2014
DOI: 10.2174/1389201015666140113100946
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Induction of Thyroid Neoplasm Following Plant Medicine Marine Algae (Sargassum): A Rare Case and Review of the Literature

Abstract: In this study induction of neoplasm in thyroid gland of one postoperative patient with breast cancer was conducted by marine algae (also seaweed, sargassum), which is presented here. A 41-year-old women was diagnosed as her right breast cancer complicated with lymph node metastasis in her right axilla on February, 1999. In June 19, 1999 she was given the combination chemotherapy of vincristine, cyclophosphamide, 5-Fluorouracil and cinobufacini drugs due to two lymph nodes on her right superclavicular following… Show more

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Cited by 12 publications
(10 citation statements)
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“…Aberrant EGFR activation becomes oncogenic due to overexpression and/or amplification of the EGFR gene or by autocrine/paracrine growth factor loops, whereas activating dimerized mutations promote EGFR signaling, which lead to ligandindependent [2][3]. Phosphorylation of this oncogenic receptor at residues Tyr845,Tyr1045 and Tyr1173 leads to receptor activation and downstream signaling [4][5][6][7][8][9][10][11].And oncogenic receptor EGFR can transfer its oncogenic activity among cancer cells [12][13][14].Oncogenic EGFR mutations are found in 10% to 35% of lung adenocarcinomas, with predominant in a subset of patients with non-small cell lung cancer(NSCLC) [15][16][17].These mutations, which commonly occur as either small inframe deletions in exon 19 or point mutations T790M and L858R in exon 21 within the EGFR tyrosine kinase domain, confer constitutive activity and sensitivity to EGFR tyrosine kinase inhibitors(TKI) [18][19].Recent, Gallant [18]identified a novel EGFR alterations in lung cancer: EGFR exon18-25 kinase domain duplication(EGFR-KDD).EGFR-KDD is oncogenic and oncogenic EGFR-KDD-transformed cells are sensitive to the EGFR-TKI afatinib. Konduri and colleagues [19] reported five patients with metastatic lung cancer whose tumors harbored EGFR fusion, most commonly RAD5, are recurrent in lung cancer.…”
Section: Discussionmentioning
confidence: 99%
“…Aberrant EGFR activation becomes oncogenic due to overexpression and/or amplification of the EGFR gene or by autocrine/paracrine growth factor loops, whereas activating dimerized mutations promote EGFR signaling, which lead to ligandindependent [2][3]. Phosphorylation of this oncogenic receptor at residues Tyr845,Tyr1045 and Tyr1173 leads to receptor activation and downstream signaling [4][5][6][7][8][9][10][11].And oncogenic receptor EGFR can transfer its oncogenic activity among cancer cells [12][13][14].Oncogenic EGFR mutations are found in 10% to 35% of lung adenocarcinomas, with predominant in a subset of patients with non-small cell lung cancer(NSCLC) [15][16][17].These mutations, which commonly occur as either small inframe deletions in exon 19 or point mutations T790M and L858R in exon 21 within the EGFR tyrosine kinase domain, confer constitutive activity and sensitivity to EGFR tyrosine kinase inhibitors(TKI) [18][19].Recent, Gallant [18]identified a novel EGFR alterations in lung cancer: EGFR exon18-25 kinase domain duplication(EGFR-KDD).EGFR-KDD is oncogenic and oncogenic EGFR-KDD-transformed cells are sensitive to the EGFR-TKI afatinib. Konduri and colleagues [19] reported five patients with metastatic lung cancer whose tumors harbored EGFR fusion, most commonly RAD5, are recurrent in lung cancer.…”
Section: Discussionmentioning
confidence: 99%
“…Another 12 thyrotoxicosis caused by weightreducing herbal medicine [63]. In 2001, Zhu [70] reported a case of thyroid neoplasm following marine algae in a breast cancer. From epidemiologic studies in Korean population, high intake of iodine from marine products may increase thyroid cancer risk,particularly in women [71,72].Accumulated data, seaweed accounts for about 80% of Japanase people's iodine intake, seaweed consumption was clearly associated with an increased risk of papillary carcinoma (PTC)in postmenopausal women [73].…”
Section: Iodine Induced Hyperthyroidism (Iit)and Thyrotoxicosis (Iit)mentioning
confidence: 99%
“…In a series of long list of oncogenic receptors which discriminated tumorigenic in partial origin of tumours from receptors in normal health people and then better to potential targeting therapy benefits are presented in clear in previous references [ Table 1] [1][2][3][4][5][6] . Because It is no need to targeting receptors in normal condition, actually, targeting therapy now is shift mainly toward oncogenic receptors in tumours in tumor hospitals, even if we won't citing in literature 7 .…”
Section: Introductionmentioning
confidence: 99%