgen, Robak, Tadeusz, Kantarjian, Hagop M., Novák, Jan, Jedrzejczak, Wieslaw W., Thomas, Xavier, Ojeda-Uribe, Mario, Miyazaki, Yasushi, Min, Yoo Hong, Yeh, Su-Peng, Brandwein, Joseph M., Gercheva, Liana, Demeter, Judit, Griffiths, Elizabeth A., Yee, Karen W.L., Issa, Jean-Pierre J., Bewersdorf, Jan Philipp, Keer, Harold, Hao, Yong, Azab, Mohammad, and Döhner, Hartmut

Published
2022
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41. Non-pathogenic microbiota accelerate age-related CpG Island methylation in colonic mucosa.

Author

Ang Sun, Pyounghwa Park, Cole, Lauren, Vaidya, Himani, Maegawa, Shinji, Keith, Kelsey, Calendo, Gennaro, Madzo, Jozef, Jelinek, Jaroslav, Jobin, Christian, and Issa, Jean-Pierre J.

Subjects
METHYLATION, DNA methylation, COLON cancer, MUCOUS membranes, COLORECTAL cancer
Abstract

DNA methylation is an epigenetic process altered in cancer and ageing. Age-related methylation drift can be used to estimate lifespan and can be influenced by extrinsic factors such as diet. Here, we report that non-pathogenic microbiota accelerate age-related methylation drift in the colon when compared with germ-free mice. DNA methylation analyses showed that microbiota and IL10KO were associated with changes in 5% and 4.1% of CpG sites, while mice with both factors had 18% alterations. Microbiota, IL10KO, and their combination altered 0.4%, 0.4%, and 4% of CpG island methylation, respectively. These are comparable to what is seen in colon cancer. Ageing changes were accelerated in the IL10KO mice with microbiota, and the affected genes were more likely to be altered in colon cancer. Thus, the microbiota affect DNA methylation of the colon in patterns reminiscent of what is observed in ageing and colorectal cancer. [ABSTRACT FROM AUTHOR]

Published
2023
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50. Selective CDK9 Inhibition by Natural Compound Toyocamycin in Cancer Cells.

Author

Pandey, Somnath, Djibo, Rahinatou, Darracq, Anaïs, Calendo, Gennaro, Zhang, Hanghang, Henry, Ryan A., Andrews, Andrew J., Baylin, Stephen B., Madzo, Jozef, Najmanovich, Rafael, Issa, Jean-Pierre J., and Raynal, Noël J.-M.

Subjects
PROTEINS, CLINICAL drug trials, NUCLEOSIDES, ANTINEOPLASTIC agents, TRANSFERASES, CELL lines, DRUG development, COMPUTER-assisted molecular modeling, EPIGENOMICS, PHOSPHORYLATION, PHARMACODYNAMICS
Abstract

Simple Summary: By combining drug screens, transcriptomic studies, and in vitro assays, our study identified the natural product toyocamycin as a potent and selective CDK9 inhibitor. Thus, toyocamycin can be used as a new small molecule to modulate CDK9 activity in preclinical research. Through docking simulations, we identified its specific binding sites, which could spark some interest to design novel small molecule CDK9 inhibitors. Aberrant transcription in cancer cells involves the silencing of tumor suppressor genes (TSGs) and activation of oncogenes. Transcriptomic changes are associated with epigenomic alterations such as DNA-hypermethylation, histone deacetylation, and chromatin condensation in promoter regions of silenced TSGs. To discover novel drugs that trigger TSG reactivation in cancer cells, we used a GFP-reporter system whose expression is silenced by promoter DNA hypermethylation and histone deacetylation. After screening a natural product drug library, we identified that toyocamycin, an adenosine-analog, induces potent GFP reactivation and loss of clonogenicity in human colon cancer cells. Connectivity-mapping analysis revealed that toyocamycin produces a pharmacological signature mimicking cyclin-dependent kinase (CDK) inhibitors. RNA-sequencing revealed that the toyocamycin transcriptomic signature resembles that of a specific CDK9 inhibitor (HH1). Specific inhibition of RNA Pol II phosphorylation level and kinase assays confirmed that toyocamycin specifically inhibits CDK9 (IC50 = 79 nM) with a greater efficacy than other CDKs (IC50 values between 0.67 and 15 µM). Molecular docking showed that toyocamycin efficiently binds the CDK9 catalytic site in a conformation that differs from other CDKs, explained by the binding contribution of specific amino acids within the catalytic pocket and protein backbone. Altogether, we demonstrated that toyocamycin exhibits specific CDK9 inhibition in cancer cells, highlighting its potential for cancer chemotherapy. [ABSTRACT FROM AUTHOR]

Published
2022
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