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		<id>http://istoriya.soippo.edu.ua/api.php?action=feedcontributions&amp;feedformat=atom&amp;user=Bridge64water</id>
		<title>HistoryPedia - Внесок користувача [uk]</title>
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		<updated>2026-04-11T01:19:20Z</updated>
		<subtitle>Внесок користувача</subtitle>
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	<entry>
		<id>http://istoriya.soippo.edu.ua/index.php?title=Metabolic_Yeast_Enzyme_Dietary_Supplements&amp;diff=186367</id>
		<title>Metabolic Yeast Enzyme Dietary Supplements</title>
		<link rel="alternate" type="text/html" href="http://istoriya.soippo.edu.ua/index.php?title=Metabolic_Yeast_Enzyme_Dietary_Supplements&amp;diff=186367"/>
				<updated>2017-06-07T16:48:29Z</updated>
		
		<summary type="html">&lt;p&gt;Bridge64water: Створена сторінка: fact that stathmin level has an  independent prognostic value in individuals getting paclitaxel for metastatic disease, not present in individuals who do 	 not,...&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;fact that stathmin level has an  independent prognostic value in individuals getting paclitaxel for metastatic disease, not present in individuals who do 	 not, in survival analyses, supports the likelihood that the amount of stathmin level may perhaps act not just as a prognostic marker but additionally as a predictive marker for response to paclitaxel remedy in endometrial carcinomas. In contrast to preceding studies taking a look at stathmin as a potential predictive marker, predominantly in in vitro breast cancer research, in this study we had been able to test and confirm the association in clinical samples from sufferers treated using the drug of interest; working with data from a well-annotated prospectively collected patient series. Each the preclinical and clinical testing help that stathmin level influences sensitivity to paclitaxel. We've got explored and [http://www.medchemexpress.com/SAR405838.html SAR405838 site] excluded that this impact may be generalized to other chemotherapeutic agents for example carboplatin, also regularly applied in endometrial cancer. Reporting suggestions for tumor marker prognostic studies guidelines have already been created with all the aim to enhance the methodological high-quality and reporting transparency in such studies. The existing study has been performed in accordance to these recommendations to improve the top quality and common validity of its final results. Taxanes, originally isolated from the bark on the yew tree, belong for the family members of anti-microtubule chemotherapeutic agents, with paclitaxel as their prototype. Merely place, taxanes bind to b tubulin, causing microtubules to resist depolymerization, inhibiting cell cycle progression and promoting mitotic arrest and cell death. Carboplatin, in contrast, is among the platinum based agents, interacting with DNA and interfering with DNA repair. As stathmin is often a crucial regulator of microtubule dynamics, taken into consideration the mode of action of your drugs, the constructive impact of stathmin knock-down on paclitaxel response and also the absence of it to carboplatin sensitivity, can also be biologically plausible. We show a greater proportion of high stathmin level in metastatic compared with principal lesions. Discrepancy in stathmin status was noted within a quarter of paired samples, paralleling findings in e.g. breast cancer exactly where discrepancies among main and metastatic lesions are shown in 1455% and 040% for hormone receptors and HER2 respectively. In endometrial cancer, few research go over differences in marker status amongst primary and metastatic lesions. Intratumoral heterogeneity is effectively described in cancer along with a possible confounding issue in a lot of studies, irrespective of making use of fulltissue slides or TMA. Inter-observer variation is unlikely to become the sole explanation for these described variations. Also, a recent study assessing mutation status, a system considered less subjective than immunohistochemical scoring, in multiple metastatic lesions from 1 patient with renal cell carcinoma, assistance that detected biomarker adjustments from primary to metastatic lesions are real and might be connected to and relevant for tumor progression. The modifications in biomarker status from key to metastatic lesions support the will need for repeated biopsies in metastatic lesions, to improved relate therapy response to potential predictive biomarkers but additionally to only provide therapies with probably constructive impact when predictive biomarkers are readily available. For breast cancer, The American society of clinical oncology advised in 2007 currently that for hormone receptor status, testing must be deemed to&lt;/div&gt;</summary>
		<author><name>Bridge64water</name></author>	</entry>

	<entry>
		<id>http://istoriya.soippo.edu.ua/index.php?title=What_Regulates_Enzyme_Activity_In_Metabolic_Pathways&amp;diff=185300</id>
		<title>What Regulates Enzyme Activity In Metabolic Pathways</title>
		<link rel="alternate" type="text/html" href="http://istoriya.soippo.edu.ua/index.php?title=What_Regulates_Enzyme_Activity_In_Metabolic_Pathways&amp;diff=185300"/>
				<updated>2017-06-05T23:42:52Z</updated>
		
		<summary type="html">&lt;p&gt;Bridge64water: &lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;reality that stathmin level has an  independent prognostic value in sufferers receiving paclitaxel for metastatic illness, not present in individuals who do 	 not, in survival analyses, supports the likelihood that the amount of stathmin level may perhaps act not simply as a prognostic marker but also as a predictive marker for response to paclitaxel therapy in endometrial carcinomas. As opposed to preceding research looking at stathmin as a possible predictive marker, predominantly in in vitro breast cancer studies, within this study we were in a position to test and confirm the association in clinical samples from sufferers treated with the drug of interest; utilizing data from a well-annotated prospectively collected patient series. Each the preclinical and clinical testing assistance that stathmin level influences sensitivity to paclitaxel. We've explored and excluded that this [http://www.medchemexpress.com/MK-0773.html PF05314882] impact is often generalized to other chemotherapeutic agents including carboplatin, also often utilised in endometrial cancer. Reporting suggestions for tumor marker prognostic studies recommendations have already been created with all the aim to improve the methodological high-quality and reporting transparency in such research. The current study has been performed in accordance to these guidelines to enhance the top quality and basic validity of its final results. Taxanes, initially isolated in the bark of your yew tree, belong towards the loved ones of anti-microtubule chemotherapeutic agents, with paclitaxel as their prototype. Merely put, taxanes bind to b tubulin, causing microtubules to resist depolymerization, inhibiting cell cycle progression and advertising mitotic arrest and cell death. Carboplatin, in contrast, is one of the platinum based agents, interacting with DNA and interfering with DNA repair. As stathmin is usually a crucial regulator of microtubule dynamics, taken into consideration the mode of action of your drugs, the good impact of stathmin knock-down on paclitaxel response plus the absence of it to carboplatin sensitivity, can also be biologically plausible. We show a greater proportion of higher stathmin level in metastatic compared with key lesions. Discrepancy in stathmin status was noted within a quarter of paired samples, paralleling findings in e.g. breast cancer where discrepancies involving primary and metastatic lesions are shown in 1455% and 040% for hormone receptors and HER2 respectively. In endometrial cancer, few studies talk about variations in marker status amongst primary and metastatic lesions. Intratumoral heterogeneity is well described in cancer as well as a prospective confounding aspect in many studies, irrespective of applying fulltissue slides or TMA. Inter-observer variation is unlikely to be the sole explanation for these described differences. Also, a current study assessing mutation status, a approach considered significantly less subjective than immunohistochemical scoring, in various metastatic lesions from one particular patient with renal cell carcinoma, help that detected biomarker adjustments from major to metastatic lesions are actual and might be connected to and relevant for tumor progression. The adjustments in biomarker status from key to metastatic lesions help the have to have for repeated biopsies in metastatic lesions, to superior relate therapy response to potential predictive biomarkers but in addition to only supply therapies with likely positive impact when predictive biomarkers are accessible. For breast cancer, The American society of clinical oncology advised in 2007 already that for hormone receptor status, testing need to be considered to&lt;/div&gt;</summary>
		<author><name>Bridge64water</name></author>	</entry>

	<entry>
		<id>http://istoriya.soippo.edu.ua/index.php?title=How_Can_One_Enzyme_Regulate_A_Metabolic_Pathway&amp;diff=184913</id>
		<title>How Can One Enzyme Regulate A Metabolic Pathway</title>
		<link rel="alternate" type="text/html" href="http://istoriya.soippo.edu.ua/index.php?title=How_Can_One_Enzyme_Regulate_A_Metabolic_Pathway&amp;diff=184913"/>
				<updated>2017-06-05T07:49:54Z</updated>
		
		<summary type="html">&lt;p&gt;Bridge64water: Створена сторінка: truth that stathmin level has an  independent prognostic worth in sufferers getting paclitaxel for metastatic disease, not present in sufferers who do 	 not, in...&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;truth that stathmin level has an  independent prognostic worth in sufferers getting paclitaxel for metastatic disease, not present in sufferers who do 	 not, in survival analyses, supports the likelihood that the amount of stathmin level may act not simply as a prognostic marker but also as a predictive marker for response to paclitaxel therapy in endometrial carcinomas. As opposed to preceding studies looking at stathmin as a possible predictive marker, predominantly in in vitro breast cancer research, in this study we were capable to test and confirm the association in clinical samples from sufferers treated using the drug of interest; making use of data from a well-annotated prospectively collected patient series. Each the preclinical and clinical testing help that stathmin level influences sensitivity to paclitaxel. We've got explored and excluded that this impact is often generalized to other chemotherapeutic agents for example carboplatin, also often applied in endometrial cancer. Reporting recommendations for tumor marker prognostic research recommendations have already been created together with the aim to enhance the methodological quality and reporting transparency in such research. The current study has been performed in accordance to these guidelines to enhance the good quality and general validity of its benefits. Taxanes, initially isolated in the bark of the yew tree, belong for the household of anti-microtubule chemotherapeutic agents, with paclitaxel as their prototype. Just place, taxanes bind to b tubulin, causing microtubules to resist depolymerization, inhibiting cell cycle progression and promoting mitotic arrest and cell death. Carboplatin, in contrast, is one of the platinum based agents, interacting with DNA and interfering with DNA repair. As stathmin is a crucial regulator of microtubule dynamics, taken into consideration the mode of action of your drugs, the good impact of stathmin knock-down on paclitaxel response and the absence of it to carboplatin sensitivity, can also be biologically plausible. We show a larger proportion of higher stathmin level in metastatic compared with key lesions. Discrepancy in stathmin status was noted within a quarter of paired samples, paralleling findings in e.g. breast cancer where discrepancies between main and metastatic lesions are shown in 1455% and 040% for hormone receptors and HER2 respectively. In endometrial cancer, couple of studies talk about variations in marker status involving main and metastatic lesions. Intratumoral heterogeneity is nicely described in cancer as well as a prospective confounding element in many studies, irrespective of using fulltissue [http://www.medchemexpress.com/SAR405838.html MedChemExpress 1303607-60-4] slides or TMA. Inter-observer variation is unlikely to be the sole explanation for these described variations. Also, a current study assessing mutation status, a strategy considered less subjective than immunohistochemical scoring, in multiple metastatic lesions from one patient with renal cell carcinoma, support that detected biomarker alterations from principal to metastatic lesions are true and could be connected to and relevant for tumor progression. The adjustments in biomarker status from key to metastatic lesions support the need for repeated biopsies in metastatic lesions, to improved relate therapy response to possible predictive biomarkers but in addition to only offer you therapies with likely positive impact when predictive biomarkers are obtainable. For breast cancer, The American society of clinical oncology advised in 2007 already that for hormone receptor status, testing need to be regarded as to&lt;/div&gt;</summary>
		<author><name>Bridge64water</name></author>	</entry>

	<entry>
		<id>http://istoriya.soippo.edu.ua/index.php?title=What_Regulates_Enzyme_Activity_In_Metabolic_Pathways&amp;diff=183674</id>
		<title>What Regulates Enzyme Activity In Metabolic Pathways</title>
		<link rel="alternate" type="text/html" href="http://istoriya.soippo.edu.ua/index.php?title=What_Regulates_Enzyme_Activity_In_Metabolic_Pathways&amp;diff=183674"/>
				<updated>2017-06-02T06:12:17Z</updated>
		
		<summary type="html">&lt;p&gt;Bridge64water: Створена сторінка: fact that stathmin level has an  independent prognostic worth in sufferers receiving paclitaxel for metastatic illness, not present in sufferers who do 	 not, i...&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;fact that stathmin level has an  independent prognostic worth in sufferers receiving paclitaxel for metastatic illness, not present in sufferers who do 	 not, in survival analyses, supports the likelihood that the amount of stathmin level may act not only as a prognostic marker but also as a predictive marker for response to paclitaxel treatment in endometrial carcinomas. In contrast to preceding research looking at stathmin as a potential predictive marker, predominantly in in vitro breast [http://www.redditbookmark.in/login.php?return=/submit.php Title Loaded From File] cancer studies, within this study we were able to test and confirm the association in clinical samples from individuals treated using the drug of interest; using data from a well-annotated prospectively collected patient series. Each the preclinical and clinical testing help that stathmin level influences sensitivity to paclitaxel. We have explored and excluded that this effect is often generalized to other chemotherapeutic agents like carboplatin, also often utilized in endometrial cancer. Reporting suggestions for tumor marker prognostic studies recommendations have been developed with the aim to improve the methodological high quality and reporting transparency in such research. The current study has been performed in accordance to these recommendations to enhance the good quality and basic validity of its results. Taxanes, originally isolated in the bark on the yew tree, belong for the family of anti-microtubule chemotherapeutic agents, with paclitaxel as their prototype. Simply place, taxanes bind to b tubulin, causing microtubules to resist depolymerization, inhibiting cell cycle progression and advertising mitotic arrest and cell death. Carboplatin, in contrast, is one of the platinum based agents, interacting with DNA and interfering with DNA repair. As stathmin is often a important regulator of microtubule dynamics, taken into consideration the mode of action with the drugs, the good effect of stathmin knock-down on paclitaxel response and also the absence of it to carboplatin sensitivity, is also biologically plausible. We show a greater proportion of high stathmin level in metastatic compared with primary lesions. Discrepancy in stathmin status was noted in a quarter of paired samples, paralleling findings in e.g. breast cancer exactly where discrepancies between primary and metastatic lesions are shown in 1455% and 040% for hormone receptors and HER2 respectively. In endometrial cancer, couple of studies discuss differences in marker status amongst primary and metastatic lesions. Intratumoral heterogeneity is properly described in cancer and also a possible confounding factor in a lot of studies, irrespective of utilizing fulltissue slides or TMA. Inter-observer variation is unlikely to be the sole explanation for these described variations. Also, a recent study assessing mutation status, a approach considered less subjective than immunohistochemical scoring, in a number of metastatic lesions from one particular patient with renal cell carcinoma, support that detected biomarker adjustments from key to metastatic lesions are actual and may be associated to and relevant for tumor progression. The adjustments in biomarker status from main to metastatic lesions support the require for repeated biopsies in metastatic lesions, to greater relate therapy response to possible predictive biomarkers but in addition to only offer you therapies with probably constructive impact when predictive biomarkers are available. For breast cancer, The American society of clinical oncology advised in 2007 already that for hormone receptor status, testing needs to be thought of to&lt;/div&gt;</summary>
		<author><name>Bridge64water</name></author>	</entry>

	<entry>
		<id>http://istoriya.soippo.edu.ua/index.php?title=Metabolic_Enzyme_Complex&amp;diff=183669</id>
		<title>Metabolic Enzyme Complex</title>
		<link rel="alternate" type="text/html" href="http://istoriya.soippo.edu.ua/index.php?title=Metabolic_Enzyme_Complex&amp;diff=183669"/>
				<updated>2017-06-02T05:48:59Z</updated>
		
		<summary type="html">&lt;p&gt;Bridge64water: Створена сторінка: rtz LH, Sargent D, et al. New response evaluation criteria in strong tumours: revised RECIST guideline. European journal of cancer 45: 228247. 33. Kononen J, Bu...&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;rtz LH, Sargent D, et al. New response evaluation criteria in strong tumours: revised RECIST guideline. European journal of cancer 45: 228247. 33. Kononen J, Bubendorf L, Kallioniemi A, Barlund M, Schraml P, et al. Tissue microarrays for high-throughput molecular profiling of tumor [http://www.bucksportnext.net/vanilla/discussion/783947/rate-limiting-enzyme-metabolic-pathways Rate Limiting Enzyme Metabolic Pathways] specimens. Nat Med four: 844847. 34. Engelsen IB, Stefansson IM, Akslen LA, Salvesen HB GATA3 expression in estrogen receptor alpha-negative  endometrial carcinomas identifies aggressive tumors with high proliferation and poor patient survival. Am J Obstet Gynecol 199: 543 e541547. 35. Salvesen HB, Das S, Akslen LA Loss of nuclear p16 protein expression isn't connected with promoter methylation but defines a subgroup of aggressive endometrial carcinomas with poor prognosis. Clin Cancer Res 6: 153159. 36. Paik D, Cocco E, Bellone S, Casagrande F, Bellone M, et al. Greater sensitivity to patupilone versus paclitaxel chemotherapy in primary uterine serous papillary carcinoma cell lines  with high versus low HER-2/neu expression in vitro. Gynecol Oncol 119: 140145. 37. Hiramatsu HP, Kikuchi Y, Seto H, Nagata I In vitro sensitivity of human endometrial cancer cell lines to paclitaxel or irinotecan in mixture with other aniticancer drugs. Anticancer Drugs 11: 573578. 38. Vandenput I, Trovik J, Leunen K, Wik E, Stefansson I, et al. Evolution in endometrial cancer: evidence from an immunohistochemical study. Int J Gynecol Cancer 21: 316322. 39. Amant F, Mirza MR, Creutzberg CL Cancer of your corpus uteri. Int J Gynaecol Obstet 119 Suppl 2: S110117. 40. Halle MK, Werner HM, Krakstad C, Birkeland E, Wik E, et al. Stratification determined by high tumour cell content material in fresh frozen tissue promotes choice of aggressive endometrial carcinomas. Histopathology 60: 516519. 41. Galluzzi L, Maiuri MC, Vitale I, Zischka H, Castedo M, et al. Cell death modalities: classification and pathophysiological implications. Cell death and differentiation 14: 12371243. 8 Stathmin Predicts Response in Endometrial Cancer 42. Taatjes DJ, Sobel BE, Budd RC Morphological and cytochemical determination of cell death by apoptosis. Histochemistry and cell biology 129: 3343. 43. McShane LM, Altman DG, Sauerbrei W, Taube SE, Gion M, et al. Reporting recommendations for tumor marker prognostic studies. Journal in the National Cancer Institute 97: 11801184. 44. Xiao H, Verdier-Pinard P, Fernandez-Fuentes N, Burd B, Angeletti R, et al. Insights in to the mechanism of microtubule stabilization by Taxol. Proceedings of your National Academy of Sciences from the United states of America 103: 1016610173. 45. Arslan C, Sari E, Aksoy S, Altundag K Variation in hormone receptor and HER-2 status in between major and metastatic breast cancer: critique of your literature. Professional opinion on therapeutic targets 15: 2130. 46. Khasraw M, Brogi E, Seidman AD The must examine metastatic tissue at the time of progression of breast cancer: is re-biopsy a necessity or perhaps a luxury Present oncology reports 13: 1725. 47. Simmons C, Miller N, Geddie W, Gianfelice D, Oldfield M, et al. Does confirmatory tumor biopsy alter the management of breast cancer sufferers with 48. 49. 50. 51. 52. distant metastases Annals of oncology: official journal on the European Society for Medical Oncology/ESMO 20: 14991504. Krakstad C, Trovik J, Wik E, Engelsen IB, Werner HM, et al. Loss of GPER identifies new targets for therapy among a subgroup of ERalpha-positive endometrial cancer patients with poor outcome.&lt;/div&gt;</summary>
		<author><name>Bridge64water</name></author>	</entry>

	<entry>
		<id>http://istoriya.soippo.edu.ua/index.php?title=What_Is_A_Metabolic_Enzyme&amp;diff=183666</id>
		<title>What Is A Metabolic Enzyme</title>
		<link rel="alternate" type="text/html" href="http://istoriya.soippo.edu.ua/index.php?title=What_Is_A_Metabolic_Enzyme&amp;diff=183666"/>
				<updated>2017-06-02T05:42:38Z</updated>
		
		<summary type="html">&lt;p&gt;Bridge64water: Створена сторінка: ee K, Sgagias M, Cowan KH Ectopic expression of von Hippel-Lindau tumor suppressor induces apoptosis in 786-O renal cell carcinoma cells and regresses tumor gro...&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;ee K, Sgagias M, Cowan KH Ectopic expression of von Hippel-Lindau tumor suppressor induces apoptosis in 786-O renal cell carcinoma cells and regresses tumor growth of 786-O cells in nude mouse. Biochem Biophys Res Commun 320: 945950. 9 Cadherin-11 in Kidney Bone Metastasis 22. Guise TA Molecular mechanisms of osteolytic bone metastases. Cancer 88: 28922898. 23. Mundy GR Metastasis to bone: causes, consequences and therapeutic possibilities. Nat Rev  Cancer 2: 584593. 24. Pan T, Zhu J, Hwu WJ, Jankovic J The function of alpha-synuclein in melanin synthesis in melanoma and dopaminergic neuronal cells. PLoS One particular 7: e45183. 25. Lee YC, Bilen MA, Yu G, Lin SC, Huang CF, et al. Inhibition of Cell Adhesion by an Anti-cadherin 11 Antibody Prevents Bone Metastasis. Mol Cancer Res. 26. Fukuhara S, Sako K, Noda K, Zhang J, Minami M, et al. Angiopoietin1/Tie2 receptor signaling in vascular quiescence and angiogenesis. Histol Histopathol 25: 387396. 27. Gibney GT, Aziz SA, Camp RL, Conrad P, Schwartz BE, et al. c-Met is actually a prognostic marker and possible therapeutic target in clear cell renal cell carcinoma. Ann Oncol 24: 343349. 28. Harshman LC, Choueiri TK Targeting the Hepatocyte Development Factor/ c-Met Signaling Pathway in Renal Cell Carcinoma. Cancer J 19: 316323. 29. Guise TA, Yin JJ, Thomas RJ, Dallas M, Cui Y, et al. Parathyroid hormone-related protein - isoform is effectively secreted in vitro and enhances breast cancer metastasis to bone in vivo. Bone 30: 670676. 30. Kakonen SM, Mundy GR Mechanisms of osteolytic bone metastases in breast carcinoma. Cancer 97: 834839. 31. Sottnik JL, Keller ET Understanding and targeting osteoclastic activity in prostate cancer bone metastases. Curr Mol Med 13: 626639. 32. Chang SK, Noss EH, Chen M, Gu Z, Townsend K, et al. Cadherin-11 regulates fibroblast inflammation. Proc Natl Acad Sci U S A 108: 84028407. 33. Kalluri R, Weinberg RA The fundamentals of epithelial-mesenchymal transition. J Clin Invest 119: 14201428. 34. Thiery JP, Acloque H, Huang RY, Nieto MA Epithelial-mesenchymal transitions in development and illness. Cell 139: 871890. 35. Zeisberg M, Neilson EG Biomarkers for epithelial-mesenchymal transitions. J Clin Invest 119: 14291437. 36. Hazan RB, Qiao R, Keren R, Badano I, Suyama K Cadherin switch in tumor progression. Ann N Y Acad Sci 1014: 155163. 37. Wheelock MJ, Shintani Y, Maeda M, Fukumoto Y, Johnson KR Cadherin switching. J Cell Sci 121: 727735. 38. Haviv YS, van Houdt WJ, Lu B, Curiel DT, Zhu ZB Transcriptional targeting in renal cancer cell lines via the human CXCR4 promoter. Mol Cancer Ther three: 687691. 39. Murakami T, Maki W, Cardones AR, Fang H, Tun Kyi A, et al. Expression of CXC chemokine receptor-4 enhances the pulmonary metastatic prospective of murine B16 melanoma cells. Cancer Res 62: 73287334. 40. D'Alterio C, Consales C, Polimeno M, Franco R, Cindolo L, et al. Concomitant CXCR4 and CXCR7 expression predicts poor prognosis in renal cancer. Curr Cancer Drug  Targets 10: 772781. 41. Wehler TC, Graf C, [http://antiqueradios.com/forums/ucp.php?mode=login Regulation Of Gene Expression By A Metabolic Enzyme] Biesterfeld S, Brenner W, Schadt J, et al. Powerful expression of chemokine receptor CXCR4 by renal cell carcinoma correlates with sophisticated disease. J Oncol 2008: 626340. 42. Pan J, Mestas J, Burdick MD, Phillips RJ, Thomas GV, et al. Stromal derived factor-1 and CXCR4 in renal cell carcinoma metastasis. Mol Cancer five: 56. 43.&lt;/div&gt;</summary>
		<author><name>Bridge64water</name></author>	</entry>

	<entry>
		<id>http://istoriya.soippo.edu.ua/index.php?title=How_Can_An_Enzyme_Control_The_Rate_Of_A_Metabolic_Reaction&amp;diff=183480</id>
		<title>How Can An Enzyme Control The Rate Of A Metabolic Reaction</title>
		<link rel="alternate" type="text/html" href="http://istoriya.soippo.edu.ua/index.php?title=How_Can_An_Enzyme_Control_The_Rate_Of_A_Metabolic_Reaction&amp;diff=183480"/>
				<updated>2017-06-01T14:27:48Z</updated>
		
		<summary type="html">&lt;p&gt;Bridge64water: Створена сторінка: be repeated in Stathmin Predicts Response in Endometrial Cancer metastatic disease in the event the benefits have been to influence patient management. Acknowle...&lt;/p&gt;
&lt;hr /&gt;
&lt;div&gt;be repeated in Stathmin Predicts Response in Endometrial Cancer metastatic disease in the event the benefits have been to influence patient management. Acknowledgments Britt Edvardsen, Ellen Valen, Gerd Lillian Hallseth, Bendik Nordanger, Kadri Madissoo and Tormund Njlstad are heartily thanked for technical help. We are quite grateful for the clinical employees in the gynaecological oncology department in Haukeland University Hospital for their enormous efforts in  patient inclusion into our study and sample collection and to all sufferers for [http://www.ncbi.nlm.nih.gov/pubmed/1676428 1676428] their voluntary participation. Conclusion These benefits, such as preclinical information and for the initial time data from clinical samples, help that stathmin may possibly be a predictive biomarker for the response to paclitaxel remedy in endometrial cancer. On the other hand, confirmatory research, ideally from randomized clinical trials are necessary. The biomarker discordance on tumor progression is in line with other studies on tumor biomarker heterogeneity and supports the want for repeated biopsy in metastatic disease. Author Contributions Conceived and designed the experiments: HMJW JT CK HBS. Performed the experiments: HMJW JT ILT EW EB TB MKH CK. Analyzed the data: HMJW JT EW MKH TB CK HBS. Contributed reagents/ materials/analysis tools: HBS LAA EB CK, EW. Wrote the paper: HMJW CK JT HBS ILT EW EB TB MKH LAA. References 1. Belletti B, Baldassarre G Stathmin: a protein with numerous tasks. New biomarker and possible target in cancer. Specialist opinion on therapeutic targets 15: 12491266. two. Marklund U, Larsson N, Gradin HM, Brattsand G, Gullberg M Oncoprotein 18 can be a phosphorylation-responsive regulator of microtubule dynamics. The EMBO journal 15: 52905298. 3. Mistry SJ, Li HC, Atweh GF Function for protein phosphatases in the cellcycle-regulated phosphorylation of stathmin. The Biochemical journal 334: 2329. four. Rubin CI, Atweh GF The function of stathmin within the regulation of your cell cycle. Journal of cellular biochemistry 93: 242250. five. Biomarkers Definitions Operating G Biomarkers and surrogate endpoints: preferred definitions and conceptual framework. Clinical pharmacology and therapeutics 69: 8995. six. Baquero MT, Hanna JA, Neumeister V, Cheng H, Molinaro AM, et al. Stathmin expression and its connection to microtubule-associated protein tau and outcome in breast cancer. Cancer 118: 46604669. 7. Bieche I, Lachkar S, Becette V, Cifuentes-Diaz C, Sobel A, et al. Overexpression in the stathmin gene within a subset of human breast cancer. British journal of cancer 78: 701709. 8. Jeon TY, Han ME, Lee YW, Lee YS, Kim GH, et al. Overexpression of stathmin1 in the diffuse variety of gastric cancer and its roles in proliferation and migration of gastric cancer cells. British journal of cancer 102: 710718. 9. Kang W, Tong JH, Chan AW, Lung RW, Chau SL, et al. Stathmin1 plays oncogenic part and is really a target of microRNA-223 in gastric cancer. PLoS A single 7: e33919. 10. Kouzu Y, Uzawa K, Koike H, Saito K, Nakashima D, et al. Overexpression of stathmin in oral squamous-cell carcinoma: correlation with tumour progression and poor prognosis. British journal of cancer 94: [http://www.medchemexpress.com/CTEP.html CTEP web] 717723. 11. Liu F, Sun YL, Xu Y, Liu F, Wang LS, et al. Expression and phosphorylation of stathmin correlate with cell migration in esophageal squamous cell carcinoma. Oncology reports 29: 419424. 12. Salvesen HB, Carter SL, Mannelqvist M, Dutt A, Getz G, et al. Integrated genomic profiling of endometrial carcinoma associates aggressive tumors with indicators of PI3 kinase activation. Proceedings&lt;/div&gt;</summary>
		<author><name>Bridge64water</name></author>	</entry>

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