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      Tumor therapy with Amanita phalloides (Death Cap): stabilization of mammary duct cancer

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      https://www.riss.kr/link?id=A105949428

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      다국어 초록 (Multilingual Abstract)

      Molecular events that cause tumor formation enhance a number of HOX genes, called switch genes, coding for RNApolymeraseII transcription factors. Thus, in tumor cells, RNApolymeraseII is more active than in other somatic cells. Amanita phalloides cont...

      Molecular events that cause tumor formation enhance a number of HOX genes, called switch genes, coding for RNApolymeraseII transcription factors. Thus, in tumor cells, RNApolymeraseII is more active than in other somatic cells. Amanita phalloides contains amanitin which inhibits RNApolymeraseII. Partial inhibition with amanitin influences tumor cell - but not normal cell - activity. To widen the treatment spectrum, dilutions of Amanita phalloides, containing amanitin, are applied to a patient with mammary duct cancer. For monitoring tumormarkers, different doses of amanitin are applied. The former duplication time of tumor growth represented three months; however within a period of 18 months the patient can be stabilized without further growth of the tumor. There are also no severe symptoms, no liver damage and no continuous erythrocyte deprivation. This new principle of tumor therapy shows high potential to provide a medical treatment.

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      참고문헌 (Reference)

      1 Bishop JM, "Viral oncogenes" 42 : 23-38, 1985

      2 Rozovskaia T, "Upregulation of Meis1 and HoxA9 in acute lymphocytic leukemias with the t(4 : 11) abnormality" 20 : 874-878, 2001

      3 Riede, I, "Tumor Therapy with Amanita phalloides (Death Cap): Stabilization of B-Cell Chronic Lymphatic Leukemia" 16 : 1129-1132, 2010

      4 Yang ZQ, "Transforming properties of 8p11-12 amplified genes in human breast cancer" 70 : 8487-8497, 2010

      5 Gu Y, "The t(4;11) chromosome translocation of human acute leukemias fuses the ALL-1 gene, related to Drosophila trithorax, to the AF-4 gene" 71 : 701-708, 1992

      6 Riede I, "Switch Genes in Tumor Formation" 87 : 54-59, 2004

      7 Barrett JC, "Role of oncogenes and tumor suppressor genes in a multistep model of carcinogenesis" 39 : 45-56, 1986

      8 Riede I, "Proliferative genes induce somatic pairing defects in Drosophila melanogaster and allow replication" 97 : 143-154, 1997

      9 Imam JS, "MicroRNA-185 suppresses tumor growth and progression by targeting the Six1 oncogen in human cancers" 29 : 4971-4979, 2010

      10 Orlovsky K, "Down-regulation of homeobox genes MEIS1 and HOXA in MLL-rearranged acute leukemia impairs engraftment and reduces proliferation" 108 : 7956-7961, 2011

      1 Bishop JM, "Viral oncogenes" 42 : 23-38, 1985

      2 Rozovskaia T, "Upregulation of Meis1 and HoxA9 in acute lymphocytic leukemias with the t(4 : 11) abnormality" 20 : 874-878, 2001

      3 Riede, I, "Tumor Therapy with Amanita phalloides (Death Cap): Stabilization of B-Cell Chronic Lymphatic Leukemia" 16 : 1129-1132, 2010

      4 Yang ZQ, "Transforming properties of 8p11-12 amplified genes in human breast cancer" 70 : 8487-8497, 2010

      5 Gu Y, "The t(4;11) chromosome translocation of human acute leukemias fuses the ALL-1 gene, related to Drosophila trithorax, to the AF-4 gene" 71 : 701-708, 1992

      6 Riede I, "Switch Genes in Tumor Formation" 87 : 54-59, 2004

      7 Barrett JC, "Role of oncogenes and tumor suppressor genes in a multistep model of carcinogenesis" 39 : 45-56, 1986

      8 Riede I, "Proliferative genes induce somatic pairing defects in Drosophila melanogaster and allow replication" 97 : 143-154, 1997

      9 Imam JS, "MicroRNA-185 suppresses tumor growth and progression by targeting the Six1 oncogen in human cancers" 29 : 4971-4979, 2010

      10 Orlovsky K, "Down-regulation of homeobox genes MEIS1 and HOXA in MLL-rearranged acute leukemia impairs engraftment and reduces proliferation" 108 : 7956-7961, 2011

      11 Svingen T, "Altered HOX gene expression in human skin and breast cancer cells" 2 : 518-523, 2003

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2024 평가예정 재인증평가 신청대상 (재인증)
      2021-01-01 평가 등재학술지 선정 (계속평가) KCI등재
      2020-05-11 학술지명변경 한글명 : TANG [HUMANITAS MEDICINE] -> 셀메드
      외국어명 : TANG [HUMANITAS MEDICINE] -> CELLMED
      KCI등재후보
      2019-01-22 학회명변경 한글명 : 후마니타스 세포교정의학회 -> 셀메드 세포교정의약학회
      영문명 : Humanitas Orthocellular Medicine Association -> Cellmed Orthocellular Medicine and Pharmaceutical Association
      KCI등재후보
      2019-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
      2018-12-01 평가 등재후보 탈락 (계속평가)
      2018-11-26 학회명변경 한글명 : 후마니타스의학회 -> 후마니타스 세포교정의학회
      영문명 : Association of Humanitas Medicine -> Humanitas Orthocellular Medicine Association
      KCI등재후보
      2017-01-01 평가 등재후보학술지 유지 (계속평가) KCI등재후보
      2015-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.07 0.07 0.07
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.06 0.05 0.226 0.14
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