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PKC activation sensitizes basal-like breast cancer cell lines to Smac mimetics.

Cell death discovery

Cornmark L, Holmgren C, Masoumi K, Larsson C.
PMID: 27551497
Cell Death Discov. 2016 Feb 29;2:16002. doi: 10.1038/cddiscovery.2016.2. eCollection 2016.

There is a need for novel strategies to initiate cancer cell death. One approach is the use of Smac mimetics, which antagonize inhibitor of apoptosis proteins (IAPs). Recent studies have shown that combinations of Smac mimetics such as LBW242...

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Cornmark L, Holmgren C, Masoumi K, et al. PKC activation sensitizes basal-like breast cancer cell lines to Smac mimetics. Cell Death Discov. 2016;2:16002doi: 10.1038/cddiscovery.2016.2.
Cornmark, L., Holmgren, C., Masoumi, K., & Larsson, C. (2016). PKC activation sensitizes basal-like breast cancer cell lines to Smac mimetics. Cell death discovery, 216002. https://doi.org/10.1038/cddiscovery.2016.2
Cornmark, L, et al. "PKC activation sensitizes basal-like breast cancer cell lines to Smac mimetics." Cell death discovery vol. 2 (2016): 16002. doi: https://doi.org/10.1038/cddiscovery.2016.2
Cornmark L, Holmgren C, Masoumi K, Larsson C. PKC activation sensitizes basal-like breast cancer cell lines to Smac mimetics. Cell Death Discov. 2016 Feb 29;2:16002. doi: 10.1038/cddiscovery.2016.2. eCollection 2016. PMID: 27551497; PMCID: PMC4979953.
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Inducing death in tumor cells: roles of the inhibitor of apoptosis proteins.

F1000Research

Finlay D, Teriete P, Vamos M, Cosford NDP, Vuori K.
PMID: 28529715
F1000Res. 2017 Apr 27;6:587. doi: 10.12688/f1000research.10625.1. eCollection 2017.

The heterogeneous group of diseases collectively termed cancer results not just from aberrant cellular proliferation but also from a lack of accompanying homeostatic cell death. Indeed, cancer cells regularly acquire resistance to programmed cell death, or apoptosis, which not...

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Finlay D, Teriete P, Vamos M, et al. Inducing death in tumor cells: roles of the inhibitor of apoptosis proteins. F1000Res. 2017;6:587doi: 10.12688/f1000research.10625.1.
Finlay, D., Teriete, P., Vamos, M., Cosford, N. D. P., & Vuori, K. (2017). Inducing death in tumor cells: roles of the inhibitor of apoptosis proteins. F1000Research, 6587. https://doi.org/10.12688/f1000research.10625.1
Finlay, Darren, et al. "Inducing death in tumor cells: roles of the inhibitor of apoptosis proteins." F1000Research vol. 6 (2017): 587. doi: https://doi.org/10.12688/f1000research.10625.1
Finlay D, Teriete P, Vamos M, Cosford NDP, Vuori K. Inducing death in tumor cells: roles of the inhibitor of apoptosis proteins. F1000Res. 2017 Apr 27;6:587. doi: 10.12688/f1000research.10625.1. eCollection 2017. PMID: 28529715; PMCID: PMC5414821.
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Dimeric Macrocyclic Antagonists of Inhibitor of Apoptosis Proteins for the Treatment of Cancer.

ACS medicinal chemistry letters

Zhang Y, Seigal BA, Terrett NK, Talbott RL, Fargnoli J, Naglich JG, Chaudhry C, Posy SL, Vuppugalla R, Cornelius G, Lei M, Wang C, Zhang Y, Schmidt RJ, Wei DD, Miller MM, Allen MP, Li L, Carter PH, Vite GD, Borzilleri RM.
PMID: 26191364
ACS Med Chem Lett. 2015 May 27;6(7):770-5. doi: 10.1021/acsmedchemlett.5b00091. eCollection 2015 Jul 09.

A series of dimeric macrocyclic compounds were prepared and evaluated as antagonists for inhibitor of apoptosis proteins. The most potent analogue 11, which binds to XIAP and c-IAP proteins with high affinity and induces caspase-3 activation and ultimately cell...

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Zhang Y, Seigal BA, Terrett NK, et al. Dimeric Macrocyclic Antagonists of Inhibitor of Apoptosis Proteins for the Treatment of Cancer. ACS Med Chem Lett. 2015;6(7):770-5doi: 10.1021/acsmedchemlett.5b00091.
Zhang, Y., Seigal, B. A., Terrett, N. K., Talbott, R. L., Fargnoli, J., Naglich, J. G., Chaudhry, C., Posy, S. L., Vuppugalla, R., Cornelius, G., Lei, M., Wang, C., Zhang, Y., Schmidt, R. J., Wei, D. D., Miller, M. M., Allen, M. P., Li, L., Carter, P. H., Vite, G. D., & Borzilleri, R. M. (2015). Dimeric Macrocyclic Antagonists of Inhibitor of Apoptosis Proteins for the Treatment of Cancer. ACS medicinal chemistry letters, 6(7), 770-5. https://doi.org/10.1021/acsmedchemlett.5b00091
Zhang, Yong, et al. "Dimeric Macrocyclic Antagonists of Inhibitor of Apoptosis Proteins for the Treatment of Cancer." ACS medicinal chemistry letters vol. 6,7 (2015): 770-5. doi: https://doi.org/10.1021/acsmedchemlett.5b00091
Zhang Y, Seigal BA, Terrett NK, Talbott RL, Fargnoli J, Naglich JG, Chaudhry C, Posy SL, Vuppugalla R, Cornelius G, Lei M, Wang C, Zhang Y, Schmidt RJ, Wei DD, Miller MM, Allen MP, Li L, Carter PH, Vite GD, Borzilleri RM. Dimeric Macrocyclic Antagonists of Inhibitor of Apoptosis Proteins for the Treatment of Cancer. ACS Med Chem Lett. 2015 May 27;6(7):770-5. doi: 10.1021/acsmedchemlett.5b00091. eCollection 2015 Jul 09. PMID: 26191364; PMCID: PMC4499820.
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Delivery of a survivin promoter-driven antisense survivin-expressing plasmid DNA as a cancer therapeutic: a proof-of-concept study.

OncoTargets and therapy

Lin KY, Cheng SM, Tsai SL, Tsai JY, Lin CH, Cheung CH.
PMID: 27217778
Onco Targets Ther. 2016 May 03;9:2601-13. doi: 10.2147/OTT.S101209. eCollection 2016.

Survivin is a member of the inhibitor-of-apoptosis proteins family. It is overexpressed in many different cancer types but not in the differentiated normal tissue. In addition, overexpression of survivin promotes cancer cell survival and induces chemotherapeutic drug resistance, making...

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Lin KY, Cheng SM, Tsai SL, et al. Delivery of a survivin promoter-driven antisense survivin-expressing plasmid DNA as a cancer therapeutic: a proof-of-concept study. Onco Targets Ther. 2016;9:2601-13doi: 10.2147/OTT.S101209.
Lin, K. Y., Cheng, S. M., Tsai, S. L., Tsai, J. Y., Lin, C. H., & Cheung, C. H. (2016). Delivery of a survivin promoter-driven antisense survivin-expressing plasmid DNA as a cancer therapeutic: a proof-of-concept study. OncoTargets and therapy, 92601-13. https://doi.org/10.2147/OTT.S101209
Lin, Kun-Yuan, et al. "Delivery of a survivin promoter-driven antisense survivin-expressing plasmid DNA as a cancer therapeutic: a proof-of-concept study." OncoTargets and therapy vol. 9 (2016): 2601-13. doi: https://doi.org/10.2147/OTT.S101209
Lin KY, Cheng SM, Tsai SL, Tsai JY, Lin CH, Cheung CH. Delivery of a survivin promoter-driven antisense survivin-expressing plasmid DNA as a cancer therapeutic: a proof-of-concept study. Onco Targets Ther. 2016 May 03;9:2601-13. doi: 10.2147/OTT.S101209. eCollection 2016. PMID: 27217778; PMCID: PMC4862386.
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The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia.

Leukemia research and treatment

Nestal de Moraes G, Souza PS, Costas FC, Vasconcelos FC, Reis FR, Maia RC.
PMID: 23259070
Leuk Res Treatment. 2012;2012:671702. doi: 10.1155/2012/671702. Epub 2012 Apr 24.

Chronic myeloid leukemia (CML) is a clonal hematopoietic disorder characterized by the presence of the Philadelphia chromosome which resulted from the reciprocal translocation between chromosomes 9 and 22. The pathogenesis of CML involves the constitutive activation of the BCR-ABL...

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Nestal de Moraes G, Souza PS, Costas FC, et al. The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia. Leuk Res Treatment. 2012;2012:671702doi: 10.1155/2012/671702.
Nestal de Moraes, G., Souza, P. S., Costas, F. C., Vasconcelos, F. C., Reis, F. R., & Maia, R. C. (2012). The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia. Leukemia research and treatment, 2012671702. https://doi.org/10.1155/2012/671702
Nestal de Moraes, Gabriela, et al. "The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia." Leukemia research and treatment vol. 2012 (2012): 671702. doi: https://doi.org/10.1155/2012/671702
Nestal de Moraes G, Souza PS, Costas FC, Vasconcelos FC, Reis FR, Maia RC. The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia. Leuk Res Treatment. 2012;2012:671702. doi: 10.1155/2012/671702. Epub 2012 Apr 24. PMID: 23259070; PMCID: PMC3505928.
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Long-term maintenance of prognostic value of survivin and its relationship with p53 in T4 breast cancer patients.

Experimental and therapeutic medicine

Ionta MT, Perra MT, Atzori F, Maxia C, Pusceddu V, Demurtas P, Deidda MC, Piras F, Frau B, Murtas D, Minerba L, Massidda B, Sirigu P.
PMID: 23136593
Exp Ther Med. 2010 Jan;1(1):59-64. doi: 10.3892/etm_00000010. Epub 2010 Jan 01.

A large proportion of human tumors show deregulated expression of a variety of proteins that play a crucial role in the execution of the apoptotic program. Survivin belongs to the family of inhibitor of apoptosis proteins which were originally...

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Ionta MT, Perra MT, Atzori F, et al. Long-term maintenance of prognostic value of survivin and its relationship with p53 in T4 breast cancer patients. Exp Ther Med. 2010;1(1):59-64doi: 10.3892/etm_00000010.
Ionta, M. T., Perra, M. T., Atzori, F., Maxia, C., Pusceddu, V., Demurtas, P., Deidda, M. C., Piras, F., Frau, B., Murtas, D., Minerba, L., Massidda, B., & Sirigu, P. (2010). Long-term maintenance of prognostic value of survivin and its relationship with p53 in T4 breast cancer patients. Experimental and therapeutic medicine, 1(1), 59-64. https://doi.org/10.3892/etm_00000010
Ionta, Maria Teresa, et al. "Long-term maintenance of prognostic value of survivin and its relationship with p53 in T4 breast cancer patients." Experimental and therapeutic medicine vol. 1,1 (2010): 59-64. doi: https://doi.org/10.3892/etm_00000010
Ionta MT, Perra MT, Atzori F, Maxia C, Pusceddu V, Demurtas P, Deidda MC, Piras F, Frau B, Murtas D, Minerba L, Massidda B, Sirigu P. Long-term maintenance of prognostic value of survivin and its relationship with p53 in T4 breast cancer patients. Exp Ther Med. 2010 Jan;1(1):59-64. doi: 10.3892/etm_00000010. Epub 2010 Jan 01. PMID: 23136593; PMCID: PMC3490395.
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Integrin-Targeting Dye-Doped PEG-Shell/Silica-Core Nanoparticles Mimicking the Proapoptotic Smac/DIABLO Protein.

Nanomaterials (Basel, Switzerland)

De Marco R, Rampazzo E, Zhao J, Prodi L, Paolillo M, Picchetti P, Gallo F, Calonghi N, Gentilucci L.
PMID: 32575872
Nanomaterials (Basel). 2020 Jun 21;10(6). doi: 10.3390/nano10061211.

Cancer cells demonstrate elevated expression levels of the inhibitor of apoptosis proteins (IAPs), contributing to tumor cell survival, disease progression, chemo-resistance, and poor prognosis. Smac/DIABLO is a mitochondrial protein that promotes apoptosis by neutralizing members of the IAP family....

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De Marco R, Rampazzo E, Zhao J, et al. Integrin-Targeting Dye-Doped PEG-Shell/Silica-Core Nanoparticles Mimicking the Proapoptotic Smac/DIABLO Protein. Nanomaterials (Basel). 2020;10(6)doi: 10.3390/nano10061211.
De Marco, R., Rampazzo, E., Zhao, J., Prodi, L., Paolillo, M., Picchetti, P., Gallo, F., Calonghi, N., & Gentilucci, L. (2020). Integrin-Targeting Dye-Doped PEG-Shell/Silica-Core Nanoparticles Mimicking the Proapoptotic Smac/DIABLO Protein. Nanomaterials (Basel, Switzerland), 10(6), . https://doi.org/10.3390/nano10061211
De Marco, Rossella, et al. "Integrin-Targeting Dye-Doped PEG-Shell/Silica-Core Nanoparticles Mimicking the Proapoptotic Smac/DIABLO Protein." Nanomaterials (Basel, Switzerland) vol. 10,6 (2020). doi: https://doi.org/10.3390/nano10061211
De Marco R, Rampazzo E, Zhao J, Prodi L, Paolillo M, Picchetti P, Gallo F, Calonghi N, Gentilucci L. Integrin-Targeting Dye-Doped PEG-Shell/Silica-Core Nanoparticles Mimicking the Proapoptotic Smac/DIABLO Protein. Nanomaterials (Basel). 2020 Jun 21;10(6). doi: 10.3390/nano10061211. PMID: 32575872; PMCID: PMC7353088.
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Combination of IAP Antagonists and TNF-α-Armed Oncolytic Viruses Induce Tumor Vascular Shutdown and Tumor Regression.

Molecular therapy oncolytics

Beug ST, Pichette SJ, St-Jean M, Holbrook J, Walker DE, LaCasse EC, Korneluk RG.
PMID: 30101187
Mol Ther Oncolytics. 2018 Jun 21;10:28-39. doi: 10.1016/j.omto.2018.06.002. eCollection 2018 Sep 28.

Smac mimetic compounds (SMCs) are anti-cancer drugs that antagonize Inhibitor of Apoptosis proteins, which consequently sensitize cancer cells to death in the presence of proinflammatory ligands such as tumor necrosis factor alpha (TNF-α). SMCs synergize with the attenuated oncolytic...

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Beug ST, Pichette SJ, St-Jean M, et al. Combination of IAP Antagonists and TNF-α-Armed Oncolytic Viruses Induce Tumor Vascular Shutdown and Tumor Regression. Mol Ther Oncolytics. 2018;10:28-39doi: 10.1016/j.omto.2018.06.002.
Beug, S. T., Pichette, S. J., St-Jean, M., Holbrook, J., Walker, D. E., LaCasse, E. C., & Korneluk, R. G. (2018). Combination of IAP Antagonists and TNF-α-Armed Oncolytic Viruses Induce Tumor Vascular Shutdown and Tumor Regression. Molecular therapy oncolytics, 1028-39. https://doi.org/10.1016/j.omto.2018.06.002
Beug, Shawn T, et al. "Combination of IAP Antagonists and TNF-α-Armed Oncolytic Viruses Induce Tumor Vascular Shutdown and Tumor Regression." Molecular therapy oncolytics vol. 10 (2018): 28-39. doi: https://doi.org/10.1016/j.omto.2018.06.002
Beug ST, Pichette SJ, St-Jean M, Holbrook J, Walker DE, LaCasse EC, Korneluk RG. Combination of IAP Antagonists and TNF-α-Armed Oncolytic Viruses Induce Tumor Vascular Shutdown and Tumor Regression. Mol Ther Oncolytics. 2018 Jun 21;10:28-39. doi: 10.1016/j.omto.2018.06.002. eCollection 2018 Sep 28. PMID: 30101187; PMCID: PMC6076221.
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Clinicopathological and functional implications of the inhibitor of apoptosis proteins survivin and XIAP in esophageal cancer.

Oncology letters

Dizdar L, Jünemann LM, Werner TA, Verde PE, Baldus SE, Stoecklein NH, Knoefel WT, Krieg A.
PMID: 29467895
Oncol Lett. 2018 Mar;15(3):3779-3789. doi: 10.3892/ol.2018.7755. Epub 2018 Jan 09.

Based on their overexpression and important roles in progression and therapy-resistance in malignant diseases, the inhibitor of apoptosis protein family (IAP) members, survivin and X-linked inhibitor of apoptosis protein (XIAP), represent attractive candidates for targeted therapy. The present study...

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Dizdar L, Jünemann LM, Werner TA, et al. Clinicopathological and functional implications of the inhibitor of apoptosis proteins survivin and XIAP in esophageal cancer. Oncol Lett. 2018;15(3):3779-3789doi: 10.3892/ol.2018.7755.
Dizdar, L., Jünemann, L. M., Werner, T. A., Verde, P. E., Baldus, S. E., Stoecklein, N. H., Knoefel, W. T., & Krieg, A. (2018). Clinicopathological and functional implications of the inhibitor of apoptosis proteins survivin and XIAP in esophageal cancer. Oncology letters, 15(3), 3779-3789. https://doi.org/10.3892/ol.2018.7755
Dizdar, Levent, et al. "Clinicopathological and functional implications of the inhibitor of apoptosis proteins survivin and XIAP in esophageal cancer." Oncology letters vol. 15,3 (2018): 3779-3789. doi: https://doi.org/10.3892/ol.2018.7755
Dizdar L, Jünemann LM, Werner TA, Verde PE, Baldus SE, Stoecklein NH, Knoefel WT, Krieg A. Clinicopathological and functional implications of the inhibitor of apoptosis proteins survivin and XIAP in esophageal cancer. Oncol Lett. 2018 Mar;15(3):3779-3789. doi: 10.3892/ol.2018.7755. Epub 2018 Jan 09. PMID: 29467895; PMCID: PMC5796362.
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miR-874-3p mitigates cisplatin resistance through modulating NF-κB/inhibitor of apoptosis protein signaling pathway in epithelial ovarian cancer cells.

Molecular and cellular biochemistry

Wang Y, Yan C, Qi J, Liu C, Yu J, Wang H.
PMID: 34716858
Mol Cell Biochem. 2022 Jan;477(1):307-317. doi: 10.1007/s11010-021-04271-6. Epub 2021 Oct 30.

The resistance to cisplatin, the most common platinum chemotherapy drug, may confine the efficacy of treatment in epithelial ovarian cancer patients. Aberrant expression of inhibitor of apoptosis proteins set the stage for resistance to cisplatin in EOC; besides, chemosensitivity...

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Wang Y, Yan C, Qi J, et al. miR-874-3p mitigates cisplatin resistance through modulating NF-κB/inhibitor of apoptosis protein signaling pathway in epithelial ovarian cancer cells. Mol Cell Biochem. 2021;477(1):307-317doi: 10.1007/s11010-021-04271-6.
Wang, Y., Yan, C., Qi, J., Liu, C., Yu, J., & Wang, H. (2022). miR-874-3p mitigates cisplatin resistance through modulating NF-κB/inhibitor of apoptosis protein signaling pathway in epithelial ovarian cancer cells. Molecular and cellular biochemistry, 477(1), 307-317. https://doi.org/10.1007/s11010-021-04271-6
Wang, Ying, et al. "miR-874-3p mitigates cisplatin resistance through modulating NF-κB/inhibitor of apoptosis protein signaling pathway in epithelial ovarian cancer cells." Molecular and cellular biochemistry vol. 477,1 (2022): 307-317. doi: https://doi.org/10.1007/s11010-021-04271-6
Wang Y, Yan C, Qi J, Liu C, Yu J, Wang H. miR-874-3p mitigates cisplatin resistance through modulating NF-κB/inhibitor of apoptosis protein signaling pathway in epithelial ovarian cancer cells. Mol Cell Biochem. 2022 Jan;477(1):307-317. doi: 10.1007/s11010-021-04271-6. Epub 2021 Oct 30. PMID: 34716858.
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The Curcumin Analog EF24 is Highly Active Against Chemotherapy- Resistant Melanoma Cells.

Current cancer drug targets

He Y, Li W, Zhang J, Yang Y, Qian Y, Zhou D.
PMID: 33655859
Curr Cancer Drug Targets. 2021;21(7):608-618. doi: 10.2174/1568009621666210303092921.

BACKGROUND: Malignant melanoma (MM) is an aggressive type of skin cancer with a poor prognosis, because MM cells are characterized by unresponsiveness to chemotherapy.OBJECTIVE: In this study, we evaluated the effectiveness of several curcumin analogs on four MM cell...

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He Y, Li W, Zhang J, et al. The Curcumin Analog EF24 is Highly Active Against Chemotherapy- Resistant Melanoma Cells. Curr Cancer Drug Targets. 2021;21(7):608-618doi: 10.2174/1568009621666210303092921.
He, Y., Li, W., Zhang, J., Yang, Y., Qian, Y., & Zhou, D. (2021). The Curcumin Analog EF24 is Highly Active Against Chemotherapy- Resistant Melanoma Cells. Current cancer drug targets, 21(7), 608-618. https://doi.org/10.2174/1568009621666210303092921
He, Yonghan, et al. "The Curcumin Analog EF24 is Highly Active Against Chemotherapy- Resistant Melanoma Cells." Current cancer drug targets vol. 21,7 (2021): 608-618. doi: https://doi.org/10.2174/1568009621666210303092921
He Y, Li W, Zhang J, Yang Y, Qian Y, Zhou D. The Curcumin Analog EF24 is Highly Active Against Chemotherapy- Resistant Melanoma Cells. Curr Cancer Drug Targets. 2021;21(7):608-618. doi: 10.2174/1568009621666210303092921. PMID: 33655859.
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The combination of TRAIL and the Smac mimetic LCL-161 induces an irreversible phenotypic change of MCF-7 breast cancer cells.

Experimental and molecular pathology

Granqvist V, Holmgren C, Larsson C.
PMID: 35007560
Exp Mol Pathol. 2022 Jan 07;104739. doi: 10.1016/j.yexmp.2021.104739. Epub 2022 Jan 07.

BACKGROUND: Breast cancer is the most common malignancy affecting women. Although the prognosis generally is good, a substantial number of patients still suffer from relapse, emphasizing the need for novel treatments. Smac mimetics were developed to facilitate cell death...

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Granqvist V, Holmgren C, Larsson C. The combination of TRAIL and the Smac mimetic LCL-161 induces an irreversible phenotypic change of MCF-7 breast cancer cells. Exp Mol Pathol. 2022;104739doi: 10.1016/j.yexmp.2021.104739.
Granqvist, V., Holmgren, C., & Larsson, C. (2022). The combination of TRAIL and the Smac mimetic LCL-161 induces an irreversible phenotypic change of MCF-7 breast cancer cells. Experimental and molecular pathology, 104739. https://doi.org/10.1016/j.yexmp.2021.104739
Granqvist, Victoria, et al. "The combination of TRAIL and the Smac mimetic LCL-161 induces an irreversible phenotypic change of MCF-7 breast cancer cells." Experimental and molecular pathology vol. (2022): 104739. doi: https://doi.org/10.1016/j.yexmp.2021.104739
Granqvist V, Holmgren C, Larsson C. The combination of TRAIL and the Smac mimetic LCL-161 induces an irreversible phenotypic change of MCF-7 breast cancer cells. Exp Mol Pathol. 2022 Jan 07;104739. doi: 10.1016/j.yexmp.2021.104739. Epub 2022 Jan 07. PMID: 35007560.
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