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Confidence intervals for the difference of median failure times applied to censored tumor growth delay data.

Statistics in biopharmaceutical research

Wu J.
PMID: 28966720
Stat Biopharm Res. 2011;3(3):488-496. doi: 10.1198/sbr.2011.10020. Epub 2012 Jan 24.

In tumor xenograft experiments, tumor response to the anti-cancer agents is often assessed by tumor growth delay, the difference in median tumor quadrupling times between treatment and control. Tumor quadrupling time is often subjected to right censoring because death...

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Wu J. Confidence intervals for the difference of median failure times applied to censored tumor growth delay data. Stat Biopharm Res. 2012;3(3):488-496doi: 10.1198/sbr.2011.10020.
Wu, J. (2011). Confidence intervals for the difference of median failure times applied to censored tumor growth delay data. Statistics in biopharmaceutical research, 3(3), 488-496. https://doi.org/10.1198/sbr.2011.10020
Wu, Jianrong. "Confidence intervals for the difference of median failure times applied to censored tumor growth delay data." Statistics in biopharmaceutical research vol. 3,3 (2011): 488-496. doi: https://doi.org/10.1198/sbr.2011.10020
Wu J. Confidence intervals for the difference of median failure times applied to censored tumor growth delay data. Stat Biopharm Res. 2011;3(3):488-496. doi: 10.1198/sbr.2011.10020. Epub 2012 Jan 24. PMID: 28966720; PMCID: PMC5621763.
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Single-Arm Phase II Survival Trial Design Under the Proportional Hazards Model.

Statistics in biopharmaceutical research

Wu J.
PMID: 28966721
Stat Biopharm Res. 2017;9(1):25-34. doi: 10.1080/19466315.2016.1174147. Epub 2017 Mar 02.

For designing single-arm phase II trials with time-to-event endpoints, a sample size formula is derived for the modified one-sample log-rank test under the proportional hazards model. The derived formula enables new methods for designing trials that allow a flexible...

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Wu J. Single-Arm Phase II Survival Trial Design Under the Proportional Hazards Model. Stat Biopharm Res. 2017;9(1):25-34doi: 10.1080/19466315.2016.1174147.
Wu, J. (2017). Single-Arm Phase II Survival Trial Design Under the Proportional Hazards Model. Statistics in biopharmaceutical research, 9(1), 25-34. https://doi.org/10.1080/19466315.2016.1174147
Wu, Jianrong. "Single-Arm Phase II Survival Trial Design Under the Proportional Hazards Model." Statistics in biopharmaceutical research vol. 9,1 (2017): 25-34. doi: https://doi.org/10.1080/19466315.2016.1174147
Wu J. Single-Arm Phase II Survival Trial Design Under the Proportional Hazards Model. Stat Biopharm Res. 2017;9(1):25-34. doi: 10.1080/19466315.2016.1174147. Epub 2017 Mar 02. PMID: 28966721; PMCID: PMC5619878.
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Use of Fungal Diagnostics and Therapy in Pediatric Cancer Patients in Resource-Limited Settings.

Current clinical microbiology reports

Mukkada S, Kirby J, Apiwattanakul N, Hayden RT, Caniza MA.
PMID: 27672551
Curr Clin Microbiol Rep. 2016 Sep;3(3):120-131. doi: 10.1007/s40588-016-0038-2. Epub 2016 Apr 18.

Fungal diseases are an important cause of mortality in immunocompromised hosts, and their incidence in pediatric cancer patients in low- to middle-income countries is underestimated. In this review, we present relevant, up-to-date information about the most common opportunistic and...

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Mukkada S, Kirby J, Apiwattanakul N, et al. Use of Fungal Diagnostics and Therapy in Pediatric Cancer Patients in Resource-Limited Settings. Curr Clin Microbiol Rep. 2016;3(3):120-131doi: 10.1007/s40588-016-0038-2.
Mukkada, S., Kirby, J., Apiwattanakul, N., Hayden, R. T., & Caniza, M. A. (2016). Use of Fungal Diagnostics and Therapy in Pediatric Cancer Patients in Resource-Limited Settings. Current clinical microbiology reports, 3(3), 120-131. https://doi.org/10.1007/s40588-016-0038-2
Mukkada, Sheena, et al. "Use of Fungal Diagnostics and Therapy in Pediatric Cancer Patients in Resource-Limited Settings." Current clinical microbiology reports vol. 3,3 (2016): 120-131. doi: https://doi.org/10.1007/s40588-016-0038-2
Mukkada S, Kirby J, Apiwattanakul N, Hayden RT, Caniza MA. Use of Fungal Diagnostics and Therapy in Pediatric Cancer Patients in Resource-Limited Settings. Curr Clin Microbiol Rep. 2016 Sep;3(3):120-131. doi: 10.1007/s40588-016-0038-2. Epub 2016 Apr 18. PMID: 27672551; PMCID: PMC5034939.
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Inhibition of mTORC1/C2 signaling improves anti-leukemia efficacy of JAK/STAT blockade in .

Oncotarget

Zhang Q, Shi C, Han L, Jain N, Roberts KG, Ma H, Cai T, Cavazos A, Tabe Y, Jacamo RO, Mu H, Zhao Y, Wang J, Wu SC, Cao F, Zeng Z, Zhou J, Mi Y, Jabbour EJ, Levine R, Tasian SK, Mullighan CG, Weinstock DM, Fruman DA, Konopleva M.
PMID: 29487712
Oncotarget. 2018 Jan 17;9(8):8027-8041. doi: 10.18632/oncotarget.24261. eCollection 2018 Jan 30.

Patients with cytokine receptor-like factor 2 rearranged (

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Zhang Q, Shi C, Han L, et al. Inhibition of mTORC1/C2 signaling improves anti-leukemia efficacy of JAK/STAT blockade in . Oncotarget. 2018;9(8):8027-8041doi: 10.18632/oncotarget.24261.
Zhang, Q., Shi, C., Han, L., Jain, N., Roberts, K. G., Ma, H., Cai, T., Cavazos, A., Tabe, Y., Jacamo, R. O., Mu, H., Zhao, Y., Wang, J., Wu, S. C., Cao, F., Zeng, Z., Zhou, J., Mi, Y., Jabbour, E. J., Levine, R., Tasian, S. K., Mullighan, C. G., Weinstock, D. M., Fruman, D. A., & Konopleva, M. (2018). Inhibition of mTORC1/C2 signaling improves anti-leukemia efficacy of JAK/STAT blockade in . Oncotarget, 9(8), 8027-8041. https://doi.org/10.18632/oncotarget.24261
Zhang, Qi, et al. "Inhibition of mTORC1/C2 signaling improves anti-leukemia efficacy of JAK/STAT blockade in ." Oncotarget vol. 9,8 (2018): 8027-8041. doi: https://doi.org/10.18632/oncotarget.24261
Zhang Q, Shi C, Han L, Jain N, Roberts KG, Ma H, Cai T, Cavazos A, Tabe Y, Jacamo RO, Mu H, Zhao Y, Wang J, Wu SC, Cao F, Zeng Z, Zhou J, Mi Y, Jabbour EJ, Levine R, Tasian SK, Mullighan CG, Weinstock DM, Fruman DA, Konopleva M. Inhibition of mTORC1/C2 signaling improves anti-leukemia efficacy of JAK/STAT blockade in . Oncotarget. 2018 Jan 17;9(8):8027-8041. doi: 10.18632/oncotarget.24261. eCollection 2018 Jan 30. PMID: 29487712; PMCID: PMC5814279.
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Double small bowel intussusception complicating bilateral partial nephrectomies.

Journal of pediatric surgery case reports

Wahid FN, Malkan AD, McCarville MB, Davidoff AM.
PMID: 24795858
J Pediatr Surg Case Rep. 2014 Jan;2(1):30-32. doi: 10.1016/j.epsc.2013.12.003.

An 11.5-month-old male, diagnosed with bilateral Wilms tumor at 10 months of age, received 6 weeks of chemotherapy and subsequently underwent bilateral partial nephrectomies. On postoperative day 5, he had crampy abdominal pain and bilious vomiting. Abdominal ultrasound confirmed...

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Wahid FN, Malkan AD, McCarville MB, et al. Double small bowel intussusception complicating bilateral partial nephrectomies. J Pediatr Surg Case Rep. 2014;2(1):30-32doi: 10.1016/j.epsc.2013.12.003.
Wahid, F. N., Malkan, A. D., McCarville, M. B., & Davidoff, A. M. (2014). Double small bowel intussusception complicating bilateral partial nephrectomies. Journal of pediatric surgery case reports, 2(1), 30-32. https://doi.org/10.1016/j.epsc.2013.12.003
Wahid, Fazal N, et al. "Double small bowel intussusception complicating bilateral partial nephrectomies." Journal of pediatric surgery case reports vol. 2,1 (2014): 30-32. doi: https://doi.org/10.1016/j.epsc.2013.12.003
Wahid FN, Malkan AD, McCarville MB, Davidoff AM. Double small bowel intussusception complicating bilateral partial nephrectomies. J Pediatr Surg Case Rep. 2014 Jan;2(1):30-32. doi: 10.1016/j.epsc.2013.12.003. PMID: 24795858; PMCID: PMC4005927.
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Generation of a lentiviral vector producer cell clone for human Wiskott-Aldrich syndrome gene therapy.

Molecular therapy. Methods & clinical development

Wielgosz MM, Kim YS, Carney GG, Zhan J, Reddivari M, Coop T, Heath RJ, Brown SA, Nienhuis AW.
PMID: 26052531
Mol Ther Methods Clin Dev. 2015 Jan 21;2:14063. doi: 10.1038/mtm.2014.63. eCollection 2015.

We have developed a producer cell line that generates lentiviral vector particles of high titer. The vector encodes the Wiskott-Aldrich syndrome (WAS) protein. An insulator element has been added to the long terminal repeats of the integrated vector to...

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Wielgosz MM, Kim YS, Carney GG, et al. Generation of a lentiviral vector producer cell clone for human Wiskott-Aldrich syndrome gene therapy. Mol Ther Methods Clin Dev. 2015;2:14063doi: 10.1038/mtm.2014.63.
Wielgosz, M. M., Kim, Y. S., Carney, G. G., Zhan, J., Reddivari, M., Coop, T., Heath, R. J., Brown, S. A., & Nienhuis, A. W. (2015). Generation of a lentiviral vector producer cell clone for human Wiskott-Aldrich syndrome gene therapy. Molecular therapy. Methods & clinical development, 214063. https://doi.org/10.1038/mtm.2014.63
Wielgosz, Matthew M, et al. "Generation of a lentiviral vector producer cell clone for human Wiskott-Aldrich syndrome gene therapy." Molecular therapy. Methods & clinical development vol. 2 (2015): 14063. doi: https://doi.org/10.1038/mtm.2014.63
Wielgosz MM, Kim YS, Carney GG, Zhan J, Reddivari M, Coop T, Heath RJ, Brown SA, Nienhuis AW. Generation of a lentiviral vector producer cell clone for human Wiskott-Aldrich syndrome gene therapy. Mol Ther Methods Clin Dev. 2015 Jan 21;2:14063. doi: 10.1038/mtm.2014.63. eCollection 2015. PMID: 26052531; PMCID: PMC4449020.
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Regulated lysosomal exocytosis mediates cancer progression.

Science advances

Machado E, White-Gilbertson S, van de Vlekkert D, Janke L, Moshiach S, Campos Y, Finkelstein D, Gomero E, Mosca R, Qiu X, Morton CL, Annunziata I, d'Azzo A.
PMID: 26824057
Sci Adv. 2015 Dec 18;1(11):e1500603. doi: 10.1126/sciadv.1500603. eCollection 2015 Dec.

Understanding how tumor cells transition to an invasive and drug-resistant phenotype is central to cancer biology, but the mechanisms underlying this transition remain unclear. We show that sarcomas gain these malignant traits by inducing lysosomal exocytosis, a ubiquitous physiological...

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Machado E, White-Gilbertson S, van de Vlekkert D, et al. Regulated lysosomal exocytosis mediates cancer progression. Sci Adv. 2015;1(11):e1500603doi: 10.1126/sciadv.1500603.
Machado, E., White-Gilbertson, S., van de Vlekkert, D., Janke, L., Moshiach, S., Campos, Y., Finkelstein, D., Gomero, E., Mosca, R., Qiu, X., Morton, C. L., Annunziata, I., & d'Azzo, A. (2015). Regulated lysosomal exocytosis mediates cancer progression. Science advances, 1(11), e1500603. https://doi.org/10.1126/sciadv.1500603
Machado, Eda, et al. "Regulated lysosomal exocytosis mediates cancer progression." Science advances vol. 1,11 (2015): e1500603. doi: https://doi.org/10.1126/sciadv.1500603
Machado E, White-Gilbertson S, van de Vlekkert D, Janke L, Moshiach S, Campos Y, Finkelstein D, Gomero E, Mosca R, Qiu X, Morton CL, Annunziata I, d'Azzo A. Regulated lysosomal exocytosis mediates cancer progression. Sci Adv. 2015 Dec 18;1(11):e1500603. doi: 10.1126/sciadv.1500603. eCollection 2015 Dec. PMID: 26824057; PMCID: PMC4730843.
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A Spline-Based Lack-Of-Fit Test for Independent Variable Effect in Poisson Regression.

Journal of modern applied statistical methods : JMASM

Li CS, Tu W.
PMID: 18997877
J Mod Appl Stat Methods. 2007 May;6(1):239-247. doi: 10.22237/jmasm/1177993260.

In regression analysis of count data, independent variables are often modeled by their linear effects under the assumption of log-linearity. In reality, the validity of such an assumption is rarely tested, and its use is at times unjustifiable. A...

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Li CS, Tu W. A Spline-Based Lack-Of-Fit Test for Independent Variable Effect in Poisson Regression. J Mod Appl Stat Methods. 2007;6(1):239-247doi: 10.22237/jmasm/1177993260.
Li, C. S., & Tu, W. (2007). A Spline-Based Lack-Of-Fit Test for Independent Variable Effect in Poisson Regression. Journal of modern applied statistical methods : JMASM, 6(1), 239-247. https://doi.org/10.22237/jmasm/1177993260
Li, Chin-Shang, and Tu, Wanzhu. "A Spline-Based Lack-Of-Fit Test for Independent Variable Effect in Poisson Regression." Journal of modern applied statistical methods : JMASM vol. 6,1 (2007): 239-247. doi: https://doi.org/10.22237/jmasm/1177993260
Li CS, Tu W. A Spline-Based Lack-Of-Fit Test for Independent Variable Effect in Poisson Regression. J Mod Appl Stat Methods. 2007 May;6(1):239-247. doi: 10.22237/jmasm/1177993260. PMID: 18997877; PMCID: PMC2581423.
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Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity.

Current immunology reviews

Ulett GC, Adderson EE.
PMID: 19081777
Curr Immunol Rev. 2006 May;2(2):119-141. doi: 10.2174/157339506776843033.

Apoptosis, or programmed cell death (PCD), is an important physiological mechanism, through which the human immune system regulates homeostasis and responds to diverse forms of cellular damage. PCD may also be involved in immune counteraction to microbial infection. Over...

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Ulett GC, Adderson EE. Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity. Curr Immunol Rev. 2006;2(2):119-141doi: 10.2174/157339506776843033.
Ulett, G. C., & Adderson, E. E. (2006). Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity. Current immunology reviews, 2(2), 119-141. https://doi.org/10.2174/157339506776843033
Ulett, Glen C, and Adderson, Elisabeth E. "Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity." Current immunology reviews vol. 2,2 (2006): 119-141. doi: https://doi.org/10.2174/157339506776843033
Ulett GC, Adderson EE. Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity. Curr Immunol Rev. 2006 May;2(2):119-141. doi: 10.2174/157339506776843033. PMID: 19081777; PMCID: PMC2600511.
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Alexander Disease: An Important Mimicker of Focal Brainstem Glioma-Response.

Pediatric blood & cancer

Van Poppel K, Ellison D, Broniscer A, Patay Z, Morris EB.
PMID: 21552504
Pediatr Blood Cancer. 2010 Mar;54(3):487. doi: 10.1002/pbc.22335.

No abstract available.

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Van Poppel K, Ellison D, Broniscer A, et al. Alexander Disease: An Important Mimicker of Focal Brainstem Glioma-Response. Pediatr Blood Cancer. 2010;54(3):487doi: 10.1002/pbc.22335.
Van Poppel, K., Ellison, D., Broniscer, A., Patay, Z., & Morris, E. B. (2010). Alexander Disease: An Important Mimicker of Focal Brainstem Glioma-Response. Pediatric blood & cancer, 54(3), 487. https://doi.org/10.1002/pbc.22335
Van Poppel, Katherine, et al. "Alexander Disease: An Important Mimicker of Focal Brainstem Glioma-Response." Pediatric blood & cancer vol. 54,3 (2010): 487. doi: https://doi.org/10.1002/pbc.22335
Van Poppel K, Ellison D, Broniscer A, Patay Z, Morris EB. Alexander Disease: An Important Mimicker of Focal Brainstem Glioma-Response. Pediatr Blood Cancer. 2010 Mar;54(3):487. doi: 10.1002/pbc.22335. PMID: 21552504; PMCID: PMC3087160.
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The epidermis of grhl3-null mice displays altered lipid processing and cellular hyperproliferation.

Organogenesis

Ting SB, Caddy J, Wilanowski T, Auden A, Cunningham JM, Elias PM, Holleran WM, Jane SM.
PMID: 19521564
Organogenesis. 2005 Apr;2(2):33-5. doi: 10.4161/org.2.2.2167.

The presence of an impermeable surface barrier is an essential homeostatic mechanism in almost all living organisms. We have recently described a novel gene that is critical for the developmental instruction and repair of the integument in mammals. This...

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Ting SB, Caddy J, Wilanowski T, et al. The epidermis of grhl3-null mice displays altered lipid processing and cellular hyperproliferation. Organogenesis. 2005;2(2):33-5doi: 10.4161/org.2.2.2167.
Ting, S. B., Caddy, J., Wilanowski, T., Auden, A., Cunningham, J. M., Elias, P. M., Holleran, W. M., & Jane, S. M. (2005). The epidermis of grhl3-null mice displays altered lipid processing and cellular hyperproliferation. Organogenesis, 2(2), 33-5. https://doi.org/10.4161/org.2.2.2167
Ting, Stephen B, et al. "The epidermis of grhl3-null mice displays altered lipid processing and cellular hyperproliferation." Organogenesis vol. 2,2 (2005): 33-5. doi: https://doi.org/10.4161/org.2.2.2167
Ting SB, Caddy J, Wilanowski T, Auden A, Cunningham JM, Elias PM, Holleran WM, Jane SM. The epidermis of grhl3-null mice displays altered lipid processing and cellular hyperproliferation. Organogenesis. 2005 Apr;2(2):33-5. doi: 10.4161/org.2.2.2167. PMID: 19521564; PMCID: PMC2634083.
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HNRNPH1 is required for rhabdomyosarcoma cell growth and survival.

Oncogenesis

Li Y, Bakke J, Finkelstein D, Zeng H, Wu J, Chen T.
PMID: 29362363
Oncogenesis. 2018 Jan 24;7(1):9. doi: 10.1038/s41389-017-0024-4.

Rhabdomyosarcoma (RMS) is an aggressive and difficult to treat cancer characterized by a muscle-like phenotype. Although the average 5-y survival rate is 65% for newly diagnosed RMS, the treatment options for metastatic disease are limited in efficacy, with the...

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Li Y, Bakke J, Finkelstein D, et al. HNRNPH1 is required for rhabdomyosarcoma cell growth and survival. Oncogenesis. 2018;7(1):9doi: 10.1038/s41389-017-0024-4.
Li, Y., Bakke, J., Finkelstein, D., Zeng, H., Wu, J., & Chen, T. (2018). HNRNPH1 is required for rhabdomyosarcoma cell growth and survival. Oncogenesis, 7(1), 9. https://doi.org/10.1038/s41389-017-0024-4
Li, Yanfeng, et al. "HNRNPH1 is required for rhabdomyosarcoma cell growth and survival." Oncogenesis vol. 7,1 (2018): 9. doi: https://doi.org/10.1038/s41389-017-0024-4
Li Y, Bakke J, Finkelstein D, Zeng H, Wu J, Chen T. HNRNPH1 is required for rhabdomyosarcoma cell growth and survival. Oncogenesis. 2018 Jan 24;7(1):9. doi: 10.1038/s41389-017-0024-4. PMID: 29362363; PMCID: PMC5833419.
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Showing 1 to 12 of 270 entries