| 研究生: |
林明賢 Lin, Ming-Hsien |
|---|---|
| 論文名稱: |
台灣地區砷暴露與淋巴及造血組織癌症之相關性 The Association between Arsenic Exposure and Lymphoid & Hematopoietic Malignancies in Taiwan |
| 指導教授: |
郭浩然
Guo, How-Ran |
| 學位類別: |
博士 Doctor |
| 系所名稱: |
醫學院 - 環境醫學研究所 Department of Environmental and Occupational Health |
| 論文出版年: | 2024 |
| 畢業學年度: | 112 |
| 語文別: | 英文 |
| 論文頁數: | 80 |
| 中文關鍵詞: | 急性前骨髓性白血病 、砷 、三氧化二砷 、致癌性 、飲用水 、發生率 、血癌 、淋巴癌 、第二原發惡性腫瘤 |
| 外文關鍵詞: | acute promyelocytic leukemia (APL), arsenic, arsenic trioxide (ATO), carcinogenesis, drinking water, incidence, leukemia, lymphoma, second primary malignancy (SPM) |
| 相關次數: | 點閱:33 下載:1 |
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飲用水中砷已被公認為對人類具有致癌性,並可導致肺癌、膀胱癌、和皮膚癌。過去的研究顯示,砷的攝入與腎臟癌、肝癌、和前列腺癌之間存在正相關的關係。然而,三氧化二砷已被成功用於治療急性前骨髓性白血病。因此,砷可能在實體癌和血液癌的致癌作用中發揮不同的效應。
飲用水中砷的含量與血液癌發病率之間的關係尚未得到充分研究。我們建立了一個台灣全人口的世代,並使用0.05 mg/L為切點,將台灣的319個鄉鎮分為兩個暴露類別。然後,我們將這些數據與台灣癌症登記資料串聯,按性別、暴露類別、和時間區段,計算淋巴瘤和白血病的標準化發生比,並評估標準化發生比從1981-1990到1991-2000、再到2001-2010隨時間變化的趨勢。
我們發現,在淋巴瘤和白血病中,較高濃度的暴露類別在男性和女性都有較低的標準化發生比。就時間趨勢而言,雖然飲用水中砷的暴露量會隨時間而降低,淋巴瘤和白血病的標準化發生比在兩性中均呈現上升趨勢。因此,飲用水中砷的濃度與男性和女性的淋巴瘤和白血病的發病率呈現負相關,研究結果支持砷的致癌性具有雙重作用,對血液癌具有潛在的保護效應。
三氧化二砷結合全反式維甲酸已經成為急性前骨髓性白血病患者的第一線治療藥物;儘管這種方法的治癒率很高,但存活者面臨著罹患第二原發性惡性腫瘤的潛在風險。我們進行了一項統合分析,評估接受含三氧化二砷治療的急性前骨髓性白血病患者發生第二原發性惡性腫瘤的風險,並對以三氧化二砷為基礎的無化學治療與化學治療進行比較。我們從Embase、Ovid MEDLINE、Web of Science、Cochrane Library 和 Scopus資料庫中檢索了截至2022年11月發表的研究,使用隨機效應模型進行統合分析和分組分析,以評估三氧化二砷暴露與第二原發性惡性腫瘤風險之間的關聯。
統合分析共納入12項研究,涵蓋3,169名急性前骨髓性白血病患者。其中,6項研究的治療包括以三氧化二砷為基礎的無化學治療。在12項研究的統合分析中,含三氧化二砷的治療與第二原發性惡性腫瘤風險的相關性沒有達到統計的顯著。然而,在分組分析中,採用完全基於三氧化二砷的無化學治療的風險較低。結果顯示,在急性前骨髓性白血病患者,以三氧化二砷為基礎的無化學治療與化學治療相比,發生第二原發性惡性腫瘤的風險較低。
Arsenic in drinking water has been recognized as carcinogenic to humans and can cause solid cancers of lung, urinary bladder, and skin. Positive associations have also been reported between arsenic ingestion and cancers of kidney, liver, and prostate. Nevertheless, arsenic trioxide has been used successfully in the treatment of acute promyelocytic leukemia. Therefore, arsenic might play different roles in the carcinogenesis of solid cancers and hematologic malignancies.
The relationship between arsenic in drinking water and the incidences of hematologic malignancies has not been fully investigated. We established a cohort of Taiwanese population and assorted 319 townships of Taiwan into two exposure categories using 0.05 mg/L as the cutoff. Then, we linked these data to the Taiwan Cancer Registry and computed standardized incidence ratios of lymphoma and leukemia by sex, exposure category and time period. The trend of changes in the standardized incidence ratios over time was assessed, from 1981–1990 to 1991–2000 and then to 2001–2010.
We found that in both lymphoma and leukemia, the higher exposure category was associated with lower standardized incidence ratios in both men and women. In terms of time trends, the standardized incidence ratios in both lymphoma and leukemia showed increasing trends in both sexes, while exposure to arsenic in drinking water decreased over time. The arsenic level in drinking water was negatively associated with the incidences of lymphoma and leukemia in both men and women. This study supports the dual effects of arsenic on carcinogenesis, with a potential protective effect against hematologic malignancies.
On the other hand, arsenic trioxide combined with all-trans retinoic acid has been the first line treatment for patients with acute promyelocytic leukemia. Despite the high cure rate of this approach, survivors face the potential risk of developing second primary malignancy. We conducted a meta-analysis aimed to assess the risk of second primary malignancy in acute promyelocytic leukemia patients treated by arsenic trioxide-containing regimens, with subgroup comparison between arsenic trioxide-based chemotherapy-free versus chemotherapy-based regimens. We searched studies published until November 2022 from the following electronic databases: Embase, Ovid MEDLINE, Web of Science, Cochrane Library, and Scopus. Meta-analysis and subgroup analyses using random-effects modeling were conducted to examine the associations between exposure of arsenic trioxide and the risk of second primary malignancy.
A total of 12 studies involving 3,169 patients with acute promyelocytic leukemia were included in the meta-analysis. Of these, treatment in 6 studies included an arsenic trioxide-based chemotherapy-free regimens. In the meta-analysis of the 12 studies, the change in the risk of developing second primary malignancy associated with arsenic trioxide-containing regimens did not reach statistical significance. However, in the subgroup analysis, there was a risk reduction after treatment with a completely arsenic trioxide-based chemotherapy-free regimens. The results showed that in patients with acute promyelocytic leukemia who were treated with arsenic trioxide, chemotherapy-free regimens were associated with a lower risk of developing second primary malignancy compared with chemotherapy-based regimens.
1. Boyle RW, Jonasson IR. The geochemistry of arsenic and its use as an indicator element in geochemical prospecting. J Geochem Explor. 1973;2(3):251-296. doi:https://doi.org/10.1016/0375-6742(73)90003-4
2. Cullen WR, Reimer KJ. Arsenic speciation in the environment. Chem Rev. 1989;89(4):713-764. doi:https://pubs.acs.org/doi/pdf/10.1021/cr00094a002
3. Matschullat J. Arsenic in the geosphere — a review. Sci Total Environ. 2000;249(1-3):297-312. doi:https://doi.org/10.1016/S0048-9697(99)00524-0
4. Smedley PL, Kinniburgh DG. A review of the source, behaviour and distribution of arsenic in natural waters. Applied Geochemistry. 2002;17(5):517-568. doi:https://doi.org/10.1016/S0883-2927(02)00018-5
5. IARC. Monographs on the Evaluation of Carcinogenic Risks to Humans: Some drinking-water disinfectants and contaminants, including arsenic. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans; 2004:1-477. https://publications.iarc.fr/102
6. WHO. Arsenic and arsenic compounds (Environmental Health Criteria 224). Second ed. WHO Inter-Organization Programme for the Sound Management of Chemicals; 2001:1-114.
7. Vahter M. Genetic polymorphism in the biotransformation of inorganic arsenic and its role in toxicity. Toxicol Lett. 2000;112:209-217. doi:https://doi.org/10.1016/S0378-4274(99)00271-4
8. Thomas DJ, Styblo M, Lin S. The cellular metabolism and systemic toxicity of arsenic. Toxicol Appl Pharmacol. 2001;176(2):127-144. doi:https://doi.org/10.1006/taap.2001.9258
9. Drobna Z, Styblo M, Thomas DJ. An overview of arsenic metabolism and toxicity. Curr Protoc Toxicol. 2009;42(1):4.31.1-4.31.6. doi:https://doi.org/10.1002/0471140856.tx0431s42
10. Orloff K, Mistry K, Metcalf S. Biomonitoring for environmental exposures to arsenic. J Toxicol Env Health - Pt b - Crit Rev. 2009;12(7):509-524. doi:https://doi.org/10.1080/10937400903358934
11. Carlin DJ, Naujokas MF, Bradham KD, et al. Arsenic and environmental health: state of the science and future research opportunities. Environ Health Perspect. 2016;124(7):890-899. doi:https://doi.org/10.1289/ehp.1510209
12. Marczynski B. Carcinogenesis as the result of the deficiency of some essential trace elements. Med Hypotheses. 1988;26(4):239-249. doi:https://doi.org/10.1016/0306-9877(88)90127-2
13. Uthus EO. Evidence for arsenic essentiality. Environ Geochem Health. 1992;14(2):55-58. doi:https://doi.org/10.1007/BF01783629
14. Mayer DR, Kosmus W, Pogglitsch H, mayer D, Beyer W. Essential trace elements in humans. Biol Trace Elem Res. 1993;37(1):27-38. doi:https://doi.org/10.1007/BF02789399
15. Chen J, Yoshinaga M, Garbinski LD, Rosen BP. Synergistic interaction of glyceraldehydes-3-phosphate dehydrogenase and ArsJ, a novel organoarsenical efflux permease, confers arsenate resistance. Mol Microbiol. 2016;100(6):945-953. doi:https://doi.org/10.1111/mmi.13371
16. Cai C, Lanman NA, Withers KA, et al. Three Genes Define a Bacterial-Like Arsenic Tolerance Mechanism in the Arsenic Hyperaccumulating Fern Pteris vittata. Curr Biol. 2019;29(10):1625-1633 e3. doi:https://doi.org/10.1016/j.cub.2019.04.029
17. IARC. Monographs on the Evaluation of Carcinogenic Risks to Humans: Some metals and metallic compounds. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans; 1980:1-438. doi:https://publications.iarc.fr/41
18. Bates MN, Smith AH, Hopenhayn-Rich C. Arsenic ingestion and internal cancers: a review. Am J Epidemiol. 1992;135(5):462-476. doi:https://doi.org/10.1093/oxfordjournals.aje.a116313
19. Wang ZY, Chen Z. Acute promyelocytic leukemia: from highly fatal to highly curable. Blood. 2008;111(5):2505-2515. doi:https://doi.org/10.1182/blood-2007-07-102798
20. Martinez VD, Vucic EA, Becker-Santos DD, Gil L, Lam WL. Arsenic exposure and the induction of human cancers. J Toxicol. 2011;2011:1-13. doi:https://doi.org/10.1155/2011/431287
21. Stýblo M, Drobná Z, Jaspers I, Lin S, Thomas DJ. The role of biomethylation in toxicity and carcinogenicity of arsenic: a research update. Environ Health Perspect. 2002;110(Suppl 5):767. doi:https://doi.org/10.1289/ehp.110-1241242
22. Simeonova PP, Luster MI. Mechanisms of arsenic carcinogenicity: genetic or epigenetic mechanisms? J Environ Pathol Toxicol Oncol. 2000 2000;19(3):281-286. doi:http://europepmc.org/abstract/MED/10983894
23. Kessel M, Liu SX, Xu A, Santella R, Heil TK. Arsenic induces oxidative DNA damage in mammalian cells. Oxygen/Nitrogen Radicals: Cell Injury and Disease. Springer; 2002:301-308.
24. Kitchin KT, Ahmad S. Oxidative stress as a possible mode of action for arsenic carcinogenesis. Toxicol Lett. 2003;137(1-2):3-13.
doi:https://doi.org/10.1016/S0378-4274(02)00376-4
25. Shi H, Shi X, Liu KJ. Oxidative mechanism of arsenic toxicity and carcinogenesis. Mol Cell Biochem. 2004;255(1-2):67-78. doi:https://link.springer.com/article/10.1023/B:MCBI.0000007262.26044.e8
26. Lantz RC, Hays AM. Role of oxidative stress in arsenic-induced toxicity. Drug Metab Rev. 2006;38(4):791-804. doi:https://doi.org/10.1080/03602530600980108
27. Valko M, Rhodes C, Moncol J, Izakovic M, Mazur M. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chem-Biol Interact. 2006;160(1):1-40. doi:https://doi.org/10.1016/j.cbi.2005.12.009
28. Matsui M, Nishigori C, Imamura S, et al. The role of oxidative DNA damage in human arsenic carcinogenesis: detection of 8-hydroxy-2′-deoxyguanosine in arsenic-related Bowen's disease. J Invest Dermatol. 1999;113(1):26-31. doi:https://doi.org/10.1046/j.1523-1747.1999.00630.x
29. An Y, Gao Z, Wang Z, et al. Immunohistochemical analysis of oxidative DNA damage in arsenic-related human skin samples from arsenic-contaminated area of China. Cancer Lett. 2004;214(1):11-18. doi:https://doi.org/10.1016/j.canlet.2004.04.005
30. Korswagen HC. Regulation of the Wnt/β-catenin pathway by redox signaling. Dev Cell. 2006;10(6):687-688. doi:https://doi.org/10.1016/j.devcel.2006.05.007
31. Hidalgo C, Donoso P. Crosstalk between calcium and redox signaling: from molecular mechanisms to health implications. Antioxid Redox Signal. 2008;10(7):1275-1312. doi:https://doi.org/10.1089/ars.2007.1886
32. Ying S, Myers K, Bottomley S, Helleday T, Bryant HE. BRCA2-dependent homologous recombination is required for repair of arsenite-induced replication lesions in mammalian cells. Nucleic Acids Res. 2009;37(15):5105-5113. doi:https://doi.org/10.1093/nar/gkp538
33. Kligerman AD, Malik SI, Campbell JA. Cytogenetic insights into DNA damage and repair of lesions induced by a monomethylated trivalent arsenical. Mutat Res Genet Toxicol Environ Mutagen. 2010;695(1):2-8. doi:https://doi.org/10.1016/j.mrgentox.2009.09.007
34. Zhao CQ, Young MR, Diwan BA, Coogan TP, Waalkes MP. Association of arsenic-induced malignant transformation with DNA hypomethylation and aberrant gene expression. Proc Natl Acad Sci USA. 1997;94(20):10907-10912. doi:https://doi.org/10.1073/pnas.94.20.10907
35. Mass MJ, Wang L. Arsenic alters cytosine methylation patterns of the promoter of the tumor suppressor gene p53 in human lung cells: a model for a mechanism of carcinogenesis. Mutat Res-Rev Mutat Res. 1997;386(3):263-277. doi:https://doi.org/10.1016/S1383-5742(97)00008-2
36. Marsit CJ, Karagas MR, Schned A, Kelsey KT. Carcinogen exposure and epigenetic silencing in bladder cancer. Ann NY Acad Sci. 2006;1076(1):810-821. doi:https://doi.org/10.1196/annals.1371.031
37. Chanda S, Dasgupta UB, GuhaMazumder D, et al. DNA hypermethylation of promoter of gene p53 and p16 in arsenic-exposed people with and without malignancy. Toxicol Sci. 2005;89(2):431-437. doi:https://doi.org/10.1093/toxsci/kfj030
38. Zhou X, Sun H, Ellen TP, Chen H, Costa M. Arsenite alters global histone H3 methylation. Carcinogenesis. 2008;29(9):1831-1836. doi:https://doi.org/10.1093/carcin/bgn063
39. Jensen TJ, Novak P, Eblin KE, Gandolfi AJ, Futscher BW. Epigenetic remodeling during arsenical-induced malignant transformation. Carcinogenesis. 2008;29(8):1500-1508. doi:https://doi.org/10.1093/carcin/bgn102
40. Marsit CJ, Eddy K, Kelsey KT. MicroRNA responses to cellular stress. Cancer Res. 2006;66(22):10843-10848. doi:https://doi.org/10.1158/0008-5472.CAN-06-1894
41. Cui Y, Han Z, Hu Y, et al. MicroRNA‐181b and microRNA‐9 mediate arsenic‐induced angiogenesis via NRP1. J Cell Physiol. 2012;227(2):772-783. doi:https://doi.org/10.1002/jcp.22789
42. Saumet A, Vetter G, Bouttier M, et al. Transcriptional repression of microRNA genes by PML-RARA increases expression of key cancer proteins in acute promyelocytic leukemia. Blood. 2009;113(2):412-421. doi:https://doi.org/10.1182/blood-2008-05-158139
43. Soto AM, Sonnenschein C. Emergentism as a default: cancer as a problem of tissue organization. J Biosci. 2005;30(1):103-118. doi:https://doi.org/10.1007/BF02705155
44. Brücher BL, Jamall IS. Epistemology of the origin of cancer: a new paradigm. BMC Cancer. 2014;14(1):1-15. doi:https://doi.org/10.1186/1471-2407-14-331
45. Ren X, McHale CM, Skibola CF, Smith AH, Smith MT, Zhang L. An emerging role for epigenetic dysregulation in arsenic toxicity and carcinogenesis. Environ Health Perspect. 2011;119(1):11-19. doi:https://doi.org/10.1289/ehp.1002114
46. Chrun ES, Modolo F, Daniel FI. Histone modifications: a review about the presence of this epigenetic phenomenon in carcinogenesis. Pathol Res Pract 2017;213(11):1329-1339. doi:https://doi.org/10.1016/j.prp.2017.06.013
47. Tsuji JS, Chang ET, Gentry PR, Clewell HJ, Boffetta P, Cohen SM. Dose-response for assessing the cancer risk of inorganic arsenic in drinking water: the scientific basis for use of a threshold approach. Crit Rev Toxicol. 2019;49(1):36-84. doi:https://doi.org/10.1080/10408444.2019.1573804
48. Liu CW, Liang CP, Huang FM, Hsueh YM. Assessing the human health risks from exposure of inorganic arsenic through oyster (Crassostrea gigas) consumption in Taiwan. Sci Total Environ. 2006;361(1-3):57-66. doi:https://doi.org/10.1016/j.scitotenv.2005.06.005
49. Neubauer O. Arsenical cancer: a review. Br J Cancer. 1947;1(2):192. doi:https://doi.org/10.1038/bjc.1947.22
50. Tseng WP, Chu HM, How SW, Fong JM, Lin CS, Yeh S. Prevalence of skin cancer in an endemic area of chronic arsenicism in Taiwan. J Natl Cancer Inst. 1968;40(3):453-463. doi:https://doi.org/10.1093/jnci/40.3.453
51. Chen CJ, Chuang YC, Lin TM, Wu HY. Malignant neoplasms among residents of a blackfoot disease-endemic area in Taiwan: high-arsenic artesian well water and cancers. Cancer Res. 1985;45(11 Part 2):5895-5899. doi:https://aacrjournals.org/cancerres/article/45/11_Part_2/5895/489085
52. Chen CJ, Kuo TL, Wu MM. Arsenic and cancers. Lancet. Feb 20 1988;1(8582):414-5. doi:https://doi.org/10.1016/s0140-6736(88)91207-x
53. Wu MM, Kuo TL, Hwang YH, Chen CJ. Dose-response relation between arsenic concentration in well water and mortality from cancers and vascular diseases. Am J Epidemiol. 1989;130(6):1123-1132. doi:https://doi.org/10.1093/oxfordjournals.aje.a115439
54. Chen CJ, Wang CJ. Ecological correlation between arsenic level in well water and age-adjusted mortality from malignant neoplasms. Cancer Res. 1990;50(17):5470-5474. doi:https://aacrjournals.org/cancerres/article/50/17/5470/495633
55. Guo HR, Lipsitz SR, Hu H, Monson RR. Using ecological data to estimate a regression model for individual data: the association between arsenic in drinking water and incidence of skin cancer. Environ Res. 1998;79(2):82-93. doi:https://doi.org/10.1006/enrs.1998.3863
56. Tsai SM, Wang TN, Ko YC. Mortality for certain diseases in areas with high levels of arsenic in drinking water. Arch Environ Occup Health. 1999;54(3):186-193. doi:https://doi.org/10.1080/00039899909602258
57. Chen CJ, Wu MM, Lee SS, Wang JD, Cheng SH, Wu HY. Atherogenicity and carcinogenicity of high-arsenic artesian well water. Multiple risk factors and related malignant neoplasms of blackfoot disease. Arterioscler Thromb Vasc Biol. 1988;8(5):452-460. doi:https://doi.org/10.1161/01.ATV.8.5.452
58. Hsueh YM, Chiou HY, Huang YL, et al. Serum beta-carotene level, arsenic methylation capability, and incidence of skin cancer. Cancer Epidemiol Biomarkers Prev. 1997;6(8):589-596. doi:https://aacrjournals.org/cebp/article/6/8/589/154281
59. Chung YL, Liaw YP, Hwang BF, et al. Arsenic in drinking and lung cancer mortality in Taiwan. J Asian Earth Sci. 2013;77:327-331. doi:https://doi.org/10.1016/j.jseaes.2013.04.038
60. Kuo YC, Lo YS, Guo HR. Lung cancer associated with arsenic ingestion: cell-type specificity and dose response. Epidemiology. 2017;28 Suppl 1(1):S106-S112. doi:https://doi.org/10.1097/EDE.0000000000000743
61. Chen CJ, Chuang YC, You SL, Lin TM, Wu HY. A retrospective study on malignant neoplasms of bladder, lung and liver in blackfoot disease endemic area in Taiwan. Br J Cancer. 1986;53(3):399-405. doi:https://doi.org/10.1038/bjc.1986.65
62. Chiou HY, Hsueh YM, Liaw KF, et al. Incidence of internal cancers and ingested inorganic arsenic: a seven-year follow-up study in Taiwan. Cancer Res. 1995;55(6):1296-1300. doi:https://aacrjournals.org/cancerres/article/55/6/1296/502159
63. Chen CL, Hsu LI, Chiou HY, et al. Ingested arsenic, cigarette smoking, and lung cancer risk: a follow-up study in arseniasis-endemic areas in Taiwan. JAMA-J Am Med Assoc. 2004;292(24):2984-2990. doi:https://doi.org/10.1001/jama.292.24.2984
64. Lin HJ, Sung TI, Chen CY, Guo HR. Arsenic levels in drinking water and mortality of liver cancer in Taiwan. J Hazard Mater. 2013;262:1132-1138. doi:https://doi.org/10.1016/j.jhazmat.2012.12.049
65. Guo HR, Chiang HS, Hu H, Lipsitz SR, Monson RR. Arsenic in drinking water and incidence of urinary cancers. Epidemiology. 1997;8:545-550. doi:http://www.jstor.org/stable/3702686
66. IARC. Monographs on the Evaluation of Carcinogenic Risks to Humans: Arsenic, metals, fibres, and dusts. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans; 2012:1-465. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4781271
67. Han YY, Weissfeld JL, Davis DL, Talbott EO. Arsenic levels in ground water and cancer incidence in Idaho: an ecologic study. Int Arch Occup Environ Health. 2009;82(7):843-849. doi:https://doi.org/10.1007/s00420-008-0362-9
68. Kumar A, Ali M, Kumar R, et al. Arsenic exposure in Indo Gangetic plains of Bihar causing increased cancer risk. Sci Rep. 2021;11(1):2376. doi:https://doi.org/10.1038/s41598-021-81579-9
69. Hinwood AL, Jolley DJ, Sim MR. Cancer incidence and high environmental arsenic concentrations in rural populations: results of an ecological study. Int J Environ Health Res. 1999;9(2):131-141. doi:https://doi.org/10.1080/09603129973272
70. García-Esquinas E, Pollán M, Umans JG, et al. Arsenic exposure and cancer mortality in a US-based prospective cohort: the strong heart study. Cancer Epidemiol Biomarkers Prev. 2013;22(11):1944-1953. doi:https://doi.org/10.1158/1055-9965.EPI-13-0234-T
71. Glaser SL. Regional variation in Hodgkin's disease incidence by histologic subtype in the US. Cancer. 1987;60(11):2841-2847. doi:https://doi.org/10.1002/1097-0142(19871201)60:11<2841::aid-cncr2820601140>3.0.co;2-2
72. Linabery AM, Erhardt EB, Fonstad RK, et al. Infectious, autoimmune and allergic diseases and risk of Hodgkin lymphoma in children and adolescents: a Children's Oncology Group study. Int J Cancer. 2014;135(6):1454-1469. doi:https://doi.org/10.1002/ijc.28785
73. Tinguely M, Vonlanthen R, Müller E, et al. Hodgkin's disease-like lymphoproliferative disorders in patients with different underlying immunodeficiency states. Mod Pathol. 1998;11(4):307-312. doi:https://europepmc.org/article/med/9578079
74. Landgren O, Engels EA, Pfeiffer RM, et al. Autoimmunity and susceptibility to Hodgkin lymphoma: a population-based case–control study in Scandinavia. JNCI-J Natl Cancer Inst. 2006;98(18):1321-1330. doi:https://doi.org/10.1093/jnci/djj361
75. Morton LM, Slager SL, Cerhan JR, et al. Etiologic heterogeneity among non-Hodgkin lymphoma subtypes: the InterLymph non-Hodgkin lymphoma subtypes project. J Natl Cancer Inst Monographs. 2014;2014(48):130-144. doi:https://doi.org/10.1093/jncimonographs/lgu013
76. Zintzaras E, Voulgarelis M, Moutsopoulos HM. The risk of lymphoma development in autoimmune diseases: a meta-analysis. Arch Intern Med. 2005;165(20):2337-2344. doi:https://doi.org/10.1001/archinte.165.20.2337
77. Shiels MS, Engels EA, Linet M, et al. The epidemic of non-Hodgkin lymphoma in the United States: disentangling the effect of HIV, 1992-2009. Cancer Epidemiol Biomarkers Prev. 2013;22(6):1069-1078. doi:https://doi.org/10.1158/1055-9965.EPI-13-0040
78. Bayerdörffer E, Rudolph B, Neubauer A, et al. Regression of primary gastric lymphoma of mucosa-associated lymphoid tissue type after cure of Helicobacter pylori infection. Lancet. 1995;345(8965):1591-1594. doi:https://doi.org/10.1016/S0140-6736(95)90113-2
79. Giordano TP, Henderson L, Landgren O, et al. Risk of non-Hodgkin lymphoma and lymphoproliferative precursor diseases in US veterans with hepatitis C virus. JAMA-J Am Med Assoc. 2007;297(18):2010-2017. doi:https://doi.org/10.1001/jama.297.18.2010
80. Saha A, Robertson ES. Epstein-Barr virus associated B-cell lymphomas: pathogenesis and clinical outcomes. Clin Cancer Res. 2011;17(10):3056-3063. doi:https://doi.org/10.1158/1078-0432.CCR-10-2578
81. Morton LM, Hartge P, Holford TR, et al. Cigarette smoking and risk of non-Hodgkin lymphoma: a pooled analysis from the International Lymphoma Epidemiology Consortium (interlymph). Cancer Epidemiol Biomarkers Prev. 2005;14(4):925-933. doi:https://doi.org/10.1158/1055-9965.EPI-04-0693
82. Wang SS, Flowers CR, Kadin ME, et al. Medical history, lifestyle, family history, and occupational risk factors for peripheral T-cell lymphomas: the InterLymph Non-Hodgkin Lymphoma Subtypes Project. J Natl Cancer Inst Monographs. 2014;2014(48):66-75. doi:https://doi.org/10.1093/jncimonographs/lgu012
83. Riedel DA, Pottern LM. The epidemiology of multiple myeloma. Hematol Oncol Clin N Am 1992;6(2):225-247. doi:https://doi.org/10.1016/S0889-8588(18)30341-1
84. Kyle RA, Rajkumar SV. Monoclonal gammopathy of undetermined significance and smouldering multiple myeloma: emphasis on risk factors for progression. Br J Haematol. 2007;139(5):730-743. doi:https://doi.org/10.1111/j.1365-2141.2007.06873.x
85. Iwanaga M, Tagawa M, Tsukasaki K, et al. Relationship between monoclonal gammopathy of undetermined significance and radiation exposure in Nagasaki atomic bomb survivors. Blood. 2009;113(8):1639-1650. doi:https://doi.org/10.1182/blood-2008-05-159665
86. Smith M, Barnett M, Bassan R, Gatta G, Tondini C, Kern W. Adult acute myeloid leukaemia. Crit Rev Oncol/Hematol. 2004;50(3):197-222. doi:https://doi.org/10.1016/j.critrevonc.2003.11.002
87. Larson RA. Etiology and management of therapy-related myeloid leukemia. Hematology Am Soc Hematol Educ Program. 2007;2007(1):453-459. doi:https://doi.org/10.1182/asheducation-2007.1.453
88. Leone G, Pagano L, Ben-Yehuda D, Voso MT. Therapy-related leukemia and myelodysplasia: susceptibility and incidence. Haematologica. 2007;92(10):1389-1398. doi:https://doi.org/10.3324/haematol.11034
89. Czader M, Orazi A. Therapy-related myeloid neoplasms. Am J Clin Pathol. 2009;132(3):410-425. doi:https://doi.org/10.1309/AJCPD85MCOHHCOMQ
90. Jabbour EJ, Faderl S, Kantarjian HM. Adult acute lymphoblastic leukemia. Mayo Clin Proc. 2005;80(11):1517-1527. doi:https://doi.org/10.1016/j.mayocp.2016.09.010
91. Whitlock JA. Down syndrome and acute lymphoblastic leukaemia. Br J Haematol. 2006;135(5):595-602. doi:https://doi.org/10.1111/j.1365-2141.2006.06337.x
92. Sears DA. History of the treatment of chronic myelocytic leukemia. Am J Med Sci. 1988;296(2):85-86. doi:https://doi.org/10.1097/00000441-198808000-00001
93. Jolliffe D. A history of the use of arsenicals in man. J R Soc Med. 1993;86(5):287. doi:https://doi.org/10.1177/014107689308600515
94. Hillestad LK. Acute promyelocytc leukemia. Acta Medica Scandinavica. 1957;159(3):189-194. doi:https://doi.org/10.1111/j.0954-6820.1957.tb00124.x
95. Degos L. The history of acute promyelocytic leukaemia. Br J Haematol. 2003;122(4):539-553. doi:https://doi.org/10.1046/j.1365-2141.2003.04460.x
96. Zhou GB, Zhao WL, Wang ZY, Chen SJ, Chen Z. Retinoic acid and arsenic for treating acute promyelocytic leukemia. PLos Med. 2005;2(1):e12. doi:https://doi.org/10.1371/journal.pmed.0020012
97. Chen GQ, Zhu J, Shi XG, et al. In vitro studies on cellular and molecular mechanisms of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia: As2O3 induces NB4 cell apoptosis with downregulation of Bcl-2 expression and modulation of PML-RARα/PML proteins. Blood. 1996;88(3):1052-1061. doi:https://doi.org/10.1182/blood.V88.3.1052.1052
98. Chen GQ, Shi XG, Tang W, et al. Use of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia (APL): I. As2O3 exerts dose-dependent dual effects on APL cells. Blood. 1997;89(9):3345-3353. doi:https://ashpublications.org/blood/article/89/9/3345/139261
99. Shen ZX, Chen GQ, Ni JH, et al. Use of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia (APL): II. Clinical efficacy and pharmacokinetics in relapsed patients. Blood. 1997;89(9):3354-3360. doi:https://ashpublications.org/blood/article/89/9/3354/139279
100. Niu C, Yan H, Yu T, et al. Studies on treatment of acute promyelocytic leukemia with arsenic trioxide: remission induction, follow-up, and molecular monitoring in 11 newly diagnosed and 47 relapsed acute promyelocytic leukemia patients. Blood. 1999;94(10):3315-3324. doi:https://doi.org/10.1182/blood.V94.10.3315.422k16_3315_3324
101. Soignet SL, Frankel SR, Douer D, et al. United States multicenter study of arsenic trioxide in relapsed acute promyelocytic leukemia. J Clin Oncol.2001;19(18):3852-3860. doi:https://doi.org/10.1200/JCO.2001.19.18.3852
102. Shigeno K, Naito K, Sahara N, et al. Arsenic trioxide therapy in relapsed or refractory Japanese patients with acute promyelocytic leukemia: updated outcomes of the phase II study and postremission therapies. Int J Hematol. 2005;82(3):224-229. doi:https://doi.org/10.1532/IJH97.05044
103. Mathews V, George B, Chendamarai E, et al. Single-agent arsenic trioxide in the treatment of newly diagnosed acute promyelocytic leukemia: long-term follow-up data. J Clin Oncol. 2010;28(24):3866-3871. doi:https://doi.org/10.1200/JCO.2010.28.5031
104. Zhou J, Zhang Y, Li J, et al. Single-agent arsenic trioxide in the treatment of children with newly diagnosed acute promyelocytic leukemia. Blood. 2010;115(9):1697-1702. doi:https://doi.org/10.1182/blood-2009-07-230805
105. Vey N, Bosly A, Guerci A, et al. Arsenic trioxide in patients with myelodysplastic syndromes: a phase II multicenter study. J Clin Oncol. 2006;24(16):2465-2471. doi:https://doi.org/10.1200/JCO.2005.03.9503
106. Berenson JR, Matous J, Swift RA, Mapes R, Morrison B, Yeh HS. A phase I/II study of arsenic trioxide/bortezomib/ascorbic acid combination therapy for the treatment of relapsed or refractory multiple myeloma. Clin Cancer Res. 2007;13(6):1762-1768. doi:https://doi.org/10.1158/1078-0432.CCR-06-1812
107. Chang J, Voorhees P, Kolesar J, et al. Phase II study of arsenic trioxide and ascorbic acid for relapsed or refractory lymphoid malignancies: a Wisconsin Oncology Network study. Hematol Oncol. 2009;27(1):11-16. doi:https://doi.org/10.1002/hon.870
108. Hermine O, Dombret H, Poupon J, et al. Phase II trial of arsenic trioxide and alpha interferon in patients with relapsed/refractory adult T-cell leukemia/lymphoma. Haematol-Hematol J. 2004;5(2):130-134. doi:https://doi.org/10.1038/sj.thj.6200374
109. Kchour G, Tarhini M, Kooshyar MM, et al. Phase 2 study of the efficacy and safety of the combination of arsenic trioxide, interferon alpha, and zidovudine in newly diagnosed chronic adult T-cell leukemia/lymphoma (ATL). Blood. 2009;113(26):6528-6532. doi:https://doi.org/10.1182/blood-2009-03-211821
110. Bazarbachi A, El-Sabban ME, Nasr R, et al. Arsenic trioxide and interferon-α synergize to induce cell cycle arrest and apoptosis in human T-cell lymphotropic virus type I–transformed cells. Blood. 1999;93(1):278-283. doi:https://doi.org/10.1182/blood.V93.1.278
111. El-Sabban ME, Nasr R, Dbaibo G, et al. Arsenic-interferon-α–triggered apoptosis in HTLV-I transformed cells is associated with Tax down-regulation and reversal of NF-κB activation. Blood. 2000;96(8):2849-2855. doi:https://doi.org/10.1182/blood.V96.8.2849
112. Nasr R, Rosenwald A, El-Sabban ME, et al. Arsenic/interferon specifically reverses 2 distinct gene networks critical for the survival of HTLV-1–infected leukemic cells. Blood. 2003;101(11):4576-4582. doi:https://doi.org/10.1182/blood-2002-09-2986
113. Huang ME, Ye YC, Chen SR, et al. Use of all-trans retinoic acid in the treatment of acute promyelocytic leukemia. Blood. 1988;72(2):567-572. doi:https://doi.org/10.1182/blood.V72.2.567.567
114. Chen ZX, Xue YQ, Zhang R, et al. A clinical and experimental study on all-trans retinoic acid-treated acute promyelocytic leukemia patients. Blood. 1991;78(6):1413-1419. doi:https://doi.org/10.1182/blood.V78.6.1413.1413
115. Warrell RP, Frankel SR, Miller WH, et al. Differentiation therapy of acute promyelocytic leukemia with tretinoin (all-trans-retinoic acid). N Engl J Med. 1991;324(20):1385-1393. doi:https://www.nejm.org/doi/full/10.1056/NEJM199105163242002
116. Tallman MS, Nabhan C, Feusner JH, Rowe JM. Acute promyelocytic leukemia: evolving therapeutic strategies. Blood. 2002;99(3):759-767. doi:https://doi.org/10.1182/blood.V99.3.759
117. Coombs CC, Tavakkoli M, Tallman MS. Acute promyelocytic leukemia: where did we start, where are we now, and the future. Blood Cancer J. 2015/04/01 2015;5(4):e304-e304. doi:https://doi.org/10.1038/bcj.2015.25
118. Latagliata R, Petti MC, Fenu S, et al. Therapy-related myelodysplastic syndrome–acute myelogenous leukemia in patients treated for acute promyelocytic leukemia: an emerging problem. Blood. 2002;99(3):822-824. doi:https://doi.org/10.1182/blood.V99.3.822
119. Zompi S, Viguié F. Therapy-related acute myeloid leukemia and myelodysplasia after successful treatment of acute promyelocytic leukemia. Leuk Lymphoma. 2002/01/01 2002;43(2):275-280. doi:https://doi.org/10.1080/10428190290006044
120. Montesinos P, González JD, González J, et al. Therapy-related myeloid neoplasms in patients with acute promyelocytic leukemia treated with all-trans-retinoic acid and anthracycline-based chemotherapy. J Clin Oncol. 2010;28(24):3872-3879. doi:https://doi.org/10.1200/JCO.2010.29.2268
121. Hu J, Liu YF, Wu CF, et al. Long-term efficacy and safety of all-trans retinoic acid/arsenic trioxide-based therapy in newly diagnosed acute promyelocytic leukemia. Proc Natl Acad Sci U S A. 2009;106(9):3342-3347. doi:https://doi.org/10.1073/pnas.0813280106
122. Ravandi F, Estey E, Jones D, et al. Effective treatment of acute promyelocytic leukemia with all-trans-retinoic acid, arsenic trioxide, and gemtuzumab ozogamicin. J Clin Oncol. 2009;27(4):504-10. doi:https://doi.org/10.1200/jco.2008.18.6130
123. Lo-Coco F, Avvisati G, Vignetti M, et al. Retinoic acid and arsenic trioxide for acute promyelocytic leukemia. N Engl J Med. 2013;369(2):111-121. doi:https://doi.org/10.1056/NEJMoa1300874
124. Burnett AK, Russell NH, Hills RK, et al. Arsenic trioxide and all-trans retinoic acid treatment for acute promyelocytic leukaemia in all risk groups (AML17): results of a randomised, controlled, phase 3 trial. Lancet Oncol. 2015;16(13):1295-1305. doi:https://doi.org/10.1016/S1470-2045(15)00193-X
125. Platzbecker U, Avvisati G, Cicconi L, et al. Improved outcomes with retinoic acid and arsenic trioxide compared with retinoic acid and chemotherapy in non-high-risk acute promyelocytic leukemia: final results of the randomized Italian-German APL0406 trial. J Clin Oncol. 2017;35(6):605-612. doi:https://doi.org/10.1200/JCO.2016.67.1982
126. TRISENOX Prescribing Information. 2022. doi:https://www.trisenox.com/globalassets/trisenoxhcp/trisenox-prescribing-information.pdf
127. Yang CY, Chiu HF, Chang CC, Ho SC, Wu TN. Bladder cancer mortality reduction after installation of a tap-water supply system in an arsenious-endemic area in southwestern Taiwan. Environ Res. 2005;98(1):127-132. doi:https://doi.org/10.1016/j.envres.2004.07.013
128. Lo MC, Hsen YC, Lin BK. The second report on the investigation of arsenic content in underground water in Taiwan Providence. 1977. https://hero.epa.gov/hero/index.cfm/reference/details/reference_id/732069
129. Page MJ, McKenzie JE, Bossuyt PM, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ-British Medical Journal. 2021;372:n71. doi:https://doi.org/10.1136/bmj.n71
130. Greenhalgh T, Peacock R. Effectiveness and efficiency of search methods in systematic reviews of complex evidence: audit of primary sources. BMJ-British Medical Journal. 2005;331(7524):1064-1065. doi:https://doi.org/10.1136/bmj.38636.593461.68
131. Higgins J, Thomas J, Chandler J, et al. Cochrane Handbook for Systematic Reviews of Interventions, version 6.3. Cochrane. Accessed 20221109, https://training.cochrane.org/handbook
132. Wells GA, Shea B, O'Connell D, et al. The Newcastle-Ottawa Scale (NOS) for assessing the quality of nonrandomised studies in meta-analyses. Accessed 20221109, https://www.ohri.ca/programs/clinical_epidemiology/oxford.asp
133. Jlashi Z, Hui J, Zhenghua L, et al. A comparison of two regimens for children with acute promyelocytic leukemia: a retrospective study. Pediatr Blood Cancer. 2013;60(Suppl 3):S73. doi:https://doi.org/10.1002/pbc.24719
134. Eghtedar A, Rodriguez I, Kantarjian H, et al. Incidence of secondary neoplasms in patients with acute promyelocytic leukemia treated with all-trans retinoic acid plus chemotherapy or with all-trans retinoic acid plus arsenic trioxide. Leuk Lymphoma. 2015;56(5):1342-1345. doi:https://doi.org/10.3109/10428194.2014.953143
135. Lo-Coco F, Di Donato L, Schlenk RF. Targeted therapy alone for acute promyelocytic leukemia. N Engl J Med. 2016;374(12):1197-1198. doi:https://doi.org/10.1056/NEJMc1513710
136. Kayser S, Krzykalla J, Elliott MA, et al. Characteristics and outcome of patients with therapy-related acute promyelocytic leukemia front-line treated with or without arsenic trioxide. Leukemia. 2017;31(11):2347-2354. doi:https://doi.org/10.1038/leu.2017.92
137. Qin R, Li X, Ll N, et al. Clinical outcomes of different regimens in patients newly diagnosed with acute promyelocytic leukemia. Blood. 2017;130(Suppl 1):2617. doi:https://www.sciencedirect.com/science/article/pii/S0006497119831336
138. Lou Y, Lu Y, Zhu Z, et al. Improved long‐term survival in all Sanz risk patients of newly diagnosed acute promyelocytic leukemia treated with a combination of retinoic acid and arsenic trioxide‐based front‐line therapy. Hematol Oncol. 2018;36(3):584-590. doi:https://doi.org/10.1002/hon.2519
139. Autore F, Chiusolo P, Sorà F, et al. Reduction of hospitalization and transfusion support in patients with acute promyelocytic leukemia treated with arsenic trioxide plus all-trans retinoic acid compared to chemotherapy plus all-trans retinoic acid. Leuk Lymphoma. 2019;60(5):1328-1330. doi:https://doi.org/10.1080/10428194.2018.1522436
140. Norsworthy KJ, Avagyan A, Bird ST, et al. Second cancers in adults with acute promyelocytic leukemia treated with or without arsenic trioxide: a SEER-medicare analysis. Leukemia. 2020;34(11):3082-3084. doi:https://doi.org/10.1038/s41375-020-0905-y
141. Chen YG, Wu YY, Ho CL, et al. Investigating the incidence of secondary primary cancer in acute promyelocytic leukemia patients. HemaSphere. 2021;5(Suppl 2):199. doi:https://www.embase.com/search/results?subaction=viewrecord&id=L635849230&from=export
142. Gill H, Raghupathy R, Ni M, et al. Epidemiology and outcomes of acute promyelocytic leukaemia in the era of all-trans retinoic acid: a retrospective analysis. Lancet Oncol. 2022;23(Suppl 1):S11. doi:https://doi.org/10.1016/S1470-2045(22)00410-7
143. Chiu HF, Ho SC, Yang CY. Lung cancer mortality reduction after installation of tap-water supply system in an arseniasis-endemic area in southwestern Taiwan. Lung Cancer. 2004;46(3):265-270. doi:https://doi.org/10.1016/j.lungcan.2004.05.012
144. Yang CY, Chang CC, Chiu HF. Does arsenic exposure increase the risk for prostate cancer? J Toxicol Env Health Part A. 2008;71(23):1559-1563. doi:https://doi.org/10.1080/15287390802392065
145. Chiu HF, Ho SC, Wang LY, Wu TN, Yang CY. Does arsenic exposure increase the risk for liver cancer? J Toxicol Env Health Part A. 2004;67(19):1491-1500. doi:https://doi.org/10.1080/15287390490486806
146. Levine PH, Jaffe ES, Manns A, Murphy EL, Clark J, Blattner WA. Human T-cell lymphotropic virus type I and adult T-cell leukemia/lymphoma outside Japan and the Caribbean Basin. Yale J Biol Med. 1988;61(3):215-222. doi:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2590467/
147. Lee SH, Su IJ, Chen RL, et al. A pathologic study of childhood lymphoma in Taiwan with special reference to peripheral T‐cell lymphoma and the association with Epstein‐Barr viral infection. Cancer. 1991;68(9):1954-1962. doi:https://doi.org/10.1002/1097-0142(19911101)68:9<1954::AID-CNCR2820680918>3.0.CO;2-E
148. RMC. Environmental Radiation Monitoring (2020). Radiation Monitoring Center (RMC), Atomic Energy Council, Taiwan. Accessed 2021/02/25, https://www.aec.gov.tw/english/Environmental-Radiation-Monitoring-7.html
149. HPA. Adult Smoking Behavior Survey (2019). Health Promotion Administration (HPA), Ministry of Health and Welfare, Taiwan. Accessed 2021/02/25, https://www.hpagov.tw/Pages/Detail.aspx?nodeid=1718&pid=9913
150. Marshall G, Ferreccio C, Yuan Y, et al. Fifty-year study of lung and bladder cancer mortality in Chile related to arsenic in drinking water. JNCI-J Natl Cancer Inst. 2007;99(12):920-928. doi:https://doi.org/10.1093/jnci/djm004
151. Yuan Y, Marshall G, Ferreccio C, et al. Kidney cancer mortality: fifty-year latency patterns related to arsenic exposure. Epidemiology. 2010;21(1):103-108. doi:http://www.jstor.org/stable/25662813
152. Lin MH, Li CY, Cheng YY, Guo HR. Arsenic in drinking water and incidences of leukemia and lymphoma: implication for its dual effects in carcinogenicity. Front Public Health. 2022;10. doi:https://doi.org/10.3389/fpubh.2022.863882