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Cancer research meets evolutionary biology.

Evolutionary applications

Pepper JW, Scott Findlay C, Kassen R, Spencer SL, Maley CC.
PMID: 25567847
Evol Appl. 2009 Feb;2(1):62-70. doi: 10.1111/j.1752-4571.2008.00063.x.

There is increasing evidence that Darwin's theory of evolution by natural selection provides insights into the etiology and treatment of cancer. On a microscopic scale, neoplastic cells meet the conditions for evolution by Darwinian selection: cell reproduction with heritable...

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Pepper JW, Scott Findlay C, Kassen R, et al. Cancer research meets evolutionary biology. Evol Appl. 2009;2(1):62-70doi: 10.1111/j.1752-4571.2008.00063.x.
Pepper, J. W., Scott Findlay, C., Kassen, R., Spencer, S. L., & Maley, C. C. (2009). Cancer research meets evolutionary biology. Evolutionary applications, 2(1), 62-70. https://doi.org/10.1111/j.1752-4571.2008.00063.x
Pepper, John W, et al. "Cancer research meets evolutionary biology." Evolutionary applications vol. 2,1 (2009): 62-70. doi: https://doi.org/10.1111/j.1752-4571.2008.00063.x
Pepper JW, Scott Findlay C, Kassen R, Spencer SL, Maley CC. Cancer research meets evolutionary biology. Evol Appl. 2009 Feb;2(1):62-70. doi: 10.1111/j.1752-4571.2008.00063.x. PMID: 25567847; PMCID: PMC3352411.
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Corrigendum: Landscape of the mitochondrial Hsp90 metabolome in tumours.

Nature communications

Chae YC, Angelin A, Lisanti S, Kossenkov AV, Speicher KD, Wang H, Powers JF, Tischler AS, Pacak K, Fliedner S, Michalek RD, Karoly ED, Wallace DC, Languino LR, Speicher DW, Altieri DC.
PMID: 26085380
Nat Commun. 2015 Jun 18;6:7605. doi: 10.1038/ncomms8605.

No abstract available.

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Chae YC, Angelin A, Lisanti S, et al. Corrigendum: Landscape of the mitochondrial Hsp90 metabolome in tumours. Nat Commun. 2015;6:7605doi: 10.1038/ncomms8605.
Chae, Y. C., Angelin, A., Lisanti, S., Kossenkov, A. V., Speicher, K. D., Wang, H., Powers, J. F., Tischler, A. S., Pacak, K., Fliedner, S., Michalek, R. D., Karoly, E. D., Wallace, D. C., Languino, L. R., Speicher, D. W., & Altieri, D. C. (2015). Corrigendum: Landscape of the mitochondrial Hsp90 metabolome in tumours. Nature communications, 67605. https://doi.org/10.1038/ncomms8605
Chae, Young Chan, et al. "Corrigendum: Landscape of the mitochondrial Hsp90 metabolome in tumours." Nature communications vol. 6 (2015): 7605. doi: https://doi.org/10.1038/ncomms8605
Chae YC, Angelin A, Lisanti S, Kossenkov AV, Speicher KD, Wang H, Powers JF, Tischler AS, Pacak K, Fliedner S, Michalek RD, Karoly ED, Wallace DC, Languino LR, Speicher DW, Altieri DC. Corrigendum: Landscape of the mitochondrial Hsp90 metabolome in tumours. Nat Commun. 2015 Jun 18;6:7605. doi: 10.1038/ncomms8605. PMID: 26085380; PMCID: PMC4750482.
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Design of Selective PAK1 Inhibitor G-5555: Improving Properties by Employing an Unorthodox Low-pK a Polar Moiety.

ACS medicinal chemistry letters

Ndubaku CO, Crawford JJ, Drobnick J, Aliagas I, Campbell D, Dong P, Dornan LM, Duron S, Epler J, Gazzard L, Heise CE, Hoeflich KP, Jakubiak D, La H, Lee W, Lin B, Lyssikatos JP, Maksimoska J, Marmorstein R, Murray LJ, O'Brien T, Oh A, Ramaswamy S, Wang W, Zhao X, Zhong Y, Blackwood E, Rudolph J.
PMID: 26713112
ACS Med Chem Lett. 2015 Oct 31;6(12):1241-6. doi: 10.1021/acsmedchemlett.5b00398. eCollection 2015 Dec 10.

Signaling pathways intersecting with the p21-activated kinases (PAKs) play important roles in tumorigenesis and cancer progression. By recognizing that the limitations of FRAX1036 (1) were chiefly associated with the highly basic amine it contained, we devised a mitigation strategy...

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Ndubaku CO, Crawford JJ, Drobnick J, et al. Design of Selective PAK1 Inhibitor G-5555: Improving Properties by Employing an Unorthodox Low-pK a Polar Moiety. ACS Med Chem Lett. 2015;6(12):1241-6doi: 10.1021/acsmedchemlett.5b00398.
Ndubaku, C. O., Crawford, J. J., Drobnick, J., Aliagas, I., Campbell, D., Dong, P., Dornan, L. M., Duron, S., Epler, J., Gazzard, L., Heise, C. E., Hoeflich, K. P., Jakubiak, D., La, H., Lee, W., Lin, B., Lyssikatos, J. P., Maksimoska, J., Marmorstein, R., Murray, L. J., O'Brien, T., Oh, A., Ramaswamy, S., Wang, W., Zhao, X., Zhong, Y., Blackwood, E., & Rudolph, J. (2015). Design of Selective PAK1 Inhibitor G-5555: Improving Properties by Employing an Unorthodox Low-pK a Polar Moiety. ACS medicinal chemistry letters, 6(12), 1241-6. https://doi.org/10.1021/acsmedchemlett.5b00398
Ndubaku, Chudi O, et al. "Design of Selective PAK1 Inhibitor G-5555: Improving Properties by Employing an Unorthodox Low-pK a Polar Moiety." ACS medicinal chemistry letters vol. 6,12 (2015): 1241-6. doi: https://doi.org/10.1021/acsmedchemlett.5b00398
Ndubaku CO, Crawford JJ, Drobnick J, Aliagas I, Campbell D, Dong P, Dornan LM, Duron S, Epler J, Gazzard L, Heise CE, Hoeflich KP, Jakubiak D, La H, Lee W, Lin B, Lyssikatos JP, Maksimoska J, Marmorstein R, Murray LJ, O'Brien T, Oh A, Ramaswamy S, Wang W, Zhao X, Zhong Y, Blackwood E, Rudolph J. Design of Selective PAK1 Inhibitor G-5555: Improving Properties by Employing an Unorthodox Low-pK a Polar Moiety. ACS Med Chem Lett. 2015 Oct 31;6(12):1241-6. doi: 10.1021/acsmedchemlett.5b00398. eCollection 2015 Dec 10. PMID: 26713112; PMCID: PMC4677365.
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Structure and function of the telomeric CST complex.

Computational and structural biotechnology journal

Rice C, Skordalakes E.
PMID: 27239262
Comput Struct Biotechnol J. 2016 Apr 14;14:161-7. doi: 10.1016/j.csbj.2016.04.002. eCollection 2016.

Telomeres comprise the ends of eukaryotic chromosomes and are essential for cell proliferation and genome maintenance. Telomeres are replicated by telomerase, a ribonucleoprotein (RNP) reverse transcriptase, and are maintained primarily by nucleoprotein complexes such as shelterin (TRF1, TRF2, TIN2,...

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Rice C, Skordalakes E. Structure and function of the telomeric CST complex. Comput Struct Biotechnol J. 2016;14:161-7doi: 10.1016/j.csbj.2016.04.002.
Rice, C., & Skordalakes, E. (2016). Structure and function of the telomeric CST complex. Computational and structural biotechnology journal, 14161-7. https://doi.org/10.1016/j.csbj.2016.04.002
Rice, Cory, and Skordalakes, Emmanuel. "Structure and function of the telomeric CST complex." Computational and structural biotechnology journal vol. 14 (2016): 161-7. doi: https://doi.org/10.1016/j.csbj.2016.04.002
Rice C, Skordalakes E. Structure and function of the telomeric CST complex. Comput Struct Biotechnol J. 2016 Apr 14;14:161-7. doi: 10.1016/j.csbj.2016.04.002. eCollection 2016. PMID: 27239262; PMCID: PMC4872678.
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A link between TP53 polymorphisms and metabolism.

Molecular & cellular oncology

Kung CP, Basu S, Murphy ME.
PMID: 27652322
Mol Cell Oncol. 2016 Apr 15;3(4):e1173769. doi: 10.1080/23723556.2016.1173769. eCollection 2016 Jul.

Besides being a critical tumor suppressor, the TP53 gene also plays a role in metabolism and recent studies in humans have implicated the codon 72 polymorphism of TP53 in this role. Using a humanized knock-in mouse model for these...

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Kung CP, Basu S, Murphy ME. A link between TP53 polymorphisms and metabolism. Mol Cell Oncol. 2016;3(4):e1173769doi: 10.1080/23723556.2016.1173769.
Kung, C. P., Basu, S., & Murphy, M. E. (2016). A link between TP53 polymorphisms and metabolism. Molecular & cellular oncology, 3(4), e1173769. https://doi.org/10.1080/23723556.2016.1173769
Kung, Che-Pei, et al. "A link between TP53 polymorphisms and metabolism." Molecular & cellular oncology vol. 3,4 (2016): e1173769. doi: https://doi.org/10.1080/23723556.2016.1173769
Kung CP, Basu S, Murphy ME. A link between TP53 polymorphisms and metabolism. Mol Cell Oncol. 2016 Apr 15;3(4):e1173769. doi: 10.1080/23723556.2016.1173769. eCollection 2016 Jul. PMID: 27652322; PMCID: PMC4972101.
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Mitochondrial biogenesis meets chemoresistance in BRAF-mutant melanoma.

Molecular & cellular oncology

Wu LW, Zhang G, Herlyn M.
PMID: 27652325
Mol Cell Oncol. 2016 May 02;3(4):e1179381. doi: 10.1080/23723556.2016.1179381. eCollection 2016 Jul.

The acquisition of resistance to current mitogen activated protein kinase (MAPK) inhibitors in B-Raf proto-oncogene, serine/threonine kinase (BRAF) mutant melanoma is almost inevitable. Our recent findings identify therapy-induced mitochondrial biogenesis (MitoBiogenesis) and aberrant tumor bioenergetics as therapeutic escape mechanisms...

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Wu LW, Zhang G, Herlyn M. Mitochondrial biogenesis meets chemoresistance in BRAF-mutant melanoma. Mol Cell Oncol. 2016;3(4):e1179381doi: 10.1080/23723556.2016.1179381.
Wu, L. W., Zhang, G., & Herlyn, M. (2016). Mitochondrial biogenesis meets chemoresistance in BRAF-mutant melanoma. Molecular & cellular oncology, 3(4), e1179381. https://doi.org/10.1080/23723556.2016.1179381
Wu, Lawrence W, et al. "Mitochondrial biogenesis meets chemoresistance in BRAF-mutant melanoma." Molecular & cellular oncology vol. 3,4 (2016): e1179381. doi: https://doi.org/10.1080/23723556.2016.1179381
Wu LW, Zhang G, Herlyn M. Mitochondrial biogenesis meets chemoresistance in BRAF-mutant melanoma. Mol Cell Oncol. 2016 May 02;3(4):e1179381. doi: 10.1080/23723556.2016.1179381. eCollection 2016 Jul. PMID: 27652325; PMCID: PMC4972122.
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Crosstalk in skin: melanocytes, keratinocytes, stem cells, and melanoma.

Journal of cell communication and signaling

Wang JX, Fukunaga-Kalabis M, Herlyn M.
PMID: 27553358
J Cell Commun Signal. 2016 Sep;10(3):191-196. doi: 10.1007/s12079-016-0349-3. Epub 2016 Aug 23.

In the vertebrate embryo, melanocytes arise from the neural crest, migrate to and colonize the basal layer within the skin and skin appendages. Post-migratory melanocytes are securely attached to the basement membrane, and their morphology, growth, adhesion, and migration...

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Wang JX, Fukunaga-Kalabis M, Herlyn M. Crosstalk in skin: melanocytes, keratinocytes, stem cells, and melanoma. J Cell Commun Signal. 2016;10(3):191-196doi: 10.1007/s12079-016-0349-3.
Wang, J. X., Fukunaga-Kalabis, M., & Herlyn, M. (2016). Crosstalk in skin: melanocytes, keratinocytes, stem cells, and melanoma. Journal of cell communication and signaling, 10(3), 191-196. https://doi.org/10.1007/s12079-016-0349-3
Wang, Joshua X, et al. "Crosstalk in skin: melanocytes, keratinocytes, stem cells, and melanoma." Journal of cell communication and signaling vol. 10,3 (2016): 191-196. doi: https://doi.org/10.1007/s12079-016-0349-3
Wang JX, Fukunaga-Kalabis M, Herlyn M. Crosstalk in skin: melanocytes, keratinocytes, stem cells, and melanoma. J Cell Commun Signal. 2016 Sep;10(3):191-196. doi: 10.1007/s12079-016-0349-3. Epub 2016 Aug 23. PMID: 27553358; PMCID: PMC5055506.
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Epigenetic synthetic lethality in ovarian clear cell carcinoma: EZH2 and ARID1A mutations.

Molecular & cellular oncology

Bitler BG, Aird KM, Zhang R.
PMID: 27308548
Mol Cell Oncol. 2015 Apr 14;3(1):e1032476. doi: 10.1080/23723556.2015.1032476. eCollection 2016 Jan.

The components of the Switch/Sucrose non-fermentable (SWI/SNF) complex are mutated in approximately 20% of human cancers. The A/T-rich interacting domain 1A (ARID1A) subunit has one of the highest mutation rates. Most notably, ARID1A is mutated in over 50% of...

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Bitler BG, Aird KM, Zhang R. Epigenetic synthetic lethality in ovarian clear cell carcinoma: EZH2 and ARID1A mutations. Mol Cell Oncol. 2015;3(1):e1032476doi: 10.1080/23723556.2015.1032476.
Bitler, B. G., Aird, K. M., & Zhang, R. (2016). Epigenetic synthetic lethality in ovarian clear cell carcinoma: EZH2 and ARID1A mutations. Molecular & cellular oncology, 3(1), e1032476. https://doi.org/10.1080/23723556.2015.1032476
Bitler, Benjamin G, et al. "Epigenetic synthetic lethality in ovarian clear cell carcinoma: EZH2 and ARID1A mutations." Molecular & cellular oncology vol. 3,1 (2016): e1032476. doi: https://doi.org/10.1080/23723556.2015.1032476
Bitler BG, Aird KM, Zhang R. Epigenetic synthetic lethality in ovarian clear cell carcinoma: EZH2 and ARID1A mutations. Mol Cell Oncol. 2015 Apr 14;3(1):e1032476. doi: 10.1080/23723556.2015.1032476. eCollection 2016 Jan. PMID: 27308548; PMCID: PMC4845188.
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Design, Synthesis and Biological Evaluation of β-Carboline Dimers Based on the Structure of Neokauluamine.

Tetrahedron letters

Chatwichien J, Basu S, Murphy ME, Hamann MT, Winkler JD.
PMID: 26257442
Tetrahedron Lett. 2015 Jun 03;56(23):3515-3517. doi: 10.1016/j.tetlet.2015.01.142.

The design, synthesis and biological evaluation (anticancer and antimalarial activity) of bis-β-carbolines, based on the structure of the naturally occurring alkaloid neokauluamine, is described.

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Chatwichien J, Basu S, Murphy ME, et al. Design, Synthesis and Biological Evaluation of β-Carboline Dimers Based on the Structure of Neokauluamine. Tetrahedron Lett. 2015;56(23):3515-3517doi: 10.1016/j.tetlet.2015.01.142.
Chatwichien, J., Basu, S., Murphy, M. E., Hamann, M. T., & Winkler, J. D. (2015). Design, Synthesis and Biological Evaluation of β-Carboline Dimers Based on the Structure of Neokauluamine. Tetrahedron letters, 56(23), 3515-3517. https://doi.org/10.1016/j.tetlet.2015.01.142
Chatwichien, Jaruwan, et al. "Design, Synthesis and Biological Evaluation of β-Carboline Dimers Based on the Structure of Neokauluamine." Tetrahedron letters vol. 56,23 (2015): 3515-3517. doi: https://doi.org/10.1016/j.tetlet.2015.01.142
Chatwichien J, Basu S, Murphy ME, Hamann MT, Winkler JD. Design, Synthesis and Biological Evaluation of β-Carboline Dimers Based on the Structure of Neokauluamine. Tetrahedron Lett. 2015 Jun 03;56(23):3515-3517. doi: 10.1016/j.tetlet.2015.01.142. PMID: 26257442; PMCID: PMC4527524.
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Pathological mobilization and activities of dendritic cells in tumor-bearing hosts: challenges and opportunities for immunotherapy of cancer.

Frontiers in immunology

Tesone AJ, Svoronos N, Allegrezza MJ, Conejo-Garcia JR.
PMID: 24339824
Front Immunol. 2013 Dec 10;4:435. doi: 10.3389/fimmu.2013.00435.

A common characteristic of solid tumors is the pathological recruitment of immunosuppressive myeloid cells, which in certain tumors includes dendritic cells (DCs). DCs are of particular interest in the field of cancer immunotherapy because they induce potent and highly...

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Tesone AJ, Svoronos N, Allegrezza MJ, et al. Pathological mobilization and activities of dendritic cells in tumor-bearing hosts: challenges and opportunities for immunotherapy of cancer. Front Immunol. 2013;4:435doi: 10.3389/fimmu.2013.00435.
Tesone, A. J., Svoronos, N., Allegrezza, M. J., & Conejo-Garcia, J. R. (2013). Pathological mobilization and activities of dendritic cells in tumor-bearing hosts: challenges and opportunities for immunotherapy of cancer. Frontiers in immunology, 4435. https://doi.org/10.3389/fimmu.2013.00435
Tesone, Amelia J, et al. "Pathological mobilization and activities of dendritic cells in tumor-bearing hosts: challenges and opportunities for immunotherapy of cancer." Frontiers in immunology vol. 4 (2013): 435. doi: https://doi.org/10.3389/fimmu.2013.00435
Tesone AJ, Svoronos N, Allegrezza MJ, Conejo-Garcia JR. Pathological mobilization and activities of dendritic cells in tumor-bearing hosts: challenges and opportunities for immunotherapy of cancer. Front Immunol. 2013 Dec 10;4:435. doi: 10.3389/fimmu.2013.00435. PMID: 24339824; PMCID: PMC3857526.
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Establishing Human Skin Grafts in Mice as Model for Melanoma Progression.

Methods in molecular biology (Clifton, N.J.)

Li L, Fukunaga-Kalabis M, Herlyn M.
PMID: 26659798
Methods Mol Biol. 2015 Dec 13; doi: 10.1007/7651_2015_301. Epub 2015 Dec 13.

Technological advances often dictate progress in cancer research. Melanoma research has been considerably influenced by implementation of novel techniques and has contributed to our understanding of the mechanism of tumor progression. The three-dimensional (3D) human skin reconstruct is an...

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Li L, Fukunaga-Kalabis M, Herlyn M. Establishing Human Skin Grafts in Mice as Model for Melanoma Progression. Methods Mol Biol. 2015;doi: 10.1007/7651_2015_301.
Li, L., Fukunaga-Kalabis, M., & Herlyn, M. (2015). Establishing Human Skin Grafts in Mice as Model for Melanoma Progression. Methods in molecular biology (Clifton, N.J.), . https://doi.org/10.1007/7651_2015_301
Li, Ling, et al. "Establishing Human Skin Grafts in Mice as Model for Melanoma Progression." Methods in molecular biology (Clifton, N.J.) vol. (2015). doi: https://doi.org/10.1007/7651_2015_301
Li L, Fukunaga-Kalabis M, Herlyn M. Establishing Human Skin Grafts in Mice as Model for Melanoma Progression. Methods Mol Biol. 2015 Dec 13; doi: 10.1007/7651_2015_301. Epub 2015 Dec 13. PMID: 26659798; PMCID: PMC5148711.
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Role of EZH2 in Epithelial Ovarian Cancer: From Biological Insights to Therapeutic Target.

Frontiers in oncology

Li H, Zhang R.
PMID: 23494175
Front Oncol. 2013 Mar 13;3:47. doi: 10.3389/fonc.2013.00047. eCollection 2013.

EZH2 is the catalytic subunit of polycomb repressive complex 2 (PRC2), which generates a methylation epigenetic mark at lysine 27 residue of histone H3 (H3K27me3) to silence gene expression. EZH2 target genes are involved in a variety of biological...

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Li H, Zhang R. Role of EZH2 in Epithelial Ovarian Cancer: From Biological Insights to Therapeutic Target. Front Oncol. 2013;3:47doi: 10.3389/fonc.2013.00047.
Li, H., & Zhang, R. (2013). Role of EZH2 in Epithelial Ovarian Cancer: From Biological Insights to Therapeutic Target. Frontiers in oncology, 347. https://doi.org/10.3389/fonc.2013.00047
Li, Hua, and Zhang, Rugang. "Role of EZH2 in Epithelial Ovarian Cancer: From Biological Insights to Therapeutic Target." Frontiers in oncology vol. 3 (2013): 47. doi: https://doi.org/10.3389/fonc.2013.00047
Li H, Zhang R. Role of EZH2 in Epithelial Ovarian Cancer: From Biological Insights to Therapeutic Target. Front Oncol. 2013 Mar 13;3:47. doi: 10.3389/fonc.2013.00047. eCollection 2013. PMID: 23494175; PMCID: PMC3595978.
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Showing 1 to 12 of 166 entries