| pubmed-article:7609676 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7609676 | lifeskim:mentions | umls-concept:C0027651 | lld:lifeskim |
| pubmed-article:7609676 | lifeskim:mentions | umls-concept:C0178487 | lld:lifeskim |
| pubmed-article:7609676 | lifeskim:mentions | umls-concept:C0348016 | lld:lifeskim |
| pubmed-article:7609676 | lifeskim:mentions | umls-concept:C1511636 | lld:lifeskim |
| pubmed-article:7609676 | lifeskim:mentions | umls-concept:C0729502 | lld:lifeskim |
| pubmed-article:7609676 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:7609676 | pubmed:dateCreated | 1995-8-11 | lld:pubmed |
| pubmed-article:7609676 | pubmed:abstractText | Ascorbic acid and its salts (AA) are preferentially toxic to tumor cells in vitro and in vivo. Given in high enough doses to maintain plasma concentrations above levels that have been shown to be toxic to tumor cells in vitro, AA has the potential to selectively kill tumor cells in a manner similar to other tumor cytotoxic chemotherapeutic agents. Most studies of AA and cancer to date have not utilized high enough doses of AA to maintain tumor cytotoxic plasma concentrations of AA. Data are presented which demonstrate the ability to sustain plasma levels of AA in humans above levels which are toxic to tumor cells in vitro and suggests the feasibility of using AA as a cytotoxic chemotherapeutic agent. | lld:pubmed |
| pubmed-article:7609676 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7609676 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7609676 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:7609676 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7609676 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7609676 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7609676 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:7609676 | pubmed:issn | 0306-9877 | lld:pubmed |
| pubmed-article:7609676 | pubmed:author | pubmed-author:LUMM | lld:pubmed |
| pubmed-article:7609676 | pubmed:author | pubmed-author:JacksonJ AJA | lld:pubmed |
| pubmed-article:7609676 | pubmed:author | pubmed-author:MenaBB | lld:pubmed |
| pubmed-article:7609676 | pubmed:author | pubmed-author:RiordanH DHD | lld:pubmed |
| pubmed-article:7609676 | pubmed:author | pubmed-author:RiordanN HNH | lld:pubmed |
| pubmed-article:7609676 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7609676 | pubmed:volume | 44 | lld:pubmed |
| pubmed-article:7609676 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7609676 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7609676 | pubmed:pagination | 207-13 | lld:pubmed |
| pubmed-article:7609676 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:7609676 | pubmed:meshHeading | pubmed-meshheading:7609676-... | lld:pubmed |
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| pubmed-article:7609676 | pubmed:meshHeading | pubmed-meshheading:7609676-... | lld:pubmed |
| pubmed-article:7609676 | pubmed:meshHeading | pubmed-meshheading:7609676-... | lld:pubmed |
| pubmed-article:7609676 | pubmed:meshHeading | pubmed-meshheading:7609676-... | lld:pubmed |
| pubmed-article:7609676 | pubmed:meshHeading | pubmed-meshheading:7609676-... | lld:pubmed |
| pubmed-article:7609676 | pubmed:meshHeading | pubmed-meshheading:7609676-... | lld:pubmed |
| pubmed-article:7609676 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:7609676 | pubmed:articleTitle | Intravenous ascorbate as a tumor cytotoxic chemotherapeutic agent. | lld:pubmed |
| pubmed-article:7609676 | pubmed:affiliation | Project RECNAC, Bio-Communications Research Institute, Wichita, Kansas 67219, USA. | lld:pubmed |
| pubmed-article:7609676 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7609676 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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