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DNA repair deficiency biomarkers and the 70-gene ultra-high risk signature as predictors of veliparib/carboplatin response in the I-SPY 2 breast cancer trial.

NPJ breast cancer

Wolf DM, Yau C, Sanil A, Glas A, Petricoin E, Wulfkuhle J, Severson TM, Linn S, Brown-Swigart L, Hirst G, Buxton M, DeMichele A, Hylton N, Symmans F, Yee D, Paoloni M, Esserman L, Berry D, Rugo H, Olopade O, van 't Veer L.
PMID: 28948212
NPJ Breast Cancer. 2017 Aug 25;3:31. doi: 10.1038/s41523-017-0025-7. eCollection 2017.

Veliparib combined with carboplatin (VC) was an experimental regimen evaluated in the biomarker-rich neoadjuvant I-SPY 2 trial for breast cancer. VC showed improved efficacy in the triple negative signature. However, not all triple negative patients achieved pathologic complete response...

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Wolf DM, Yau C, Sanil A, et al. DNA repair deficiency biomarkers and the 70-gene ultra-high risk signature as predictors of veliparib/carboplatin response in the I-SPY 2 breast cancer trial. NPJ Breast Cancer. 2017;3:31doi: 10.1038/s41523-017-0025-7.
Wolf, D. M., Yau, C., Sanil, A., Glas, A., Petricoin, E., Wulfkuhle, J., Severson, T. M., Linn, S., Brown-Swigart, L., Hirst, G., Buxton, M., DeMichele, A., Hylton, N., Symmans, F., Yee, D., Paoloni, M., Esserman, L., Berry, D., Rugo, H., Olopade, O., & van 't Veer, L. (2017). DNA repair deficiency biomarkers and the 70-gene ultra-high risk signature as predictors of veliparib/carboplatin response in the I-SPY 2 breast cancer trial. NPJ breast cancer, 331. https://doi.org/10.1038/s41523-017-0025-7
Wolf, Denise M, et al. "DNA repair deficiency biomarkers and the 70-gene ultra-high risk signature as predictors of veliparib/carboplatin response in the I-SPY 2 breast cancer trial." NPJ breast cancer vol. 3 (2017): 31. doi: https://doi.org/10.1038/s41523-017-0025-7
Wolf DM, Yau C, Sanil A, Glas A, Petricoin E, Wulfkuhle J, Severson TM, Linn S, Brown-Swigart L, Hirst G, Buxton M, DeMichele A, Hylton N, Symmans F, Yee D, Paoloni M, Esserman L, Berry D, Rugo H, Olopade O, van 't Veer L. DNA repair deficiency biomarkers and the 70-gene ultra-high risk signature as predictors of veliparib/carboplatin response in the I-SPY 2 breast cancer trial. NPJ Breast Cancer. 2017 Aug 25;3:31. doi: 10.1038/s41523-017-0025-7. eCollection 2017. PMID: 28948212; PMCID: PMC5572474.
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Host response during Yersinia pestis infection of human bronchial epithelial cells involves negative regulation of autophagy and suggests a modulation of survival-related and cellular growth pathways.

Frontiers in microbiology

Alem F, Yao K, Lane D, Calvert V, Petricoin EF, Kramer L, Hale ML, Bavari S, Panchal RG, Hakami RM.
PMID: 25762983
Front Microbiol. 2015 Feb 13;6:50. doi: 10.3389/fmicb.2015.00050. eCollection 2015.

Yersinia pestis (Yp) causes the re-emerging disease plague, and is classified by the CDC and NIAID as a highest priority (Category A) pathogen. Currently, there is no approved human vaccine available and advances in early diagnostics and effective therapeutics...

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Alem F, Yao K, Lane D, et al. Host response during Yersinia pestis infection of human bronchial epithelial cells involves negative regulation of autophagy and suggests a modulation of survival-related and cellular growth pathways. Front Microbiol. 2015;6:50doi: 10.3389/fmicb.2015.00050.
Alem, F., Yao, K., Lane, D., Calvert, V., Petricoin, E. F., Kramer, L., Hale, M. L., Bavari, S., Panchal, R. G., & Hakami, R. M. (2015). Host response during Yersinia pestis infection of human bronchial epithelial cells involves negative regulation of autophagy and suggests a modulation of survival-related and cellular growth pathways. Frontiers in microbiology, 650. https://doi.org/10.3389/fmicb.2015.00050
Alem, Farhang, et al. "Host response during Yersinia pestis infection of human bronchial epithelial cells involves negative regulation of autophagy and suggests a modulation of survival-related and cellular growth pathways." Frontiers in microbiology vol. 6 (2015): 50. doi: https://doi.org/10.3389/fmicb.2015.00050
Alem F, Yao K, Lane D, Calvert V, Petricoin EF, Kramer L, Hale ML, Bavari S, Panchal RG, Hakami RM. Host response during Yersinia pestis infection of human bronchial epithelial cells involves negative regulation of autophagy and suggests a modulation of survival-related and cellular growth pathways. Front Microbiol. 2015 Feb 13;6:50. doi: 10.3389/fmicb.2015.00050. eCollection 2015. PMID: 25762983; PMCID: PMC4327736.
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Correction: Phosphoproteomic analysis reveals Smad protein family activation following Rift Valley fever virus infection.

PloS one

de la Fuente C, Pinkham C, Dabbagh D, Beitzel B, Garrison A, Palacios G, Hodge KA, Petricoin EF, Schmaljohn C, Campbell CE, Narayanan A, Kehn-Hall K.
PMID: 29543894
PLoS One. 2018 Mar 15;13(3):e0194633. doi: 10.1371/journal.pone.0194633. eCollection 2018.

[This corrects the article DOI: 10.1371/journal.pone.0191983.].

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de la Fuente C, Pinkham C, Dabbagh D, et al. Correction: Phosphoproteomic analysis reveals Smad protein family activation following Rift Valley fever virus infection. PLoS One. 2018;13(3):e0194633doi: 10.1371/journal.pone.0194633.
de la Fuente, C., Pinkham, C., Dabbagh, D., Beitzel, B., Garrison, A., Palacios, G., Hodge, K. A., Petricoin, E. F., Schmaljohn, C., Campbell, C. E., Narayanan, A., & Kehn-Hall, K. (2018). Correction: Phosphoproteomic analysis reveals Smad protein family activation following Rift Valley fever virus infection. PloS one, 13(3), e0194633. https://doi.org/10.1371/journal.pone.0194633
de la Fuente, Cynthia, et al. "Correction: Phosphoproteomic analysis reveals Smad protein family activation following Rift Valley fever virus infection." PloS one vol. 13,3 (2018): e0194633. doi: https://doi.org/10.1371/journal.pone.0194633
de la Fuente C, Pinkham C, Dabbagh D, Beitzel B, Garrison A, Palacios G, Hodge KA, Petricoin EF, Schmaljohn C, Campbell CE, Narayanan A, Kehn-Hall K. Correction: Phosphoproteomic analysis reveals Smad protein family activation following Rift Valley fever virus infection. PLoS One. 2018 Mar 15;13(3):e0194633. doi: 10.1371/journal.pone.0194633. eCollection 2018. PMID: 29543894; PMCID: PMC5854416.
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Protein pathway analysis in Clinical Proteomics using protein microarrays.

Drug discovery today. Technologies

Geho DH, Espina V, Wulfkuhle J, Petricoin EF, Liotta LA.
PMID: 24982012
Drug Discov Today Technol. 2005;2(4):353-9. doi: 10.1016/j.ddtec.2005.11.008.

Molecular diagnostics research within the field of cancer is increasingly focused on detecting low-abundance protein endpoints that can be used to define a patient's disease more completely. Protein microarrays represent an important Clinical Proteomics tool for directly measuring protein...

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Geho DH, Espina V, Wulfkuhle J, et al. Protein pathway analysis in Clinical Proteomics using protein microarrays. Drug Discov Today Technol. 2005;2(4):353-9doi: 10.1016/j.ddtec.2005.11.008.
Geho, D. H., Espina, V., Wulfkuhle, J., Petricoin, E. F., & Liotta, L. A. (2005). Protein pathway analysis in Clinical Proteomics using protein microarrays. Drug discovery today. Technologies, 2(4), 353-9. https://doi.org/10.1016/j.ddtec.2005.11.008
Geho, David H, et al. "Protein pathway analysis in Clinical Proteomics using protein microarrays." Drug discovery today. Technologies vol. 2,4 (2005): 353-9. doi: https://doi.org/10.1016/j.ddtec.2005.11.008
Geho DH, Espina V, Wulfkuhle J, Petricoin EF, Liotta LA. Protein pathway analysis in Clinical Proteomics using protein microarrays. Drug Discov Today Technol. 2005;2(4):353-9. doi: 10.1016/j.ddtec.2005.11.008. PMID: 24982012.
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STUDENTJAMA. Molecular technologies for personalized cancer management.

JAMA

Hasan RK, Wulfkuhle JD, Liotta LA, Petricoin EF.
PMID: 15069056
JAMA. 2004 Apr 07;291(13):1644-5. doi: 10.1001/jama.291.13.1644.

No abstract available.

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Hasan RK, Wulfkuhle JD, Liotta LA, et al. STUDENTJAMA. Molecular technologies for personalized cancer management. JAMA. 2004;291(13):1644-5doi: 10.1001/jama.291.13.1644.
Hasan, R. K., Wulfkuhle, J. D., Liotta, L. A., & Petricoin, E. F. (2004). STUDENTJAMA. Molecular technologies for personalized cancer management. JAMA, 291(13), 1644-5. https://doi.org/10.1001/jama.291.13.1644
Hasan, Rani K, et al. "STUDENTJAMA. Molecular technologies for personalized cancer management." JAMA vol. 291,13 (2004): 1644-5. doi: https://doi.org/10.1001/jama.291.13.1644
Hasan RK, Wulfkuhle JD, Liotta LA, Petricoin EF. STUDENTJAMA. Molecular technologies for personalized cancer management. JAMA. 2004 Apr 07;291(13):1644-5. doi: 10.1001/jama.291.13.1644. PMID: 15069056.
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Tissue is alive: New technologies are needed to address the problems of protein biomarker pre-analytical variability.

Proteomics. Clinical applications

Espina V, Mueller C, Edmiston K, Sciro M, Petricoin EF, Liotta LA.
PMID: 20871745
Proteomics Clin Appl. 2009 Aug 01;3(8):874-882. doi: 10.1002/prca.200800001.

Instability of tissue protein biomarkers is a critical issue for molecular profiling. Pre-analytical variables during tissue procurement, such as time delays during which the tissue remains stored at room temperature, can cause significant variability and bias in downstream molecular...

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Espina V, Mueller C, Edmiston K, et al. Tissue is alive: New technologies are needed to address the problems of protein biomarker pre-analytical variability. Proteomics Clin Appl. 2009;3(8):874-882doi: 10.1002/prca.200800001.
Espina, V., Mueller, C., Edmiston, K., Sciro, M., Petricoin, E. F., & Liotta, L. A. (2009). Tissue is alive: New technologies are needed to address the problems of protein biomarker pre-analytical variability. Proteomics. Clinical applications, 3(8), 874-882. https://doi.org/10.1002/prca.200800001
Espina, Virginia, et al. "Tissue is alive: New technologies are needed to address the problems of protein biomarker pre-analytical variability." Proteomics. Clinical applications vol. 3,8 (2009): 874-882. doi: https://doi.org/10.1002/prca.200800001
Espina V, Mueller C, Edmiston K, Sciro M, Petricoin EF, Liotta LA. Tissue is alive: New technologies are needed to address the problems of protein biomarker pre-analytical variability. Proteomics Clin Appl. 2009 Aug 01;3(8):874-882. doi: 10.1002/prca.200800001. PMID: 20871745; PMCID: PMC2944287.
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Application of Analyte Harvesting Nanoparticle Technology to the Measurement of Urinary HGH in Healthy Individuals.

Journal of sports medicine & doping studies

Luchini A, Tamburro D, Magni R, Fredolini C, Espina V, Bosch J, Garaci E, Petricoin EF, Liotta LA.
PMID: 24014257
J Sports Med Doping Stud. 2012;2(6). doi: 10.4172/2161-0673.1000e127.

Urine represents a valuable biofluid for noninvasive measurement of Human Growth Hormone (HGH) secretion. Unfortunately, currently available commercial HGH immunoassays do not achieve the sensitivity needed for urinary HGH measurement in the low picogram per milliliter range, the expected...

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Luchini A, Tamburro D, Magni R, et al. Application of Analyte Harvesting Nanoparticle Technology to the Measurement of Urinary HGH in Healthy Individuals. J Sports Med Doping Stud. 2012;2(6)doi: 10.4172/2161-0673.1000e127.
Luchini, A., Tamburro, D., Magni, R., Fredolini, C., Espina, V., Bosch, J., Garaci, E., Petricoin, E. F., & Liotta, L. A. (2012). Application of Analyte Harvesting Nanoparticle Technology to the Measurement of Urinary HGH in Healthy Individuals. Journal of sports medicine & doping studies, 2(6), . https://doi.org/10.4172/2161-0673.1000e127
Luchini, Alessandra, et al. "Application of Analyte Harvesting Nanoparticle Technology to the Measurement of Urinary HGH in Healthy Individuals." Journal of sports medicine & doping studies vol. 2,6 (2012). doi: https://doi.org/10.4172/2161-0673.1000e127
Luchini A, Tamburro D, Magni R, Fredolini C, Espina V, Bosch J, Garaci E, Petricoin EF, Liotta LA. Application of Analyte Harvesting Nanoparticle Technology to the Measurement of Urinary HGH in Healthy Individuals. J Sports Med Doping Stud. 2012;2(6). doi: 10.4172/2161-0673.1000e127. PMID: 24014257; PMCID: PMC3761369.
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Interference with pre-B-cell receptor signaling offers a therapeutic option for TCF3-rearranged childhood acute lymphoblastic leukemia.

Blood cancer journal

van der Veer A, van der Velden VH, Willemse ME, Hoogeveen PG, Petricoin EF, Beverloo HB, Escherich G, Horstmann MA, Pieters R, den Boer ML.
PMID: 24531445
Blood Cancer J. 2014 Feb 14;4:e181. doi: 10.1038/bcj.2014.5.

No abstract available.

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van der Veer A, van der Velden VH, Willemse ME, et al. Interference with pre-B-cell receptor signaling offers a therapeutic option for TCF3-rearranged childhood acute lymphoblastic leukemia. Blood Cancer J. 2014;4:e181doi: 10.1038/bcj.2014.5.
van der Veer, A., van der Velden, V. H., Willemse, M. E., Hoogeveen, P. G., Petricoin, E. F., Beverloo, H. B., Escherich, G., Horstmann, M. A., Pieters, R., & den Boer, M. L. (2014). Interference with pre-B-cell receptor signaling offers a therapeutic option for TCF3-rearranged childhood acute lymphoblastic leukemia. Blood cancer journal, 4e181. https://doi.org/10.1038/bcj.2014.5
van der Veer, A, et al. "Interference with pre-B-cell receptor signaling offers a therapeutic option for TCF3-rearranged childhood acute lymphoblastic leukemia." Blood cancer journal vol. 4 (2014): e181. doi: https://doi.org/10.1038/bcj.2014.5
van der Veer A, van der Velden VH, Willemse ME, Hoogeveen PG, Petricoin EF, Beverloo HB, Escherich G, Horstmann MA, Pieters R, den Boer ML. Interference with pre-B-cell receptor signaling offers a therapeutic option for TCF3-rearranged childhood acute lymphoblastic leukemia. Blood Cancer J. 2014 Feb 14;4:e181. doi: 10.1038/bcj.2014.5. PMID: 24531445; PMCID: PMC3944663.
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Erratum to: 'Conditional robustness analysis for fragility discovery and target identification in biochemical networks and in cancer systems biology'.

BMC systems biology

Bianconi F, Baldelli E, Ludovini V, Petricoin EF, Crinò L, Valigi P.
PMID: 26935321
BMC Syst Biol. 2016 Mar 02;10:24. doi: 10.1186/s12918-016-0267-2.

No abstract available.

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Bianconi F, Baldelli E, Ludovini V, et al. Erratum to: 'Conditional robustness analysis for fragility discovery and target identification in biochemical networks and in cancer systems biology'. BMC Syst Biol. 2016;10:24doi: 10.1186/s12918-016-0267-2.
Bianconi, F., Baldelli, E., Ludovini, V., Petricoin, E. F., Crinò, L., & Valigi, P. (2016). Erratum to: 'Conditional robustness analysis for fragility discovery and target identification in biochemical networks and in cancer systems biology'. BMC systems biology, 1024. https://doi.org/10.1186/s12918-016-0267-2
Bianconi, Fortunato, et al. "Erratum to: 'Conditional robustness analysis for fragility discovery and target identification in biochemical networks and in cancer systems biology'." BMC systems biology vol. 10 (2016): 24. doi: https://doi.org/10.1186/s12918-016-0267-2
Bianconi F, Baldelli E, Ludovini V, Petricoin EF, Crinò L, Valigi P. Erratum to: 'Conditional robustness analysis for fragility discovery and target identification in biochemical networks and in cancer systems biology'. BMC Syst Biol. 2016 Mar 02;10:24. doi: 10.1186/s12918-016-0267-2. PMID: 26935321; PMCID: PMC4774129.
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Androgen Receptor Is a Non-canonical Inhibitor of Wild-Type and Mutant Estrogen Receptors in Hormone Receptor-Positive Breast Cancers.

iScience

Ponnusamy S, Asemota S, Schwartzberg LS, Guestini F, McNamara KM, Pierobon M, Font-Tello A, Qiu X, Xie Y, Rao PK, Thiyagarajan T, Grimes B, Johnson DL, Fleming MD, Pritchard FE, Berry MP, Oswaks R, Fine RE, Brown M, Sasano H, Petricoin EF, Long HW, Narayanan R.
PMID: 31698248
iScience. 2019 Nov 22;21:341-358. doi: 10.1016/j.isci.2019.10.038. Epub 2019 Oct 23.

Sustained treatment of estrogen receptor (ER)-positive breast cancer with ER-targeting drugs results in ER mutations and refractory unresponsive cancers. Androgen receptor (AR), which is expressed in 80%-95% of ER-positive breast cancers, could serve as an alternate therapeutic target. Although...

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Ponnusamy S, Asemota S, Schwartzberg LS, et al. Androgen Receptor Is a Non-canonical Inhibitor of Wild-Type and Mutant Estrogen Receptors in Hormone Receptor-Positive Breast Cancers. iScience. 2019;21:341-358doi: 10.1016/j.isci.2019.10.038.
Ponnusamy, S., Asemota, S., Schwartzberg, L. S., Guestini, F., McNamara, K. M., Pierobon, M., Font-Tello, A., Qiu, X., Xie, Y., Rao, P. K., Thiyagarajan, T., Grimes, B., Johnson, D. L., Fleming, M. D., Pritchard, F. E., Berry, M. P., Oswaks, R., Fine, R. E., Brown, M., Sasano, H., Petricoin, E. F., Long, H. W., & Narayanan, R. (2019). Androgen Receptor Is a Non-canonical Inhibitor of Wild-Type and Mutant Estrogen Receptors in Hormone Receptor-Positive Breast Cancers. iScience, 21341-358. https://doi.org/10.1016/j.isci.2019.10.038
Ponnusamy, Suriyan, et al. "Androgen Receptor Is a Non-canonical Inhibitor of Wild-Type and Mutant Estrogen Receptors in Hormone Receptor-Positive Breast Cancers." iScience vol. 21 (2019): 341-358. doi: https://doi.org/10.1016/j.isci.2019.10.038
Ponnusamy S, Asemota S, Schwartzberg LS, Guestini F, McNamara KM, Pierobon M, Font-Tello A, Qiu X, Xie Y, Rao PK, Thiyagarajan T, Grimes B, Johnson DL, Fleming MD, Pritchard FE, Berry MP, Oswaks R, Fine RE, Brown M, Sasano H, Petricoin EF, Long HW, Narayanan R. Androgen Receptor Is a Non-canonical Inhibitor of Wild-Type and Mutant Estrogen Receptors in Hormone Receptor-Positive Breast Cancers. iScience. 2019 Nov 22;21:341-358. doi: 10.1016/j.isci.2019.10.038. Epub 2019 Oct 23. PMID: 31698248; PMCID: PMC6889594.
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CHK1 protects oncogenic KRAS-expressing cells from DNA damage and is a target for pancreatic cancer treatment.

Cell reports

Klomp JE, Lee YS, Goodwin CM, Papke B, Klomp JA, Waters AM, Stalnecker CA, DeLiberty JM, Drizyte-Miller K, Yang R, Diehl JN, Yin HH, Pierobon M, Baldelli E, Ryan MB, Li S, Peterson J, Smith AR, Neal JT, McCormick AK, Kuo CJ, Counter CM, Petricoin EF, Cox AD, Bryant KL, Der CJ.
PMID: 34852220
Cell Rep. 2021 Nov 30;37(9):110060. doi: 10.1016/j.celrep.2021.110060.

We apply genetic screens to delineate modulators of KRAS mutant pancreatic ductal adenocarcinoma (PDAC) sensitivity to ERK inhibitor treatment, and we identify components of the ATR-CHK1 DNA damage repair (DDR) pathway. Pharmacologic inhibition of CHK1 alone causes apoptotic growth...

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Klomp JE, Lee YS, Goodwin CM, et al. CHK1 protects oncogenic KRAS-expressing cells from DNA damage and is a target for pancreatic cancer treatment. Cell Rep. 2021;37(9):110060doi: 10.1016/j.celrep.2021.110060.
Klomp, J. E., Lee, Y. S., Goodwin, C. M., Papke, B., Klomp, J. A., Waters, A. M., Stalnecker, C. A., DeLiberty, J. M., Drizyte-Miller, K., Yang, R., Diehl, J. N., Yin, H. H., Pierobon, M., Baldelli, E., Ryan, M. B., Li, S., Peterson, J., Smith, A. R., Neal, J. T., McCormick, A. K., Kuo, C. J., Counter, C. M., Petricoin, E. F., Cox, A. D., Bryant, K. L., & Der, C. J. (2021). CHK1 protects oncogenic KRAS-expressing cells from DNA damage and is a target for pancreatic cancer treatment. Cell reports, 37(9), 110060. https://doi.org/10.1016/j.celrep.2021.110060
Klomp, Jennifer E, et al. "CHK1 protects oncogenic KRAS-expressing cells from DNA damage and is a target for pancreatic cancer treatment." Cell reports vol. 37,9 (2021): 110060. doi: https://doi.org/10.1016/j.celrep.2021.110060
Klomp JE, Lee YS, Goodwin CM, Papke B, Klomp JA, Waters AM, Stalnecker CA, DeLiberty JM, Drizyte-Miller K, Yang R, Diehl JN, Yin HH, Pierobon M, Baldelli E, Ryan MB, Li S, Peterson J, Smith AR, Neal JT, McCormick AK, Kuo CJ, Counter CM, Petricoin EF, Cox AD, Bryant KL, Der CJ. CHK1 protects oncogenic KRAS-expressing cells from DNA damage and is a target for pancreatic cancer treatment. Cell Rep. 2021 Nov 30;37(9):110060. doi: 10.1016/j.celrep.2021.110060. PMID: 34852220; PMCID: PMC8665414.
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Tumor-Specific Major Histocompatibility-II Expression Predicts Benefit to Anti-PD-1/L1 Therapy in Patients With HER2-Negative Primary Breast Cancer.

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

Gonzalez-Ericsson PI, Wulfkhule JD, Gallagher RI, Sun X, Axelrod ML, Sheng Q, Luo N, Gomez H, Sanchez V, Sanders M, Pusztai L, Petricoin E, Blenman KRM, Balko JM.
PMID: 34315723
Clin Cancer Res. 2021 Jul 27; doi: 10.1158/1078-0432.CCR-21-0607. Epub 2021 Jul 27.

PURPOSE: Immunotherapies targeting PD-1/L1 enhance pathologic complete response (pCR) rates when added to standard neoadjuvant chemotherapy (NAC) regimens in early-stage triple-negative, and possibly high-risk estrogen receptor-positive breast cancer. However, immunotherapy has been associated with significant toxicity, and most patients...

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Gonzalez-Ericsson PI, Wulfkhule JD, Gallagher RI, et al. Tumor-Specific Major Histocompatibility-II Expression Predicts Benefit to Anti-PD-1/L1 Therapy in Patients With HER2-Negative Primary Breast Cancer. Clin Cancer Res. 2021;doi: 10.1158/1078-0432.CCR-21-0607.
Gonzalez-Ericsson, P. I., Wulfkhule, J. D., Gallagher, R. I., Sun, X., Axelrod, M. L., Sheng, Q., Luo, N., Gomez, H., Sanchez, V., Sanders, M., Pusztai, L., Petricoin, E., Blenman, K. R. M., Balko, J. M. (2021). Tumor-Specific Major Histocompatibility-II Expression Predicts Benefit to Anti-PD-1/L1 Therapy in Patients With HER2-Negative Primary Breast Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research, . https://doi.org/10.1158/1078-0432.CCR-21-0607
Gonzalez-Ericsson, Paula I, et al. "Tumor-Specific Major Histocompatibility-II Expression Predicts Benefit to Anti-PD-1/L1 Therapy in Patients With HER2-Negative Primary Breast Cancer." Clinical cancer research : an official journal of the American Association for Cancer Research vol. (2021). doi: https://doi.org/10.1158/1078-0432.CCR-21-0607
Gonzalez-Ericsson PI, Wulfkhule JD, Gallagher RI, Sun X, Axelrod ML, Sheng Q, Luo N, Gomez H, Sanchez V, Sanders M, Pusztai L, Petricoin E, Blenman KRM, Balko JM. Tumor-Specific Major Histocompatibility-II Expression Predicts Benefit to Anti-PD-1/L1 Therapy in Patients With HER2-Negative Primary Breast Cancer. Clin Cancer Res. 2021 Jul 27; doi: 10.1158/1078-0432.CCR-21-0607. Epub 2021 Jul 27. PMID: 34315723.
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Showing 1 to 12 of 81 entries