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Defective erythropoiesis in bone marrow is a mechanism of anemia in children with cancer
Evaluation of the mechanism of anemia in cancer patients might help to select patients for the more efficient use of erythropoietin (EPO, a growth factor for erythroid precursor cells). For this, we investigated whether the production of EPO responds to anemia and the bone marrow responds to EPO app...
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Published in: | Journal of Korean medical science 2002, 17(3), , pp.337-340 |
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creator | Kim, MunHee Lee, JungHwa Wu, ChanWuk Cho, SungWon Lee, KwangChul |
description | Evaluation of the mechanism of anemia in cancer patients might help to select patients for the more efficient use of erythropoietin (EPO, a growth factor for erythroid precursor cells). For this, we investigated whether the production of EPO responds to anemia and the bone marrow responds to EPO appropriately, and whether chronic inflammation is inhibitory to erythropoiesis in anemic cancer children. Serum levels of EPO, soluble transferrin receptor (sTfR), tumor necrosis factor (TNF)-alpha, and erythrocyte sedimentation rate (ESR) in anemic cancer children were measured by enzyme-linked immunosorbent assay and then the correlation coefficients between those parameters and hemoglobin (Hb) were determined. Both in leukemia and in solid tumor patients, there were significant inverse correlations between Hb and EPO (leukemia: tau=-0.547, p |
doi_str_mv | 10.3346/jkms.2002.17.3.337 |
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For this, we investigated whether the production of EPO responds to anemia and the bone marrow responds to EPO appropriately, and whether chronic inflammation is inhibitory to erythropoiesis in anemic cancer children. Serum levels of EPO, soluble transferrin receptor (sTfR), tumor necrosis factor (TNF)-alpha, and erythrocyte sedimentation rate (ESR) in anemic cancer children were measured by enzyme-linked immunosorbent assay and then the correlation coefficients between those parameters and hemoglobin (Hb) were determined. Both in leukemia and in solid tumor patients, there were significant inverse correlations between Hb and EPO (leukemia: tau=-0.547, p<0.0001; solid tumor: tau=-0.591, p<0.0001), and between sTfR and EPO (leukemia: tau=-0.223, p<0.05; solid tumor: tau=-0.401, p<0.05). In contrast, sTfR showed a correlation with Hb in leukemia (tau=0.216, p<0.05) but not in solid tumor patients. sTfR was suppressed in 53% of anemic episodes of leukemia and 78% of those of solid tumor patients. Our results suggest that in cancer children, the EPO production is not defective and chronic inflammation is not inhibitory to erythropoiesis. Rather, the defective erythropoiesis itself is thought to be responsible for the anemia.</description><identifier>ISSN: 1011-8934</identifier><identifier>EISSN: 1598-6357</identifier><identifier>DOI: 10.3346/jkms.2002.17.3.337</identifier><identifier>PMID: 12068136</identifier><language>eng</language><publisher>Korea (South): Korean Academy of Medical Sciences</publisher><subject>Anemia - etiology ; Anemia - physiopathology ; Blood Sedimentation ; Bone Marrow - physiology ; Child ; Erythropoiesis - physiology ; Erythropoietin - blood ; Female ; Humans ; Male ; Neoplasms - complications ; Neoplasms - physiopathology ; Receptors, Transferrin - blood ; Solubility ; Tumor Necrosis Factor-alpha - metabolism ; 의학일반</subject><ispartof>Journal of Korean Medical Science, 2002, 17(3), , pp.337-340</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c431t-67e97413869ac73acc5dc830405071ac78f12d2d0fa6ee8c50542a303608a6e43</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3054874/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3054874/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12068136$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART000922818$$DAccess content in National Research Foundation of Korea (NRF)$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, MunHee</creatorcontrib><creatorcontrib>Lee, JungHwa</creatorcontrib><creatorcontrib>Wu, ChanWuk</creatorcontrib><creatorcontrib>Cho, SungWon</creatorcontrib><creatorcontrib>Lee, KwangChul</creatorcontrib><title>Defective erythropoiesis in bone marrow is a mechanism of anemia in children with cancer</title><title>Journal of Korean medical science</title><addtitle>J Korean Med Sci</addtitle><description>Evaluation of the mechanism of anemia in cancer patients might help to select patients for the more efficient use of erythropoietin (EPO, a growth factor for erythroid precursor cells). For this, we investigated whether the production of EPO responds to anemia and the bone marrow responds to EPO appropriately, and whether chronic inflammation is inhibitory to erythropoiesis in anemic cancer children. Serum levels of EPO, soluble transferrin receptor (sTfR), tumor necrosis factor (TNF)-alpha, and erythrocyte sedimentation rate (ESR) in anemic cancer children were measured by enzyme-linked immunosorbent assay and then the correlation coefficients between those parameters and hemoglobin (Hb) were determined. Both in leukemia and in solid tumor patients, there were significant inverse correlations between Hb and EPO (leukemia: tau=-0.547, p<0.0001; solid tumor: tau=-0.591, p<0.0001), and between sTfR and EPO (leukemia: tau=-0.223, p<0.05; solid tumor: tau=-0.401, p<0.05). In contrast, sTfR showed a correlation with Hb in leukemia (tau=0.216, p<0.05) but not in solid tumor patients. sTfR was suppressed in 53% of anemic episodes of leukemia and 78% of those of solid tumor patients. Our results suggest that in cancer children, the EPO production is not defective and chronic inflammation is not inhibitory to erythropoiesis. Rather, the defective erythropoiesis itself is thought to be responsible for the anemia.</description><subject>Anemia - etiology</subject><subject>Anemia - physiopathology</subject><subject>Blood Sedimentation</subject><subject>Bone Marrow - physiology</subject><subject>Child</subject><subject>Erythropoiesis - physiology</subject><subject>Erythropoietin - blood</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Neoplasms - complications</subject><subject>Neoplasms - physiopathology</subject><subject>Receptors, Transferrin - blood</subject><subject>Solubility</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>의학일반</subject><issn>1011-8934</issn><issn>1598-6357</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNpVUV1LHDEUDaVS7do_0IeSp9KXWZPcyST7Ioi2VRAKRaFvIWbudOLOJGsyq_jvm3GX2j7dcHI-knsI-cjZEqBuTu7XY14KxsSSqyUUTL0hR1yudNWAVG_LmXFe6RXUh-R9zveFKaWAd-SQC9ZoDs0R-XWBHbrJPyLF9Dz1KW6ix-wz9YHexYB0tCnFJ1oQS0d0vQ0-jzR21AYcvZ15rvdDmzDQJz_11NngMB2Tg84OGT_s54Lcfvt6c35ZXf_4fnV-dl25GvhUNQpXquagm5V1CqxzsnUaWM0kU7xAuuOiFS3rbIOonWSyFhYYNEwXpIYF-bLzDakza-dNtP5l_o5mnczZz5srI5UsAYV6uqNutncjtg7DlOxgNsmXPz6_CP-_Cb4vNo8GSqhWc9bnvUGKD1vMkxl9djgMZRVxm43iGoQoK14QsSO6FHNO2P0N4czM3Zm5OzN3Z7gyUDBVRJ_-fd6rZF8W_AFEJJbP</recordid><startdate>20020601</startdate><enddate>20020601</enddate><creator>Kim, MunHee</creator><creator>Lee, JungHwa</creator><creator>Wu, ChanWuk</creator><creator>Cho, SungWon</creator><creator>Lee, KwangChul</creator><general>Korean Academy of Medical Sciences</general><general>대한의학회</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><scope>ACYCR</scope></search><sort><creationdate>20020601</creationdate><title>Defective erythropoiesis in bone marrow is a mechanism of anemia in children with cancer</title><author>Kim, MunHee ; Lee, JungHwa ; Wu, ChanWuk ; Cho, SungWon ; Lee, KwangChul</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c431t-67e97413869ac73acc5dc830405071ac78f12d2d0fa6ee8c50542a303608a6e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Anemia - etiology</topic><topic>Anemia - physiopathology</topic><topic>Blood Sedimentation</topic><topic>Bone Marrow - physiology</topic><topic>Child</topic><topic>Erythropoiesis - physiology</topic><topic>Erythropoietin - blood</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Neoplasms - complications</topic><topic>Neoplasms - physiopathology</topic><topic>Receptors, Transferrin - blood</topic><topic>Solubility</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>의학일반</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, MunHee</creatorcontrib><creatorcontrib>Lee, JungHwa</creatorcontrib><creatorcontrib>Wu, ChanWuk</creatorcontrib><creatorcontrib>Cho, SungWon</creatorcontrib><creatorcontrib>Lee, KwangChul</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Korean Citation Index</collection><jtitle>Journal of Korean medical science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, MunHee</au><au>Lee, JungHwa</au><au>Wu, ChanWuk</au><au>Cho, SungWon</au><au>Lee, KwangChul</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Defective erythropoiesis in bone marrow is a mechanism of anemia in children with cancer</atitle><jtitle>Journal of Korean medical science</jtitle><addtitle>J Korean Med Sci</addtitle><date>2002-06-01</date><risdate>2002</risdate><volume>17</volume><issue>3</issue><spage>337</spage><epage>340</epage><pages>337-340</pages><issn>1011-8934</issn><eissn>1598-6357</eissn><abstract>Evaluation of the mechanism of anemia in cancer patients might help to select patients for the more efficient use of erythropoietin (EPO, a growth factor for erythroid precursor cells). For this, we investigated whether the production of EPO responds to anemia and the bone marrow responds to EPO appropriately, and whether chronic inflammation is inhibitory to erythropoiesis in anemic cancer children. Serum levels of EPO, soluble transferrin receptor (sTfR), tumor necrosis factor (TNF)-alpha, and erythrocyte sedimentation rate (ESR) in anemic cancer children were measured by enzyme-linked immunosorbent assay and then the correlation coefficients between those parameters and hemoglobin (Hb) were determined. Both in leukemia and in solid tumor patients, there were significant inverse correlations between Hb and EPO (leukemia: tau=-0.547, p<0.0001; solid tumor: tau=-0.591, p<0.0001), and between sTfR and EPO (leukemia: tau=-0.223, p<0.05; solid tumor: tau=-0.401, p<0.05). In contrast, sTfR showed a correlation with Hb in leukemia (tau=0.216, p<0.05) but not in solid tumor patients. sTfR was suppressed in 53% of anemic episodes of leukemia and 78% of those of solid tumor patients. Our results suggest that in cancer children, the EPO production is not defective and chronic inflammation is not inhibitory to erythropoiesis. Rather, the defective erythropoiesis itself is thought to be responsible for the anemia.</abstract><cop>Korea (South)</cop><pub>Korean Academy of Medical Sciences</pub><pmid>12068136</pmid><doi>10.3346/jkms.2002.17.3.337</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Anemia - etiology Anemia - physiopathology Blood Sedimentation Bone Marrow - physiology Child Erythropoiesis - physiology Erythropoietin - blood Female Humans Male Neoplasms - complications Neoplasms - physiopathology Receptors, Transferrin - blood Solubility Tumor Necrosis Factor-alpha - metabolism 의학일반 |
title | Defective erythropoiesis in bone marrow is a mechanism of anemia in children with cancer |
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