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Showing 1 to 12 of 922 entries
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Erratum to: Antitumor activity of the ERK inhibitor SCH722984 against BRAF mutant, NRAS mutant and wild-type melanoma.

Molecular cancer

Wong DJ, Robert L, Atefi MS, Lassen A, Avarappatt G, Cerniglia M, Avramis E, Tsoi J, Foulad D, Graeber TG, Comin-Anduix B, Samatar A, Lo RS, Ribas A.
PMID: 26134498
Mol Cancer. 2015 Jul 02;14:128. doi: 10.1186/s12943-015-0393-2.

No abstract available.

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Wong DJ, Robert L, Atefi MS, et al. Erratum to: Antitumor activity of the ERK inhibitor SCH722984 against BRAF mutant, NRAS mutant and wild-type melanoma. Mol Cancer. 2015;14:128doi: 10.1186/s12943-015-0393-2.
Wong, D. J., Robert, L., Atefi, M. S., Lassen, A., Avarappatt, G., Cerniglia, M., Avramis, E., Tsoi, J., Foulad, D., Graeber, T. G., Comin-Anduix, B., Samatar, A., Lo, R. S., & Ribas, A. (2015). Erratum to: Antitumor activity of the ERK inhibitor SCH722984 against BRAF mutant, NRAS mutant and wild-type melanoma. Molecular cancer, 14128. https://doi.org/10.1186/s12943-015-0393-2
Wong, Deborah J L, et al. "Erratum to: Antitumor activity of the ERK inhibitor SCH722984 against BRAF mutant, NRAS mutant and wild-type melanoma." Molecular cancer vol. 14 (2015): 128. doi: https://doi.org/10.1186/s12943-015-0393-2
Wong DJ, Robert L, Atefi MS, Lassen A, Avarappatt G, Cerniglia M, Avramis E, Tsoi J, Foulad D, Graeber TG, Comin-Anduix B, Samatar A, Lo RS, Ribas A. Erratum to: Antitumor activity of the ERK inhibitor SCH722984 against BRAF mutant, NRAS mutant and wild-type melanoma. Mol Cancer. 2015 Jul 02;14:128. doi: 10.1186/s12943-015-0393-2. PMID: 26134498; PMCID: PMC4488977.
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Computational and synthetic studies towards improving rescinnamine as an inducer of MSH2-dependent apoptosis in cancer treatment.

Molecular cancer biology

AbdelHafez EM, Diamanduros A, Negureanu L, Luy Y, Bean JH, Zielke K, Crowe B, Vasilyeva A, Clodfelter JE, Aly OM, Abuo-Rahma GE, Scarpinato KD, Salsbury FR, King SB.
PMID: 25485184
Mol Cancer Biol. 2013;1(1).

We, and others, have previously shown that mismatch repair proteins, in addition to their repair function, contribute to cell death initiation. In response to some drugs, this cell death activity is independent of the repair function of the proteins....

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AbdelHafez EM, Diamanduros A, Negureanu L, et al. Computational and synthetic studies towards improving rescinnamine as an inducer of MSH2-dependent apoptosis in cancer treatment. Mol Cancer Biol. 2013;1(1)
AbdelHafez, E. M., Diamanduros, A., Negureanu, L., Luy, Y., Bean, J. H., Zielke, K., Crowe, B., Vasilyeva, A., Clodfelter, J. E., Aly, O. M., Abuo-Rahma, G. E., Scarpinato, K. D., Salsbury, F. R., & King, S. B. (2013). Computational and synthetic studies towards improving rescinnamine as an inducer of MSH2-dependent apoptosis in cancer treatment. Molecular cancer biology, 1(1), .
AbdelHafez, ElShimaa M N, et al. "Computational and synthetic studies towards improving rescinnamine as an inducer of MSH2-dependent apoptosis in cancer treatment." Molecular cancer biology vol. 1,1 (2013).
AbdelHafez EM, Diamanduros A, Negureanu L, Luy Y, Bean JH, Zielke K, Crowe B, Vasilyeva A, Clodfelter JE, Aly OM, Abuo-Rahma GE, Scarpinato KD, Salsbury FR, King SB. Computational and synthetic studies towards improving rescinnamine as an inducer of MSH2-dependent apoptosis in cancer treatment. Mol Cancer Biol. 2013;1(1). PMID: 25485184; PMCID: PMC4254817.
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Erratum: Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation.

Molecular cancer

Toricelli M, Melo FH, Peres GB, Silva DC, Jasiulionis MG.
PMID: 26297111
Mol Cancer. 2015 Aug 22;14:161. doi: 10.1186/s12943-015-0405-2.

No abstract available.

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Toricelli M, Melo FH, Peres GB, et al. Erratum: Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation. Mol Cancer. 2015;14:161doi: 10.1186/s12943-015-0405-2.
Toricelli, M., Melo, F. H., Peres, G. B., Silva, D. C., & Jasiulionis, M. G. (2015). Erratum: Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation. Molecular cancer, 14161. https://doi.org/10.1186/s12943-015-0405-2
Toricelli, Mariana, et al. "Erratum: Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation." Molecular cancer vol. 14 (2015): 161. doi: https://doi.org/10.1186/s12943-015-0405-2
Toricelli M, Melo FH, Peres GB, Silva DC, Jasiulionis MG. Erratum: Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation. Mol Cancer. 2015 Aug 22;14:161. doi: 10.1186/s12943-015-0405-2. PMID: 26297111; PMCID: PMC4546186.
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Retraction: Inactivation of MAP kinase signalling in Myc transformed cells and rescue by LiCl inhibition of GSK3.

Molecular cancer

Al-Assar O, Crouch DH.
PMID: 15877819
Mol Cancer. 2005 May 06;4(1):17. doi: 10.1186/1476-4598-4-17.

The corresponding author submitted this article 1 to Molecular Cancer on the assumption that the co-author had agreed to the submission. Since this is not the case, the authors are retracting the article. The corresponding author is deeply sorry...

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Al-Assar O, Crouch DH. Retraction: Inactivation of MAP kinase signalling in Myc transformed cells and rescue by LiCl inhibition of GSK3. Mol Cancer. 2005;4(1):17doi: 10.1186/1476-4598-4-17.
Al-Assar, O., & Crouch, D. H. (2005). Retraction: Inactivation of MAP kinase signalling in Myc transformed cells and rescue by LiCl inhibition of GSK3. Molecular cancer, 4(1), 17. https://doi.org/10.1186/1476-4598-4-17
Al-Assar, Osama, and Crouch, Dorothy H. "Retraction: Inactivation of MAP kinase signalling in Myc transformed cells and rescue by LiCl inhibition of GSK3." Molecular cancer vol. 4,1 (2005): 17. doi: https://doi.org/10.1186/1476-4598-4-17
Al-Assar O, Crouch DH. Retraction: Inactivation of MAP kinase signalling in Myc transformed cells and rescue by LiCl inhibition of GSK3. Mol Cancer. 2005 May 06;4(1):17. doi: 10.1186/1476-4598-4-17. PMID: 15877819; PMCID: PMC1097756.
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Expression Regulation of the Metastasis-Promoting Protein InsP3-Kinase-A in Tumor Cells.

Molecular cancer research : MCR

Chang L, Schwarzenbach H, Meyer-Staeckling S, Brandt B, Mayr GW, Weitzel JM, Windhorst S.
PMID: 21460179
Mol Cancer Res. 2011 Apr;9(4):497-506. doi: 10.1158/1541-7786.MCR-10-0556. Epub 2011 Apr 01.

Under physiologic conditions, the inositol-1,4,5-trisphosphate (InsP(3))-metabolizing, F-actin-bundling InsP(3)-kinase-A (ITPKA) is expressed only in neurons. Tumor cells that have gained the ability to express ITPKA show an increased metastatic potential due to the migration-promoting properties of ITPKA. Here we investigated...

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Chang L, Schwarzenbach H, Meyer-Staeckling S, et al. Expression Regulation of the Metastasis-Promoting Protein InsP3-Kinase-A in Tumor Cells. Mol Cancer Res. 2011;9(4):497-506doi: 10.1158/1541-7786.MCR-10-0556.
Chang, L., Schwarzenbach, H., Meyer-Staeckling, S., Brandt, B., Mayr, G. W., Weitzel, J. M., & Windhorst, S. (2011). Expression Regulation of the Metastasis-Promoting Protein InsP3-Kinase-A in Tumor Cells. Molecular cancer research : MCR, 9(4), 497-506. https://doi.org/10.1158/1541-7786.MCR-10-0556
Chang, Lydia, et al. "Expression Regulation of the Metastasis-Promoting Protein InsP3-Kinase-A in Tumor Cells." Molecular cancer research : MCR vol. 9,4 (2011): 497-506. doi: https://doi.org/10.1158/1541-7786.MCR-10-0556
Chang L, Schwarzenbach H, Meyer-Staeckling S, Brandt B, Mayr GW, Weitzel JM, Windhorst S. Expression Regulation of the Metastasis-Promoting Protein InsP3-Kinase-A in Tumor Cells. Mol Cancer Res. 2011 Apr;9(4):497-506. doi: 10.1158/1541-7786.MCR-10-0556. Epub 2011 Apr 01. PMID: 21460179.
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Correction to: Histone demethylase KDM4D promotes gastrointestinal stromal tumor progression through HIF1β/VEGFA signalling.

Molecular cancer

Hu F, Li H, Liu L, Xu F, Lai S, Luo X, Hu J, Yang X.
PMID: 30213277
Mol Cancer. 2018 Sep 13;17(1):135. doi: 10.1186/s12943-018-0885-y.

After the publication of this work [1] an error was noticed in Fig. 7e, in which the incorrect information is shown. The updated figure included in this correction now shows the quantification of tumor microvessel density. This correction does...

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Hu F, Li H, Liu L, et al. Correction to: Histone demethylase KDM4D promotes gastrointestinal stromal tumor progression through HIF1β/VEGFA signalling. Mol Cancer. 2018;17(1):135doi: 10.1186/s12943-018-0885-y.
Hu, F., Li, H., Liu, L., Xu, F., Lai, S., Luo, X., Hu, J., & Yang, X. (2018). Correction to: Histone demethylase KDM4D promotes gastrointestinal stromal tumor progression through HIF1β/VEGFA signalling. Molecular cancer, 17(1), 135. https://doi.org/10.1186/s12943-018-0885-y
Hu, Fuqing, et al. "Correction to: Histone demethylase KDM4D promotes gastrointestinal stromal tumor progression through HIF1β/VEGFA signalling." Molecular cancer vol. 17,1 (2018): 135. doi: https://doi.org/10.1186/s12943-018-0885-y
Hu F, Li H, Liu L, Xu F, Lai S, Luo X, Hu J, Yang X. Correction to: Histone demethylase KDM4D promotes gastrointestinal stromal tumor progression through HIF1β/VEGFA signalling. Mol Cancer. 2018 Sep 13;17(1):135. doi: 10.1186/s12943-018-0885-y. PMID: 30213277; PMCID: PMC6137922.
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Correction: PRIMA-1Met/APR-246 Displays High Antitumor Activity in Multiple Myeloma by Induction of p73 and Noxa.

Molecular cancer therapeutics

[No authors listed]
PMID: 29717080
Mol Cancer Ther. 2018 May;17(5):1143. doi: 10.1158/1535-7163.MCT-18-0096.

No abstract available.

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Correction: PRIMA-1Met/APR-246 Displays High Antitumor Activity in Multiple Myeloma by Induction of p73 and Noxa. Mol Cancer Ther. 2018;17(5):1143doi: 10.1158/1535-7163.MCT-18-0096.
(2018). Correction: PRIMA-1Met/APR-246 Displays High Antitumor Activity in Multiple Myeloma by Induction of p73 and Noxa. Molecular cancer therapeutics, 17(5), 1143. https://doi.org/10.1158/1535-7163.MCT-18-0096
"Correction: PRIMA-1Met/APR-246 Displays High Antitumor Activity in Multiple Myeloma by Induction of p73 and Noxa." Molecular cancer therapeutics vol. 17,5 (2018): 1143. doi: https://doi.org/10.1158/1535-7163.MCT-18-0096
Correction: PRIMA-1Met/APR-246 Displays High Antitumor Activity in Multiple Myeloma by Induction of p73 and Noxa. Mol Cancer Ther. 2018 May;17(5):1143. doi: 10.1158/1535-7163.MCT-18-0096. PMID: 29717080.
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Correction to: MicroRNA-30d promotes angiogenesis and tumor growth via MYPT1/c-JUN/VEGFA pathway and predicts aggressive outcome in prostate cancer.

Molecular cancer

Lin ZY, Chen G, Zhang YQ, He HC, Liang YX, Ye JH, Liang YK, Mo RJ, Lu JM, Zhuo YJ, Zheng Y, Jiang FN, Han ZD, Wu SL, Zhong WD, Wu CL.
PMID: 31387585
Mol Cancer. 2019 Aug 06;18(1):122. doi: 10.1186/s12943-019-1051-x.

After publication of the article [1], the author reported that this article contained some errors.

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Lin ZY, Chen G, Zhang YQ, et al. Correction to: MicroRNA-30d promotes angiogenesis and tumor growth via MYPT1/c-JUN/VEGFA pathway and predicts aggressive outcome in prostate cancer. Mol Cancer. 2019;18(1):122doi: 10.1186/s12943-019-1051-x.
Lin, Z. Y., Chen, G., Zhang, Y. Q., He, H. C., Liang, Y. X., Ye, J. H., Liang, Y. K., Mo, R. J., Lu, J. M., Zhuo, Y. J., Zheng, Y., Jiang, F. N., Han, Z. D., Wu, S. L., Zhong, W. D., & Wu, C. L. (2019). Correction to: MicroRNA-30d promotes angiogenesis and tumor growth via MYPT1/c-JUN/VEGFA pathway and predicts aggressive outcome in prostate cancer. Molecular cancer, 18(1), 122. https://doi.org/10.1186/s12943-019-1051-x
Lin, Zhuo-Yuan, et al. "Correction to: MicroRNA-30d promotes angiogenesis and tumor growth via MYPT1/c-JUN/VEGFA pathway and predicts aggressive outcome in prostate cancer." Molecular cancer vol. 18,1 (2019): 122. doi: https://doi.org/10.1186/s12943-019-1051-x
Lin ZY, Chen G, Zhang YQ, He HC, Liang YX, Ye JH, Liang YK, Mo RJ, Lu JM, Zhuo YJ, Zheng Y, Jiang FN, Han ZD, Wu SL, Zhong WD, Wu CL. Correction to: MicroRNA-30d promotes angiogenesis and tumor growth via MYPT1/c-JUN/VEGFA pathway and predicts aggressive outcome in prostate cancer. Mol Cancer. 2019 Aug 06;18(1):122. doi: 10.1186/s12943-019-1051-x. PMID: 31387585; PMCID: PMC6683342.
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Editor's Note: Ursolic Acid Inhibits STAT3 Activation Pathway Leading to Suppression of Proliferation and Chemosensitization of Human Multiple Myeloma Cells.

Molecular cancer research : MCR

[No authors listed]
PMID: 30181206
Mol Cancer Res. 2018 Sep;16(9):1442. doi: 10.1158/1541-7786.MCR-18-0819.

No abstract available.

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Editor's Note: Ursolic Acid Inhibits STAT3 Activation Pathway Leading to Suppression of Proliferation and Chemosensitization of Human Multiple Myeloma Cells. Mol Cancer Res. 2018;16(9):1442doi: 10.1158/1541-7786.MCR-18-0819.
(2018). Editor's Note: Ursolic Acid Inhibits STAT3 Activation Pathway Leading to Suppression of Proliferation and Chemosensitization of Human Multiple Myeloma Cells. Molecular cancer research : MCR, 16(9), 1442. https://doi.org/10.1158/1541-7786.MCR-18-0819
"Editor's Note: Ursolic Acid Inhibits STAT3 Activation Pathway Leading to Suppression of Proliferation and Chemosensitization of Human Multiple Myeloma Cells." Molecular cancer research : MCR vol. 16,9 (2018): 1442. doi: https://doi.org/10.1158/1541-7786.MCR-18-0819
Editor's Note: Ursolic Acid Inhibits STAT3 Activation Pathway Leading to Suppression of Proliferation and Chemosensitization of Human Multiple Myeloma Cells. Mol Cancer Res. 2018 Sep;16(9):1442. doi: 10.1158/1541-7786.MCR-18-0819. PMID: 30181206.
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Retraction: Nek6 Mediates Human Cancer Cell Transformation and Is a Potential Cancer Therapeutic Target.

Molecular cancer research : MCR

[No authors listed]
PMID: 28250205
Mol Cancer Res. 2017 Mar;15(3):358. doi: 10.1158/1541-7786.MCR-16-0440. Epub 2017 Feb 28.

No abstract available.

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Retraction: Nek6 Mediates Human Cancer Cell Transformation and Is a Potential Cancer Therapeutic Target. Mol Cancer Res. 2017;15(3):358doi: 10.1158/1541-7786.MCR-16-0440.
(2017). Retraction: Nek6 Mediates Human Cancer Cell Transformation and Is a Potential Cancer Therapeutic Target. Molecular cancer research : MCR, 15(3), 358. https://doi.org/10.1158/1541-7786.MCR-16-0440
"Retraction: Nek6 Mediates Human Cancer Cell Transformation and Is a Potential Cancer Therapeutic Target." Molecular cancer research : MCR vol. 15,3 (2017): 358. doi: https://doi.org/10.1158/1541-7786.MCR-16-0440
Retraction: Nek6 Mediates Human Cancer Cell Transformation and Is a Potential Cancer Therapeutic Target. Mol Cancer Res. 2017 Mar;15(3):358. doi: 10.1158/1541-7786.MCR-16-0440. Epub 2017 Feb 28. PMID: 28250205.
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Multi-omics Approach Reveals Distinct Differences in Left- and Right-Sided Colon Cancer.

Molecular cancer research : MCR

Hu W, Yang Y, Li X, Huang M, Xu F, Ge W, Zhang S, Zheng S.
PMID: 29187560
Mol Cancer Res. 2018 Mar;16(3):476-485. doi: 10.1158/1541-7786.MCR-17-0483. Epub 2017 Nov 29.

Increasing evidence suggests that left-sided colon cancer (LCC) and right-sided colon cancer (RCC) are emerging as two different colorectal cancer types with distinct clinical characteristics. However, the discrepancy in the underlying molecular event between these types of cancer has...

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Hu W, Yang Y, Li X, et al. Multi-omics Approach Reveals Distinct Differences in Left- and Right-Sided Colon Cancer. Mol Cancer Res. 2017;16(3):476-485doi: 10.1158/1541-7786.MCR-17-0483.
Hu, W., Yang, Y., Li, X., Huang, M., Xu, F., Ge, W., Zhang, S., & Zheng, S. (2018). Multi-omics Approach Reveals Distinct Differences in Left- and Right-Sided Colon Cancer. Molecular cancer research : MCR, 16(3), 476-485. https://doi.org/10.1158/1541-7786.MCR-17-0483
Hu, Wangxiong, et al. "Multi-omics Approach Reveals Distinct Differences in Left- and Right-Sided Colon Cancer." Molecular cancer research : MCR vol. 16,3 (2018): 476-485. doi: https://doi.org/10.1158/1541-7786.MCR-17-0483
Hu W, Yang Y, Li X, Huang M, Xu F, Ge W, Zhang S, Zheng S. Multi-omics Approach Reveals Distinct Differences in Left- and Right-Sided Colon Cancer. Mol Cancer Res. 2018 Mar;16(3):476-485. doi: 10.1158/1541-7786.MCR-17-0483. Epub 2017 Nov 29. PMID: 29187560.
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Retraction: MiR-125b Increases Nasopharyngeal Carcinoma Radioresistance By Targeting A20/NF-κB Signaling Pathway.

Molecular cancer therapeutics

Li LN, Xiao T, Yi HM, Zheng Z, Qu JQ, Huang W, Ye X, Yi H, Lu SS, Li XH, Xiao ZQ.
PMID: 30389812
Mol Cancer Ther. 2018 Nov;17(11):2490. doi: 10.1158/1535-7163.MCT-18-0938.

No abstract available.

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Li LN, Xiao T, Yi HM, et al. Retraction: MiR-125b Increases Nasopharyngeal Carcinoma Radioresistance By Targeting A20/NF-κB Signaling Pathway. Mol Cancer Ther. 2018;17(11):2490doi: 10.1158/1535-7163.MCT-18-0938.
Li, L. N., Xiao, T., Yi, H. M., Zheng, Z., Qu, J. Q., Huang, W., Ye, X., Yi, H., Lu, S. S., Li, X. H., & Xiao, Z. Q. (2018). Retraction: MiR-125b Increases Nasopharyngeal Carcinoma Radioresistance By Targeting A20/NF-κB Signaling Pathway. Molecular cancer therapeutics, 17(11), 2490. https://doi.org/10.1158/1535-7163.MCT-18-0938
Li, Li-Na, et al. "Retraction: MiR-125b Increases Nasopharyngeal Carcinoma Radioresistance By Targeting A20/NF-κB Signaling Pathway." Molecular cancer therapeutics vol. 17,11 (2018): 2490. doi: https://doi.org/10.1158/1535-7163.MCT-18-0938
Li LN, Xiao T, Yi HM, Zheng Z, Qu JQ, Huang W, Ye X, Yi H, Lu SS, Li XH, Xiao ZQ. Retraction: MiR-125b Increases Nasopharyngeal Carcinoma Radioresistance By Targeting A20/NF-κB Signaling Pathway. Mol Cancer Ther. 2018 Nov;17(11):2490. doi: 10.1158/1535-7163.MCT-18-0938. PMID: 30389812.
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