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Postpartum breast cancer has a distinct molecular profile that predicts poor outcomes.

Nature communications

Jindal S, Pennock ND, Sun D, Horton W, Ozaki MK, Narasimhan J, Bartlett AQ, Weinmann S, Goss PE, Borges VF, Xia Z, Schedin P.
PMID: 34732713
Nat Commun. 2021 Nov 03;12(1):6341. doi: 10.1038/s41467-021-26505-3.

Young women's breast cancer (YWBC) has poor prognosis and known interactions with parity. Women diagnosed within 5-10 years of childbirth, defined as postpartum breast cancer (PPBC), have poorer prognosis compared to age, stage, and biologic subtype-matched nulliparous patients. Genomic...

Cite
Jindal S, Pennock ND, Sun D, et al. Postpartum breast cancer has a distinct molecular profile that predicts poor outcomes. Nat Commun. 2021;12(1):6341doi: 10.1038/s41467-021-26505-3.
Jindal, S., Pennock, N. D., Sun, D., Horton, W., Ozaki, M. K., Narasimhan, J., Bartlett, A. Q., Weinmann, S., Goss, P. E., Borges, V. F., Xia, Z., & Schedin, P. (2021). Postpartum breast cancer has a distinct molecular profile that predicts poor outcomes. Nature communications, 12(1), 6341. https://doi.org/10.1038/s41467-021-26505-3
Jindal, Sonali, et al. "Postpartum breast cancer has a distinct molecular profile that predicts poor outcomes." Nature communications vol. 12,1 (2021): 6341. doi: https://doi.org/10.1038/s41467-021-26505-3
Jindal S, Pennock ND, Sun D, Horton W, Ozaki MK, Narasimhan J, Bartlett AQ, Weinmann S, Goss PE, Borges VF, Xia Z, Schedin P. Postpartum breast cancer has a distinct molecular profile that predicts poor outcomes. Nat Commun. 2021 Nov 03;12(1):6341. doi: 10.1038/s41467-021-26505-3. PMID: 34732713; PMCID: PMC8566602.
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Reversible cardiac disease features in an inducible CUG repeat RNA-expressing mouse model of myotonic dystrophy.

JCI insight

Rao AN, Campbell HM, Guan X, Word TA, Wehrens XH, Xia Z, Cooper TA.
PMID: 33497365
JCI Insight. 2021 Mar 08;6(5). doi: 10.1172/jci.insight.143465.

Myotonic dystrophy type 1 (DM1) is caused by a CTG repeat expansion in the DMPK gene. Expression of pathogenic expanded CUG repeat (CUGexp) RNA causes multisystemic disease by perturbing the functions of RNA-binding proteins, resulting in expression of fetal...

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Rao AN, Campbell HM, Guan X, et al. Reversible cardiac disease features in an inducible CUG repeat RNA-expressing mouse model of myotonic dystrophy. JCI Insight. 2021;6(5)doi: 10.1172/jci.insight.143465.
Rao, A. N., Campbell, H. M., Guan, X., Word, T. A., Wehrens, X. H., Xia, Z., & Cooper, T. A. (2021). Reversible cardiac disease features in an inducible CUG repeat RNA-expressing mouse model of myotonic dystrophy. JCI insight, 6(5), . https://doi.org/10.1172/jci.insight.143465
Rao, Ashish N, et al. "Reversible cardiac disease features in an inducible CUG repeat RNA-expressing mouse model of myotonic dystrophy." JCI insight vol. 6,5 (2021). doi: https://doi.org/10.1172/jci.insight.143465
Rao AN, Campbell HM, Guan X, Word TA, Wehrens XH, Xia Z, Cooper TA. Reversible cardiac disease features in an inducible CUG repeat RNA-expressing mouse model of myotonic dystrophy. JCI Insight. 2021 Mar 08;6(5). doi: 10.1172/jci.insight.143465. PMID: 33497365; PMCID: PMC8021116.
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BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program.

Clinical cancer research : an official journal of the American Association for Cancer Research

Kim DH, Sun D, Storck WK, Welker Leng K, Jenkins C, Coleman DJ, Sampson D, Guan X, Kumaraswamy A, Rodansky ES, Urrutia JA, Schwartzman JA, Zhang C, Beltran H, Labrecque MP, Morrissey C, Lucas JM, Coleman IM, Nelson PS, Corey E, Handelman SK, Sexton JZ, Aggarwal R, Abida W, Feng FY, Small EJ, Spratt DE, Bankhead A, Rao A, Gesner EM, Attwell S, Lakhotia S, Campeau E, Yates JA, Xia Z, Alumkal JJ.
PMID: 34145028
Clin Cancer Res. 2021 Sep 01;27(17):4923-4936. doi: 10.1158/1078-0432.CCR-20-4968. Epub 2021 Jun 18.

PURPOSE: Lineage plasticity in prostate cancer-most commonly exemplified by loss of androgen receptor (AR) signaling and a switch from a luminal to alternate differentiation program-is now recognized as a treatment resistance mechanism. Lineage plasticity is a spectrum, but neuroendocrine...

Cite
Kim DH, Sun D, Storck WK, et al. BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program. Clin Cancer Res. 2021;27(17):4923-4936doi: 10.1158/1078-0432.CCR-20-4968.
Kim, D. H., Sun, D., Storck, W. K., Welker Leng, K., Jenkins, C., Coleman, D. J., Sampson, D., Guan, X., Kumaraswamy, A., Rodansky, E. S., Urrutia, J. A., Schwartzman, J. A., Zhang, C., Beltran, H., Labrecque, M. P., Morrissey, C., Lucas, J. M., Coleman, I. M., Nelson, P. S., Corey, E., Handelman, S. K., Sexton, J. Z., Aggarwal, R., Abida, W., Feng, F. Y., Small, E. J., Spratt, D. E., Bankhead, A., Rao, A., Gesner, E. M., Attwell, S., Lakhotia, S., Campeau, E., Yates, J. A., Xia, Z., & Alumkal, J. J. (2021). BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program. Clinical cancer research : an official journal of the American Association for Cancer Research, 27(17), 4923-4936. https://doi.org/10.1158/1078-0432.CCR-20-4968
Kim, Dae-Hwan, et al. "BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program." Clinical cancer research : an official journal of the American Association for Cancer Research vol. 27,17 (2021): 4923-4936. doi: https://doi.org/10.1158/1078-0432.CCR-20-4968
Kim DH, Sun D, Storck WK, Welker Leng K, Jenkins C, Coleman DJ, Sampson D, Guan X, Kumaraswamy A, Rodansky ES, Urrutia JA, Schwartzman JA, Zhang C, Beltran H, Labrecque MP, Morrissey C, Lucas JM, Coleman IM, Nelson PS, Corey E, Handelman SK, Sexton JZ, Aggarwal R, Abida W, Feng FY, Small EJ, Spratt DE, Bankhead A, Rao A, Gesner EM, Attwell S, Lakhotia S, Campeau E, Yates JA, Xia Z, Alumkal JJ. BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program. Clin Cancer Res. 2021 Sep 01;27(17):4923-4936. doi: 10.1158/1078-0432.CCR-20-4968. Epub 2021 Jun 18. PMID: 34145028; PMCID: PMC8416959.
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BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program.

Clinical cancer research : an official journal of the American Association for Cancer Research

Kim DH, Sun D, Storck WK, Welker Leng K, Jenkins C, Coleman DJ, Sampson D, Guan X, Kumaraswamy A, Rodansky ES, Urrutia JA, Schwartzman JA, Zhang C, Beltran H, Labrecque MP, Morrissey C, Lucas JM, Coleman IM, Nelson PS, Corey E, Handelman SK, Sexton JZ, Aggarwal R, Abida W, Feng FY, Small EJ, Spratt DE, Bankhead A, Rao A, Gesner EM, Attwell S, Lakhotia S, Campeau E, Yates JA, Xia Z, Alumkal JJ.
PMID: 34145028
Clin Cancer Res. 2021 Sep 01;27(17):4923-4936. doi: 10.1158/1078-0432.CCR-20-4968. Epub 2021 Jun 18.

PURPOSE: Lineage plasticity in prostate cancer-most commonly exemplified by loss of androgen receptor (AR) signaling and a switch from a luminal to alternate differentiation program-is now recognized as a treatment resistance mechanism. Lineage plasticity is a spectrum, but neuroendocrine...

Cite
Kim DH, Sun D, Storck WK, et al. BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program. Clin Cancer Res. 2021;27(17):4923-4936doi: 10.1158/1078-0432.CCR-20-4968.
Kim, D. H., Sun, D., Storck, W. K., Welker Leng, K., Jenkins, C., Coleman, D. J., Sampson, D., Guan, X., Kumaraswamy, A., Rodansky, E. S., Urrutia, J. A., Schwartzman, J. A., Zhang, C., Beltran, H., Labrecque, M. P., Morrissey, C., Lucas, J. M., Coleman, I. M., Nelson, P. S., Corey, E., Handelman, S. K., Sexton, J. Z., Aggarwal, R., Abida, W., Feng, F. Y., Small, E. J., Spratt, D. E., Bankhead, A., Rao, A., Gesner, E. M., Attwell, S., Lakhotia, S., Campeau, E., Yates, J. A., Xia, Z., & Alumkal, J. J. (2021). BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program. Clinical cancer research : an official journal of the American Association for Cancer Research, 27(17), 4923-4936. https://doi.org/10.1158/1078-0432.CCR-20-4968
Kim, Dae-Hwan, et al. "BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program." Clinical cancer research : an official journal of the American Association for Cancer Research vol. 27,17 (2021): 4923-4936. doi: https://doi.org/10.1158/1078-0432.CCR-20-4968
Kim DH, Sun D, Storck WK, Welker Leng K, Jenkins C, Coleman DJ, Sampson D, Guan X, Kumaraswamy A, Rodansky ES, Urrutia JA, Schwartzman JA, Zhang C, Beltran H, Labrecque MP, Morrissey C, Lucas JM, Coleman IM, Nelson PS, Corey E, Handelman SK, Sexton JZ, Aggarwal R, Abida W, Feng FY, Small EJ, Spratt DE, Bankhead A, Rao A, Gesner EM, Attwell S, Lakhotia S, Campeau E, Yates JA, Xia Z, Alumkal JJ. BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program. Clin Cancer Res. 2021 Sep 01;27(17):4923-4936. doi: 10.1158/1078-0432.CCR-20-4968. Epub 2021 Jun 18. PMID: 34145028; PMCID: PMC8416959.
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Showing 1 to 4 of 4 entries