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3. Upregulation of TET2 and Resistance to DNA Methyltransferase (DNMT) Inhibitors in DNMT1 -Deleted Cancer Cells.

Author

Laranjeira, Angelo B. A., Nguyen, Dat, Pelosof, Lorraine C., Doroshow, James H., and Yang, Sherry X.

Subjects
TUMOR suppressor proteins, GENE expression, SUPPRESSOR cells, GENETIC regulation, RENAL cancer, P16 gene
Abstract

Simple Summary: Ten-eleven-translocation (TET) 2 is implicated in human cancers such as lung, breast, skin, and kidney cancers, T-cell lymphomas, and leukemia. It is unclear whether TET2 is involved in the re-expression of the p16 tumor suppressor, which was partially silenced by CDKN2A gene methylation. The effect of DNA methyltransferase (DNMT) 1 gene status on TET2 expression following DNMT inhibitor treatment remains unknown in cancer. We found that deleting the DNMT1 gene made cancer cells prone to increased TET2 expression and re-expression of p16 after drug treatment. TET2 is involved in the demethylation of the CDKN2A gene and activation of p16 expression, and concomitant resistance to DNMT inhibitors when DNMT1 is obliterated. The long-sought data for the first time revealed a link between TET2 expression and the activation of p16 expression. The findings should have an impact on reactivating tumor suppressors and cancer treatment. Background: Ten-eleven-translocation (TET) 2 is a member of the TET family of proteins (TET1-3). DNMT1 gene deletion confers resistance to DNA methyltransferase (DNMT) inhibitors in colorectal, breast, and ovarian cancer cells. Currently, the effect of DNMT1 gene status on TET2 phenotype following DNMT inhibitor treatment is unclear in human malignancies. Methods: Human colorectal carcinoma HCT116 cells (DNMT+/+) and their isogenic DNMT1 knockout (DNMT1–/–) counterpart were treated with DNMT inhibitors. Expression of TET2 and tumor suppressor (p16ink4A and p15ink4B) proteins were examined by Western blot. Apoptosis and CDKN2A promoter demethylation following drug treatment were detected by Annexin-V apoptosis assay and methylation-specific PCR. Results: TET2 expression was robustly increased in DNMT1−/− cells by 0.5 µM and 5 µM decitabine and azacitidine treatment. Augmentation of TET2 expression was accompanied by re-expression of p16ink4A and p15ink4B proteins and CDKN2A promoter demethylation. TET2 upregulation and tumor suppressor re-expression were associated with resistance conferred by DNMT1 deletion. Treatment with 5-aza-4′-thio-2′-deoxycytidine at a low 0.5 µM dose only upregulated TET2 and reduced CDKN2A promoter methylation, and re-expression of p16ink4A in DNMT1−/− cells. DNMT inhibitors showed minimal effects on TET2 upregulation and re-expression of tumor suppressor proteins in cells with intact DNMT1. Conclusions: DNMT1 gene deletion made cancer cells prone to TET2 upregulation and activation of tumor suppressor expression upon DNMT inhibitor challenge. TET2 augmentation is concomitant with resistance to DNMT inhibitors in a DNMT1-deleted state. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Data from DNA Methyltransferase Inhibitor, Zebularine, Delays Tumor Growth and Induces Apoptosis in a Genetically Engineered Mouse Model of Breast Cancer

Author

Chen, Min, primary, Shabashvili, Daniel, primary, Nawab, Akbar, primary, Yang, Sherry X., primary, Dyer, Lisa M., primary, Brown, Kevin D., primary, Hollingshead, Melinda, primary, Hunter, Kent W., primary, Kaye, Frederic J., primary, Hochwald, Steven N., primary, Marquez, Victor E., primary, Steeg, Patricia, primary, and Zajac-Kaye, Maria, primary

Published
2023
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7. Supplementary Table 2 from DNA Methyltransferase Inhibitor, Zebularine, Delays Tumor Growth and Induces Apoptosis in a Genetically Engineered Mouse Model of Breast Cancer

Author

Chen, Min, primary, Shabashvili, Daniel, primary, Nawab, Akbar, primary, Yang, Sherry X., primary, Dyer, Lisa M., primary, Brown, Kevin D., primary, Hollingshead, Melinda, primary, Hunter, Kent W., primary, Kaye, Frederic J., primary, Hochwald, Steven N., primary, Marquez, Victor E., primary, Steeg, Patricia, primary, and Zajac-Kaye, Maria, primary

Published
2023
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8. Supplementary Table 7 from DNA Methyltransferase Inhibitor, Zebularine, Delays Tumor Growth and Induces Apoptosis in a Genetically Engineered Mouse Model of Breast Cancer

Author

Chen, Min, primary, Shabashvili, Daniel, primary, Nawab, Akbar, primary, Yang, Sherry X., primary, Dyer, Lisa M., primary, Brown, Kevin D., primary, Hollingshead, Melinda, primary, Hunter, Kent W., primary, Kaye, Frederic J., primary, Hochwald, Steven N., primary, Marquez, Victor E., primary, Steeg, Patricia, primary, and Zajac-Kaye, Maria, primary

Published
2023
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9. Supplementary Table 5 from DNA Methyltransferase Inhibitor, Zebularine, Delays Tumor Growth and Induces Apoptosis in a Genetically Engineered Mouse Model of Breast Cancer

Author

Chen, Min, primary, Shabashvili, Daniel, primary, Nawab, Akbar, primary, Yang, Sherry X., primary, Dyer, Lisa M., primary, Brown, Kevin D., primary, Hollingshead, Melinda, primary, Hunter, Kent W., primary, Kaye, Frederic J., primary, Hochwald, Steven N., primary, Marquez, Victor E., primary, Steeg, Patricia, primary, and Zajac-Kaye, Maria, primary

Published
2023
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10. Supplementary Table 1 from DNA Methyltransferase Inhibitor, Zebularine, Delays Tumor Growth and Induces Apoptosis in a Genetically Engineered Mouse Model of Breast Cancer

Author

Chen, Min, primary, Shabashvili, Daniel, primary, Nawab, Akbar, primary, Yang, Sherry X., primary, Dyer, Lisa M., primary, Brown, Kevin D., primary, Hollingshead, Melinda, primary, Hunter, Kent W., primary, Kaye, Frederic J., primary, Hochwald, Steven N., primary, Marquez, Victor E., primary, Steeg, Patricia, primary, and Zajac-Kaye, Maria, primary

Published
2023
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11. Supplementary Table 3 from DNA Methyltransferase Inhibitor, Zebularine, Delays Tumor Growth and Induces Apoptosis in a Genetically Engineered Mouse Model of Breast Cancer

Author

Chen, Min, primary, Shabashvili, Daniel, primary, Nawab, Akbar, primary, Yang, Sherry X., primary, Dyer, Lisa M., primary, Brown, Kevin D., primary, Hollingshead, Melinda, primary, Hunter, Kent W., primary, Kaye, Frederic J., primary, Hochwald, Steven N., primary, Marquez, Victor E., primary, Steeg, Patricia, primary, and Zajac-Kaye, Maria, primary

Published
2023
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12. Supplementary Table 4 from DNA Methyltransferase Inhibitor, Zebularine, Delays Tumor Growth and Induces Apoptosis in a Genetically Engineered Mouse Model of Breast Cancer

Author

Chen, Min, primary, Shabashvili, Daniel, primary, Nawab, Akbar, primary, Yang, Sherry X., primary, Dyer, Lisa M., primary, Brown, Kevin D., primary, Hollingshead, Melinda, primary, Hunter, Kent W., primary, Kaye, Frederic J., primary, Hochwald, Steven N., primary, Marquez, Victor E., primary, Steeg, Patricia, primary, and Zajac-Kaye, Maria, primary

Published
2023
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13. Supplementary Table 6 from DNA Methyltransferase Inhibitor, Zebularine, Delays Tumor Growth and Induces Apoptosis in a Genetically Engineered Mouse Model of Breast Cancer

Author

Chen, Min, primary, Shabashvili, Daniel, primary, Nawab, Akbar, primary, Yang, Sherry X., primary, Dyer, Lisa M., primary, Brown, Kevin D., primary, Hollingshead, Melinda, primary, Hunter, Kent W., primary, Kaye, Frederic J., primary, Hochwald, Steven N., primary, Marquez, Victor E., primary, Steeg, Patricia, primary, and Zajac-Kaye, Maria, primary

Published
2023
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14. Supplementary Figure 3 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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16. Supplementary Figure 1 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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17. Supplementary Methods, Tables 1 - 3 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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18. Supplementary Figure 2 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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21. Supplementary Figure 6 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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22. Supplementary Figure 5 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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23. Supplementary Figure 4 from Identification and Analysis of In Vivo VEGF Downstream Markers Link VEGF Pathway Activity with Efficacy of Anti-VEGF Therapies

Author

Brauer, Matthew J., primary, Zhuang, Guanglei, primary, Schmidt, Maike, primary, Yao, Jenny, primary, Wu, Xiumin, primary, Kaminker, Joshua S., primary, Jurinka, Stefanie S., primary, Kolumam, Ganesh, primary, Chung, Alicia S., primary, Jubb, Adrian, primary, Modrusan, Zora, primary, Ozawa, Tomoko, primary, James, C. David, primary, Phillips, Heidi, primary, Haley, Benjamin, primary, Tam, Rachel N.W., primary, Clermont, Anne C., primary, Cheng, Jason H., primary, Yang, Sherry X., primary, Swain, Sandra M., primary, Chen, Daniel, primary, Scherer, Stefan J., primary, Koeppen, Hartmut, primary, Yeh, Ru-Fang, primary, Yue, Peng, primary, Stephan, Jean-Philippe, primary, Hegde, Priti, primary, Ferrara, Napoleone, primary, Singh, Mallika, primary, and Bais, Carlos, primary

Published
2023
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26. 21-Gene Recurrence Score and Survival Outcomes in the Phase III Multicenter TAILORx Clinical Trial.

Author

Yang SX, Yu J, and Wang M

Subjects
Humans, Female, Middle Aged, Prognosis, Aged, Adult, Biomarkers, Tumor genetics, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Disease-Free Survival, Chemotherapy, Adjuvant methods, Breast Neoplasms mortality, Breast Neoplasms genetics, Breast Neoplasms pathology, Breast Neoplasms therapy, Breast Neoplasms drug therapy, Neoplasm Recurrence, Local genetics, Neoplasm Recurrence, Local pathology
Abstract

Background: Recurrence score (RS) based on a 21-gene genomic assay is frequently used to estimate risk of distant recurrence for choice of adjuvant chemotherapy in breast cancer. It remains unclear whether RS is an independent prognostic factor for breast cancer-specific survival (BCSS) and overall survival (OS) in the TAILORx trial population., Methods: We evaluated the association of RS with BCSS and OS plus recurrence-free interval (RFI) and invasive disease-free survival (DFS) using multivariable Cox proportional hazards regression analysis, adjusting for clinicopathologic measures, in 8,916 patients with hormone receptor-positive, HER2-negative, node-negative breast cancer. Likelihood ratio (LR) test was used to assess the relative amount of prognostic information provided by RS to BCSS, OS, RFI, and DFS, comparatively., Results: Event rates for BCSS, OS, RFI, and DFS were 1.7%, 5.2%, 5.6%, and 12.6%, respectively, by up to 11.6 years of follow-up. Compared with low-range RS (0-10), patients with midrange (11-25) and high-range (26-100) RS had inferior BCSS (adjusted hazard ratio [aHR], 5.12 [95% CI, 2.09-16.92] and 8.03 [95% CI, 2.91-28.47], respectively) and RFI (aHR, 1.68 [95% CI, 1.23-2.36] and 3.05 [95% CI, 2.02-4.67], respectively), independent of clinicopathologic factors. High-range score was associated with an increased risk of DFS (aHR, 1.56 [95% CI, 1.20-2.04]) but not significantly associated with OS (aHR, 1.44 [95% CI, 0.95-2.18]). Midrange score was associated with neither DFS (aHR, 1.15 [95% CI, 0.96-1.38]) nor OS (HR 1.14 [95% CI, 0.87-1.52]). LR-χ2 values were 83.0 and 65.1 for RFI and BCSS, respectively, and 17.5 and 33.6 for OS and DFS, respectively (P<.0001)., Conclusions: RS is an independent measure for BCSS and recurrence prognoses relative to OS in early-stage breast cancer. It carries more prognostic information for breast cancer-specific outcomes.

Published
2024
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