Prognostic assessment of hypoxia and metabolic markers in cervical cancer using automated digital image analysis of immunohistochemistry
Background Hypoxia inducible factor-1 alpha (HIF-1α), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met, carbonic anhydrase 9 (CA9) and glucose transporter 1 (GLUT1). The prognostic significance of hypoxia and metabolic markers is not clearly defined...
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| Published in | Journal of translational medicine Vol. 11; no. 1; p. 185 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
BioMed Central
08.08.2013
BioMed Central Ltd |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1479-5876 1479-5876 |
| DOI | 10.1186/1479-5876-11-185 |
Cover
| Abstract | Background
Hypoxia inducible factor-1 alpha (HIF-1α), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met, carbonic anhydrase 9 (CA9) and glucose transporter 1 (GLUT1). The prognostic significance of hypoxia and metabolic markers is not clearly defined in cervical cancer. Here, we have examined the primary players in the hypoxia signaling pathway, by immunohistochemistry, but confirming their interactions, as well as defining which proteins are associated with outcome.
Methods
The study subjects were comprised of cervical intraepithelial neoplasia (CIN,
n
= 209), carcinoma
in situ
(CIS,
n
= 74), cervical cancer (
n
= 179), and matched nonadjacent normal tissues (
n
= 357). Immunohistochemistry (IHC) was performed to identify HIF-1α, c-Met, CA9, and GLUT1. IHC scoring was performed using automated digital image analysis and the association of hypoxic markers with prognostic outcome was evaluated.
Results
HIF-1α, c-Met, CA9 and GLUT1 expression were higher in cervical cancer than in CIN and normal cervix (all
P
< 0.001). Among these markers, expression of HIF-1α and c-Met were significantly different in FIGO stage (
P
< 0.001 and
P
= 0.019, respectively) and patients with lymph node metastasis (
P
< 0.001 and
P
= 0.010, respectively). HIF-1α expression was correlated with c-Met expression in cervical cancer (
P
< 0.001). High expression of HIF-1α and c-Met showed worse 5-year overall survival rate (
P
= 0.047 and
P
= 0.005, respectively) than low expression group, but CA9 and GLUT1 did not show significant survival difference. After adjusting the prognostic covariates, c-Met was found to be an independent risk factor (HR=3.27; 95% CI, 1.05-10.23,
P
= 0.041) for overall survival in cervical cancer.
Conclusions
We demonstrate that c-Met correlates with HIF-1α and is a poor prognostic factor in survival in cervical cancer. |
|---|---|
| AbstractList | Hypoxia inducible factor-1 alpha (HIF-1α), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met, carbonic anhydrase 9 (CA9) and glucose transporter 1 (GLUT1). The prognostic significance of hypoxia and metabolic markers is not clearly defined in cervical cancer. Here, we have examined the primary players in the hypoxia signaling pathway, by immunohistochemistry, but confirming their interactions, as well as defining which proteins are associated with outcome.BACKGROUNDHypoxia inducible factor-1 alpha (HIF-1α), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met, carbonic anhydrase 9 (CA9) and glucose transporter 1 (GLUT1). The prognostic significance of hypoxia and metabolic markers is not clearly defined in cervical cancer. Here, we have examined the primary players in the hypoxia signaling pathway, by immunohistochemistry, but confirming their interactions, as well as defining which proteins are associated with outcome.The study subjects were comprised of cervical intraepithelial neoplasia (CIN, n = 209), carcinoma in situ (CIS, n = 74), cervical cancer (n = 179), and matched nonadjacent normal tissues (n = 357). Immunohistochemistry (IHC) was performed to identify HIF-1α, c-Met, CA9, and GLUT1. IHC scoring was performed using automated digital image analysis and the association of hypoxic markers with prognostic outcome was evaluated.METHODSThe study subjects were comprised of cervical intraepithelial neoplasia (CIN, n = 209), carcinoma in situ (CIS, n = 74), cervical cancer (n = 179), and matched nonadjacent normal tissues (n = 357). Immunohistochemistry (IHC) was performed to identify HIF-1α, c-Met, CA9, and GLUT1. IHC scoring was performed using automated digital image analysis and the association of hypoxic markers with prognostic outcome was evaluated.HIF-1α, c-Met, CA9 and GLUT1 expression were higher in cervical cancer than in CIN and normal cervix (all P < 0.001). Among these markers, expression of HIF-1α and c-Met were significantly different in FIGO stage (P < 0.001 and P = 0.019, respectively) and patients with lymph node metastasis (P < 0.001 and P = 0.010, respectively). HIF-1α expression was correlated with c-Met expression in cervical cancer (P < 0.001). High expression of HIF-1α and c-Met showed worse 5-year overall survival rate (P = 0.047 and P = 0.005, respectively) than low expression group, but CA9 and GLUT1 did not show significant survival difference. After adjusting the prognostic covariates, c-Met was found to be an independent risk factor (HR=3.27; 95% CI, 1.05-10.23, P = 0.041) for overall survival in cervical cancer.RESULTSHIF-1α, c-Met, CA9 and GLUT1 expression were higher in cervical cancer than in CIN and normal cervix (all P < 0.001). Among these markers, expression of HIF-1α and c-Met were significantly different in FIGO stage (P < 0.001 and P = 0.019, respectively) and patients with lymph node metastasis (P < 0.001 and P = 0.010, respectively). HIF-1α expression was correlated with c-Met expression in cervical cancer (P < 0.001). High expression of HIF-1α and c-Met showed worse 5-year overall survival rate (P = 0.047 and P = 0.005, respectively) than low expression group, but CA9 and GLUT1 did not show significant survival difference. After adjusting the prognostic covariates, c-Met was found to be an independent risk factor (HR=3.27; 95% CI, 1.05-10.23, P = 0.041) for overall survival in cervical cancer.We demonstrate that c-Met correlates with HIF-1α and is a poor prognostic factor in survival in cervical cancer.CONCLUSIONSWe demonstrate that c-Met correlates with HIF-1α and is a poor prognostic factor in survival in cervical cancer. Hypoxia inducible factor-1 alpha (HIF-1[alpha]), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met, carbonic anhydrase 9 (CA9) and glucose transporter 1 (GLUT1). The prognostic significance of hypoxia and metabolic markers is not clearly defined in cervical cancer. Here, we have examined the primary players in the hypoxia signaling pathway, by immunohistochemistry, but confirming their interactions, as well as defining which proteins are associated with outcome. The study subjects were comprised of cervical intraepithelial neoplasia (CIN, n = 209), carcinoma in situ (CIS, n = 74), cervical cancer (n = 179), and matched nonadjacent normal tissues (n = 357). Immunohistochemistry (IHC) was performed to identify HIF-1[alpha], c-Met, CA9, and GLUT1. IHC scoring was performed using automated digital image analysis and the association of hypoxic markers with prognostic outcome was evaluated. HIF-1[alpha], c-Met, CA9 and GLUT1 expression were higher in cervical cancer than in CIN and normal cervix (all P < 0.001). Among these markers, expression of HIF-1[alpha] and c-Met were significantly different in FIGO stage (P < 0.001 and P = 0.019, respectively) and patients with lymph node metastasis (P < 0.001 and P = 0.010, respectively). HIF-1[alpha] expression was correlated with c-Met expression in cervical cancer (P < 0.001). High expression of HIF-1[alpha] and c-Met showed worse 5-year overall survival rate (P = 0.047 and P = 0.005, respectively) than low expression group, but CA9 and GLUT1 did not show significant survival difference. After adjusting the prognostic covariates, c-Met was found to be an independent risk factor (HR=3.27; 95% CI, 1.05-10.23, P = 0.041) for overall survival in cervical cancer. We demonstrate that c-Met correlates with HIF-1[alpha] and is a poor prognostic factor in survival in cervical cancer. Background Hypoxia inducible factor-1 alpha (HIF-1[alpha]), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met, carbonic anhydrase 9 (CA9) and glucose transporter 1 (GLUT1). The prognostic significance of hypoxia and metabolic markers is not clearly defined in cervical cancer. Here, we have examined the primary players in the hypoxia signaling pathway, by immunohistochemistry, but confirming their interactions, as well as defining which proteins are associated with outcome. Methods The study subjects were comprised of cervical intraepithelial neoplasia (CIN, n = 209), carcinoma in situ (CIS, n = 74), cervical cancer (n = 179), and matched nonadjacent normal tissues (n = 357). Immunohistochemistry (IHC) was performed to identify HIF-1[alpha], c-Met, CA9, and GLUT1. IHC scoring was performed using automated digital image analysis and the association of hypoxic markers with prognostic outcome was evaluated. Results HIF-1[alpha], c-Met, CA9 and GLUT1 expression were higher in cervical cancer than in CIN and normal cervix (all P < 0.001). Among these markers, expression of HIF-1[alpha] and c-Met were significantly different in FIGO stage (P < 0.001 and P = 0.019, respectively) and patients with lymph node metastasis (P < 0.001 and P = 0.010, respectively). HIF-1[alpha] expression was correlated with c-Met expression in cervical cancer (P < 0.001). High expression of HIF-1[alpha] and c-Met showed worse 5-year overall survival rate (P = 0.047 and P = 0.005, respectively) than low expression group, but CA9 and GLUT1 did not show significant survival difference. After adjusting the prognostic covariates, c-Met was found to be an independent risk factor (HR=3.27; 95% CI, 1.05-10.23, P = 0.041) for overall survival in cervical cancer. Conclusions We demonstrate that c-Met correlates with HIF-1[alpha] and is a poor prognostic factor in survival in cervical cancer. Keywords: HIF-1[alpha], c-Met, Cervical cancer, Prognosis, Automated digital image analysis Background Hypoxia inducible factor-1 alpha (HIF-1α), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met, carbonic anhydrase 9 (CA9) and glucose transporter 1 (GLUT1). The prognostic significance of hypoxia and metabolic markers is not clearly defined in cervical cancer. Here, we have examined the primary players in the hypoxia signaling pathway, by immunohistochemistry, but confirming their interactions, as well as defining which proteins are associated with outcome. Methods The study subjects were comprised of cervical intraepithelial neoplasia (CIN, n = 209), carcinoma in situ (CIS, n = 74), cervical cancer ( n = 179), and matched nonadjacent normal tissues ( n = 357). Immunohistochemistry (IHC) was performed to identify HIF-1α, c-Met, CA9, and GLUT1. IHC scoring was performed using automated digital image analysis and the association of hypoxic markers with prognostic outcome was evaluated. Results HIF-1α, c-Met, CA9 and GLUT1 expression were higher in cervical cancer than in CIN and normal cervix (all P < 0.001). Among these markers, expression of HIF-1α and c-Met were significantly different in FIGO stage ( P < 0.001 and P = 0.019, respectively) and patients with lymph node metastasis ( P < 0.001 and P = 0.010, respectively). HIF-1α expression was correlated with c-Met expression in cervical cancer ( P < 0.001). High expression of HIF-1α and c-Met showed worse 5-year overall survival rate ( P = 0.047 and P = 0.005, respectively) than low expression group, but CA9 and GLUT1 did not show significant survival difference. After adjusting the prognostic covariates, c-Met was found to be an independent risk factor (HR=3.27; 95% CI, 1.05-10.23, P = 0.041) for overall survival in cervical cancer. Conclusions We demonstrate that c-Met correlates with HIF-1α and is a poor prognostic factor in survival in cervical cancer. Doc number: 185 Abstract Background: Hypoxia inducible factor-1 alpha (HIF-1α), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met, carbonic anhydrase 9 (CA9) and glucose transporter 1 (GLUT1). The prognostic significance of hypoxia and metabolic markers is not clearly defined in cervical cancer. Here, we have examined the primary players in the hypoxia signaling pathway, by immunohistochemistry, but confirming their interactions, as well as defining which proteins are associated with outcome. Methods: The study subjects were comprised of cervical intraepithelial neoplasia (CIN, n = 209), carcinoma in situ (CIS, n = 74), cervical cancer (n = 179), and matched nonadjacent normal tissues (n = 357). Immunohistochemistry (IHC) was performed to identify HIF-1α, c-Met, CA9, and GLUT1. IHC scoring was performed using automated digital image analysis and the association of hypoxic markers with prognostic outcome was evaluated. Results: HIF-1α, c-Met, CA9 and GLUT1 expression were higher in cervical cancer than in CIN and normal cervix (all P < 0.001). Among these markers, expression of HIF-1α and c-Met were significantly different in FIGO stage (P < 0.001 and P = 0.019, respectively) and patients with lymph node metastasis (P < 0.001 and P = 0.010, respectively). HIF-1α expression was correlated with c-Met expression in cervical cancer (P < 0.001). High expression of HIF-1α and c-Met showed worse 5-year overall survival rate (P = 0.047 and P = 0.005, respectively) than low expression group, but CA9 and GLUT1 did not show significant survival difference. After adjusting the prognostic covariates, c-Met was found to be an independent risk factor (HR=3.27; 95% CI, 1.05-10.23, P = 0.041) for overall survival in cervical cancer. Conclusions: We demonstrate that c-Met correlates with HIF-1α and is a poor prognostic factor in survival in cervical cancer. Hypoxia inducible factor-1 alpha (HIF-1α), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met, carbonic anhydrase 9 (CA9) and glucose transporter 1 (GLUT1). The prognostic significance of hypoxia and metabolic markers is not clearly defined in cervical cancer. Here, we have examined the primary players in the hypoxia signaling pathway, by immunohistochemistry, but confirming their interactions, as well as defining which proteins are associated with outcome. The study subjects were comprised of cervical intraepithelial neoplasia (CIN, n = 209), carcinoma in situ (CIS, n = 74), cervical cancer (n = 179), and matched nonadjacent normal tissues (n = 357). Immunohistochemistry (IHC) was performed to identify HIF-1α, c-Met, CA9, and GLUT1. IHC scoring was performed using automated digital image analysis and the association of hypoxic markers with prognostic outcome was evaluated. HIF-1α, c-Met, CA9 and GLUT1 expression were higher in cervical cancer than in CIN and normal cervix (all P < 0.001). Among these markers, expression of HIF-1α and c-Met were significantly different in FIGO stage (P < 0.001 and P = 0.019, respectively) and patients with lymph node metastasis (P < 0.001 and P = 0.010, respectively). HIF-1α expression was correlated with c-Met expression in cervical cancer (P < 0.001). High expression of HIF-1α and c-Met showed worse 5-year overall survival rate (P = 0.047 and P = 0.005, respectively) than low expression group, but CA9 and GLUT1 did not show significant survival difference. After adjusting the prognostic covariates, c-Met was found to be an independent risk factor (HR=3.27; 95% CI, 1.05-10.23, P = 0.041) for overall survival in cervical cancer. We demonstrate that c-Met correlates with HIF-1α and is a poor prognostic factor in survival in cervical cancer. |
| Audience | Academic |
| Author | Kim, Bo Wook Chung, Joon-Yong Hewitt, Stephen M Cho, Hanbyoul Conway, Catherine Ylaya, Kris Kim, Jae-Hoon |
| AuthorAffiliation | 1 Tissue Array Research Program & Applied Molecular Pathology Lab, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA 2 Department of Obstetrics and Gynecology, Gangnam Severance Hospital, Yonsei University College of Medicine, 146-92 Dogok-Dong, Gangnam-Gu, Seoul 135-720, Korea 3 Department of Obstetrics and Gynecology, Korea Cancer Center Hospital, Seoul 139-706, Korea |
| AuthorAffiliation_xml | – name: 2 Department of Obstetrics and Gynecology, Gangnam Severance Hospital, Yonsei University College of Medicine, 146-92 Dogok-Dong, Gangnam-Gu, Seoul 135-720, Korea – name: 3 Department of Obstetrics and Gynecology, Korea Cancer Center Hospital, Seoul 139-706, Korea – name: 1 Tissue Array Research Program & Applied Molecular Pathology Lab, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA |
| Author_xml | – sequence: 1 givenname: Bo Wook surname: Kim fullname: Kim, Bo Wook organization: Tissue Array Research Program & Applied Molecular Pathology Lab, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Department of Obstetrics and Gynecology, Korea Cancer Center Hospital – sequence: 2 givenname: Hanbyoul surname: Cho fullname: Cho, Hanbyoul organization: Department of Obstetrics and Gynecology, Gangnam Severance Hospital, Yonsei University College of Medicine – sequence: 3 givenname: Joon-Yong surname: Chung fullname: Chung, Joon-Yong organization: Tissue Array Research Program & Applied Molecular Pathology Lab, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health – sequence: 4 givenname: Catherine surname: Conway fullname: Conway, Catherine organization: Tissue Array Research Program & Applied Molecular Pathology Lab, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health – sequence: 5 givenname: Kris surname: Ylaya fullname: Ylaya, Kris organization: Tissue Array Research Program & Applied Molecular Pathology Lab, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health – sequence: 6 givenname: Jae-Hoon surname: Kim fullname: Kim, Jae-Hoon email: jaehoonkim@yuhs.ac organization: Department of Obstetrics and Gynecology, Gangnam Severance Hospital, Yonsei University College of Medicine – sequence: 7 givenname: Stephen M surname: Hewitt fullname: Hewitt, Stephen M email: genejock@helix.nih.gov organization: Tissue Array Research Program & Applied Molecular Pathology Lab, Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23927384$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1002/pmic.200700199 10.1016/j.cellbi.2009.05.005 10.1016/j.febslet.2007.06.018 10.1016/j.humpath.2005.10.012 10.1007/s00595-011-0027-2 10.1146/annurev.cellbio.15.1.551 10.1158/0008-5472.CAN-06-1147 10.1091/mbc.E06-07-0593 10.1158/0008-5472.CAN-03-3566 10.1186/1471-2407-8-335 10.2353/ajpath.2007.061138 10.1016/j.ejca.2008.09.025 10.1111/j.1365-2559.2005.02322.x 10.1136/jcp.2006.044537 10.1002/ijc.20598 10.1016/j.ygyno.2006.07.040 10.1038/nature04483 10.1186/1479-5876-7-25 10.1016/S0090-8258(02)00073-2 10.1158/1078-0432.CCR-03-0135 10.1245/s10434-007-9435-3 10.1007/s10555-007-9062-2 10.1111/j.1349-7006.2008.00828.x 10.1111/j.1349-7006.2006.00220.x 10.1038/20459 10.1006/gyno.2001.6347 10.1007/s00432-005-0068-2 10.1016/j.humpath.2009.05.010 10.1186/1471-2407-5-84 10.1016/j.ygyno.2009.10.062 10.1007/978-1-61779-024-9_8 10.1007/s00109-007-0281-3 10.1158/0008-5472.CAN-05-2670 |
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| Copyright | Kim et al.; licensee BioMed Central Ltd. 2013 COPYRIGHT 2013 BioMed Central Ltd. 2013 Kim et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2013 Kim et al.; licensee BioMed Central Ltd. 2013 Kim et al.; licensee BioMed Central Ltd. |
| Copyright_xml | – notice: Kim et al.; licensee BioMed Central Ltd. 2013 – notice: COPYRIGHT 2013 BioMed Central Ltd. – notice: 2013 Kim et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. – notice: Copyright © 2013 Kim et al.; licensee BioMed Central Ltd. 2013 Kim et al.; licensee BioMed Central Ltd. |
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| Keywords | Automated digital image analysis HIF-1α c-Met Prognosis Cervical cancer |
| Language | English |
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| References | 10.1186/1479-5876-11-185-B15 10.1186/1479-5876-11-185-B14 10.1186/1479-5876-11-185-B36 10.1186/1479-5876-11-185-B13 10.1186/1479-5876-11-185-B35 10.1186/1479-5876-11-185-B34 10.1186/1479-5876-11-185-B11 10.1186/1479-5876-11-185-B33 10.1186/1479-5876-11-185-B10 10.1186/1479-5876-11-185-B32 10.1186/1479-5876-11-185-B31 10.1186/1479-5876-11-185-B30 10.1186/1479-5876-11-185-B28 10.1186/1479-5876-11-185-B27 10.1186/1479-5876-11-185-B7 10.1186/1479-5876-11-185-B40 10.1186/1479-5876-11-185-B8 10.1186/1479-5876-11-185-B9 10.1186/1479-5876-11-185-B5 10.1186/1479-5876-11-185-B6 10.1186/1479-5876-11-185-B26 10.1186/1479-5876-11-185-B25 10.1186/1479-5876-11-185-B2 10.1186/1479-5876-11-185-B23 10.1186/1479-5876-11-185-B22 - 10.1186/1479-5876-11-185-B21 10.1186/1479-5876-11-185-B43 10.1186/1479-5876-11-185-B20 10.1186/1479-5876-11-185-B19 10.1186/1479-5876-11-185-B18 10.1186/1479-5876-11-185-B17 10.1186/1479-5876-11-185-B16 19540352 - Cell Biol Int. 2009 Sep;33(9):1002-7 15455388 - Int J Cancer. 2005 Feb 10;113(4):678-82 22072148 - Surg Today. 2012 May;42(5):460-9 19716155 - Hum Pathol. 2009 Nov;40(11):1517-27 20441503 - Arch Pathol Lab Med. 2010 May;134(5):728-34 16416108 - J Cancer Res Clin Oncol. 2006 May;132(5):302-8 10640274 - Genes Dev. 2000 Jan 1;14(1):34-44 17182662 - J Clin Pathol. 2007 Oct;60(10):1112-6 17301289 - Mol Biol Cell. 2007 Apr;18(4):1437-46 16035955 - BMC Cancer. 2005;5:84 16827797 - Cancer Sci. 2006 Jul;97(7):582-8 10353251 - Nature. 1999 May 20;399(6733):271-5 14654550 - Clin Cancer Res. 2003 Nov 15;9(15):5666-74 17586500 - FEBS Lett. 2007 Jul 31;581(19):3582-91 21370029 - Methods Mol Biol. 2011;717:143-54 1534653 - Biochem J. 1992 Jun 1;284 ( Pt 2):341-8 17458507 - Cancer Metastasis Rev. 2007 Jun;26(2):319-31 17549799 - Proteomics. 2007 Jun;7(13):2142-50 18990559 - Eur J Cancer. 2008 Dec;44(18):2766-73 15623619 - Clin Cancer Res. 2004 Dec 15;10(24):8405-12 16996116 - Gynecol Oncol. 2007 Jan;104(1):181-5 17308108 - Cancer Res. 2007 Feb 15;67(4):1670-9 19344680 - Biochim Biophys Acta. 2009 Apr;1795(2):162-72 18422749 - Cancer Sci. 2008 Jul;99(7):1341-7 15313932 - Cancer Res. 2004 Aug 15;64(16):5876-81 16355214 - Nature. 2005 Dec 15;438(7070):967-74 19366452 - J Transl Med. 2009;7:25 21351269 - Int J Cancer. 2010 Dec 15;127(12):2893-917 11280732 - Cancer Res. 2001 Mar 1;61(5):1830-2 18026916 - J Mol Med (Berl). 2007 Dec;85(12):1301-7 19913895 - Gynecol Oncol. 2010 Mar;116(3):452-8 16426920 - Hum Pathol. 2006 Feb;37(2):198-204 17534684 - Ann Surg Oncol. 2007 Sep;14(9):2600-7 16585181 - Cancer Res. 2006 Apr 1;66(7):3567-75 10611972 - Annu Rev Cell Dev Biol. 1999;15:551-78 16430472 - Histopathology. 2006 Feb;48(3):258-67 10987269 - Cancer Res. 2000 Sep 1;60(17):4693-6 12538480 - Clin Cancer Res. 2003 Jan;9(1):273-84 12586590 - Gynecol Oncol. 2003 Feb;88(2):123-9 19061293 - Arch Pathol Lab Med. 2008 Dec;132(12):1929-35 17600126 - Am J Pathol. 2007 Aug;171(2):667-81 11606073 - Gynecol Oncol. 2001 Nov;83(2):205-15 19014607 - BMC Cancer. 2008;8:335 13130303 - Nat Rev Cancer. 2003 Oct;3(10):721-32 |
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Hypoxia inducible factor-1 alpha (HIF-1α), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met,... Hypoxia inducible factor-1 alpha (HIF-1α), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met, carbonic... Background Hypoxia inducible factor-1 alpha (HIF-1[alpha]), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met,... Hypoxia inducible factor-1 alpha (HIF-1[alpha]), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by up-regulation of c-Met, carbonic... Doc number: 185 Abstract Background: Hypoxia inducible factor-1 alpha (HIF-1α), induced by tumor hypoxia, regulates tumor cell metabolism and metastasis by... |
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| SubjectTerms | Adult Aged Aged, 80 and over Antigens, Neoplasm - metabolism Automation Biomedical and Life Sciences Biomedicine Breast cancer Carbonic Anhydrase IX Carbonic Anhydrases - metabolism Carcinoma in Situ - metabolism Care and treatment Cervical cancer Cervical Intraepithelial Neoplasia - metabolism Cohort Studies Development and progression Disease Biomarkers Disease-Free Survival Female Glucose Transporter Type 1 - metabolism Health aspects Humans Hypoxia Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Image Processing, Computer-Assisted Immunohistochemistry Kinases Medical research Medicine/Public Health Metabolic regulation Metastasis Middle Aged Mortality Oligonucleotide Array Sequence Analysis Prognosis Proteins Proto-Oncogene Proteins c-met - metabolism Treatment Outcome Uterine Cervical Neoplasms - diagnosis Uterine Cervical Neoplasms - metabolism Womens health Young Adult |
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| Title | Prognostic assessment of hypoxia and metabolic markers in cervical cancer using automated digital image analysis of immunohistochemistry |
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