43
edits
Changes
MDS, MDS/MPN and MPN Tables: Recurrent Genomic Alterations Detected by Chromosomal Microarray (view source)
Revision as of 11:06, 6 January 2020
, 11:06, 6 January 2020Citations
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|Prognostic poor survival
|Prognostic poor survival
|<ref name=":0">Starczynowski DT, Vercauteren S, Telenius A, Sung S, Tohyama K, Brooks-Wilson A, et al. High-resolution whole genome tiling path array CGH analysis of CD34+ cells from patients with low-risk myelodysplastic syndromes reveals cryptic copy number alterations and predicts overall and leukemia-free survival. Blood 2008;112:3412-24.[https://www.ncbi.nlm.nih.gov/pubmed/?term=High-resolution+whole+genome+tiling+path+array+CGH+analysis+of+CD34%2B+cells+from+patients+with+low-risk+myelodysplastic+syndromes+reveals+cryptic+copy+number+alterations+and+predicts+overall+and+leukemia-free+sur]</ref><ref>Yeung CCS, McElhone S, Chen XY, Ng D, Storer BE, Deeg HJ, et al. Impact of copy neutral loss of heterozygosity and total genome aberrations on survival in myelodysplastic syndrome. Mod Pathol 2017.[https://www.ncbi.nlm.nih.gov/pubmed/?term=Impact+of+copy+neutral+loss+of+heterozygosity+and+total+genome+aberrations+on+survival+in+myelodysplastic+syndrome.]</ref><ref name=":1">Arenillas L, Mallo M, Ramos F, Guinta K, Barragan E, Lumbreras E, et al. Single nucleotide polymorphism array karyotyping: a diagnostic and prognostic tool in myelodysplastic syndromes with unsuccessful conventional cytogenetic testing. Genes Chromosomes Cancer 2013;52:1167-77.[https://www.ncbi.nlm.nih.gov/pubmed/24123380]</ref><ref>Cluzeau T, Moreilhon C, Mounier N, Karsenti JM, Gastaud L, Garnier G, et al. Total genomic alteration as measured by SNP-array-based molecular karyotyping is predictive of overall survival in a cohort of MDS or AML patients treated with azacitidine. Blood Cancer J 2013;3:e155.[https://www.ncbi.nlm.nih.gov/pubmed/24185502]</ref><ref name=":2">Ganster C, Shirneshan K, Salinas-Riester G, Braulke F, Schanz J, Platzbecker U, et al. Influence of total genomic alteration and chromosomal fragmentation on response to a combination of azacitidine and lenalidomide in a cohort of patients with very high risk MDS. Leuk Res 2015;39:1079-87.[https://www.ncbi.nlm.nih.gov/pubmed/?term=26278198]</ref>
|<ref name=":0">Starczynowski DT, Vercauteren S, Telenius A, Sung S, Tohyama K, Brooks-Wilson A, et al. High-resolution whole genome tiling path array CGH analysis of CD34+ cells from patients with low-risk myelodysplastic syndromes reveals cryptic copy number alterations and predicts overall and leukemia-free survival. Blood 2008;112:3412-24.[https://www.ncbi.nlm.nih.gov/pubmed/?term=High-resolution+whole+genome+tiling+path+array+CGH+analysis+of+CD34%2B+cells+from+patients+with+low-risk+myelodysplastic+syndromes+reveals+cryptic+copy+number+alterations+and+predicts+overall+and+leukemia-free+sur]</ref><ref name=":36">Yeung CCS, McElhone S, Chen XY, Ng D, Storer BE, Deeg HJ, et al. Impact of copy neutral loss of heterozygosity and total genome aberrations on survival in myelodysplastic syndrome. Mod Pathol 2017.[https://www.ncbi.nlm.nih.gov/pubmed/?term=Impact+of+copy+neutral+loss+of+heterozygosity+and+total+genome+aberrations+on+survival+in+myelodysplastic+syndrome.]</ref><ref name=":1">Arenillas L, Mallo M, Ramos F, Guinta K, Barragan E, Lumbreras E, et al. Single nucleotide polymorphism array karyotyping: a diagnostic and prognostic tool in myelodysplastic syndromes with unsuccessful conventional cytogenetic testing. Genes Chromosomes Cancer 2013;52:1167-77.[https://www.ncbi.nlm.nih.gov/pubmed/24123380]</ref><ref>Cluzeau T, Moreilhon C, Mounier N, Karsenti JM, Gastaud L, Garnier G, et al. Total genomic alteration as measured by SNP-array-based molecular karyotyping is predictive of overall survival in a cohort of MDS or AML patients treated with azacitidine. Blood Cancer J 2013;3:e155.[https://www.ncbi.nlm.nih.gov/pubmed/24185502]</ref><ref name=":2">Ganster C, Shirneshan K, Salinas-Riester G, Braulke F, Schanz J, Platzbecker U, et al. Influence of total genomic alteration and chromosomal fragmentation on response to a combination of azacitidine and lenalidomide in a cohort of patients with very high risk MDS. Leuk Res 2015;39:1079-87.[https://www.ncbi.nlm.nih.gov/pubmed/?term=26278198]</ref>
|-
|-
|
|
|
|
|Recurrent
|Recurrent
|<ref>Singh NR, Morris CM, Koleth M, Wong K, Ward CM, Stevenson WS. Polyploidy in myelofibrosis: analysis by cytogenetic and SNP array indicates association with advancing disease. Mol Cytogenet 2013;6:59.[https://www.ncbi.nlm.nih.gov/pubmed/24341401]</ref>56]
|<ref>Singh NR, Morris CM, Koleth M, Wong K, Ward CM, Stevenson WS. Polyploidy in myelofibrosis: analysis by cytogenetic and SNP array indicates association with advancing disease. Mol Cytogenet 2013;6:59.[https://www.ncbi.nlm.nih.gov/pubmed/24341401]</ref><ref name=":37">Hahm C, Huh HJ, Mun YC, Seong CM, Chung WS, Huh J. Genomic aberrations of myeloproliferative and myelodysplastic/myeloproliferative neoplasms in chronic phase and during disease progression. Int J Lab Hematol 2015;37:181-9.[https://www.ncbi.nlm.nih.gov/pubmed/24845343]</ref>
|-
|-
|
|
|''TET2''
|''TET2''
|Prognostic for progression to AML
|Prognostic for progression to AML
|<ref name=":11" />58]
|<ref name=":11" /><ref name=":38">Klampfl T, Harutyunyan A, Berg T, Gisslinger B, Schalling M, Bagienski K, et al. Genome integrity of myeloproliferative neoplasms in chronic phase and during disease progression. Blood 2011;118:167-76.[https://www.ncbi.nlm.nih.gov/pubmed/21531982]</ref>
|-
|-
|
|
|''JAK2''
|''JAK2''
|Predictive for JAK2 inhibitors; Prognostic for PV progression to MF
|Predictive for JAK2 inhibitors; Prognostic for PV progression to MF
|<ref name=":35">Rumi E, Harutyunyan A, Elena C, Pietra D, Klampfl T, Bagienski K, et al. Identification of genomic aberrations associated with disease transformation by means of high-resolution SNP array analysis in patients with myeloproliferative neoplasm. Am J Hematol 2011;86:974-9.[https://www.ncbi.nlm.nih.gov/pubmed/21953568]</ref><ref name=":34" /><ref name=":35" />56, 113]
|<ref name=":35">Rumi E, Harutyunyan A, Elena C, Pietra D, Klampfl T, Bagienski K, et al. Identification of genomic aberrations associated with disease transformation by means of high-resolution SNP array analysis in patients with myeloproliferative neoplasm. Am J Hematol 2011;86:974-9.[https://www.ncbi.nlm.nih.gov/pubmed/21953568]</ref><ref name=":34" /><ref name=":35" /><ref name=":37" /><ref name=":39">Stegelmann F, Bullinger L, Griesshammer M, Holzmann K, Habdank M, Kuhn S, et al. High-resolution single-nucleotide polymorphism array-profiling in myeloproliferative neoplasms identifies novel genomic aberrations. Haematologica 2010;95:666-9.[https://www.ncbi.nlm.nih.gov/pubmed/20015882]</ref>
|-
|-
|
|
|
|
|Presence of CNAs/CN-LOH prognostic for progression to AML
|Presence of CNAs/CN-LOH prognostic for progression to AML
|<ref name=":35" /><ref name=":35" />56<ref name=":6" />
|<ref name=":35" /><ref name=":37" /><ref name=":6" />
|-
|-
|
|
|
|
|Recurrent
|Recurrent
|<ref name=":35" />114]
|<ref name=":35" /><ref name=":40">Huh J, Tiu RV, Gondek LP, O'Keefe CL, Jasek M, Makishima H, et al. Characterization of chromosome arm 20q abnormalities in myeloid malignancies using genome-wide single nucleotide polymorphism array analysis. Genes Chromosomes Cancer 2010;49:390-9.[https://www.ncbi.nlm.nih.gov/pubmed/20095039]</ref>
|-
|-
|CML
|CML
|''TP53''
|''TP53''
|Recurrent, progression, associated with TKI resistance
|Recurrent, progression, associated with TKI resistance
|[51, 52]
|<ref name=":41">Nowak D, Ogawa S, Muschen M, Kato M, Kawamata N, Meixel A, et al. SNP array analysis of tyrosine kinase inhibitor-resistant chronic myeloid leukemia identifies heterogeneous secondary genomic alterations. Blood 2010;115:1049-53.[https://www.ncbi.nlm.nih.gov/pubmed/19965645]</ref><ref name=":42">Boultwood J, Perry J, Zaman R, Fernandez-Santamaria C, Littlewood T, Kusec R, et al. High-density single nucleotide polymorphism array analysis and ASXL1 gene mutation screening in chronic myeloid leukemia during disease progression. Leukemia 2010;24:1139-45.[https://www.ncbi.nlm.nih.gov/pubmed/20410925]</ref>
|-
|-
|
|
|
|
|Diagnostic (only seen in BC)
|Diagnostic (only seen in BC)
|[52]
|<ref name=":42" />
|-
|-
|
|
|
|
|Diagnostic (only seen in BC)
|Diagnostic (only seen in BC)
|[52]
|<ref name=":42" />
|-
|-
|BMFS
|BMFS
|''?HLA genes''
|''?HLA genes''
|Recurrent
|Recurrent
|[78<ref name=":26" />80]
|<ref>Afable MG, 2nd, Wlodarski M, Makishima H, Shaik M, Sekeres MA, Tiu RV, et al. SNP array-based karyotyping: differences and similarities between aplastic anemia and hypocellular myelodysplastic syndromes. Blood 2011;117:6876-84.[https://www.ncbi.nlm.nih.gov/pubmed/21527527]</ref><ref name=":26" /><ref>Betensky M, Babushok D, Roth JJ, Mason PJ, Biegel JA, Busse TM, et al. Clonal evolution and clinical significance of copy number neutral loss of heterozygosity of chromosome arm 6p in acquired aplastic anemia. Cancer Genet 2016;209:1-10.[https://www.ncbi.nlm.nih.gov/pubmed/26702937]</ref>
|}
|}
|Recurrent
|Recurrent
|2
|2
|<ref name=":3" /><ref name=":21" /><ref name=":17" />115]
|<ref name=":3" /><ref name=":21" /><ref name=":17" /><ref>Hahm C, Mun YC, Seong CM, Han SH, Chung WS, Huh J. Single nucleotide polymorphism array-based karyotyping in acute myeloid leukemia or myelodysplastic syndrome with trisomy 8 as the sole chromosomal abnormality. Acta Haematol 2013;129:154-8.[https://www.ncbi.nlm.nih.gov/pubmed/23208021]</ref>
|-
|-
|3
|3
|Recurrent
|Recurrent
|3
|3
|<ref name=":3" /><ref name=":14" />19, 35, 61]
|<ref name=":3" /><ref name=":14" /><ref name=":43">Merkerova MD, Bystricka D, Belickova M, Krejcik Z, Zemanova Z, Polak J, et al. From cryptic chromosomal lesions to pathologically relevant genes: integration of SNP-array with gene expression profiling in myelodysplastic syndrome with normal karyotype. Genes Chromosomes Cancer 2012;51:419-[https://www.ncbi.nlm.nih.gov/pubmed/22250017 28]</ref><ref name=":1" /><ref name=":6" />
|-
|-
|4
|4
|T***
|T***
|2
|2
|<ref name=":3" /><ref name=":23" /><ref name=":8" /><ref name=":10" /><ref name=":11" />32<ref name=":12" />
|<ref name=":3" /><ref name=":23" /><ref name=":8" /><ref name=":10" /><ref name=":11" /><ref name=":24" /><ref name=":12" />
|-
|-
|4
|4
|Recurrent
|Recurrent
|2
|2
|<ref name=":13" /><ref name=":3" /><ref name=":14" /><ref name=":8" />29<ref name=":9" /><ref name=":5" /><ref name=":15" /><ref name=":16" /><ref name=":17" /><ref name=":18" />
|<ref name=":13" /><ref name=":3" /><ref name=":14" /><ref name=":8" /><ref name=":44">Mohamedali AM, Gaken J, Ahmed M, Malik F, Smith AE, Best S, et al. High concordance of genomic and cytogenetic aberrations between peripheral blood and bone marrow in myelodysplastic syndrome (MDS). Leukemia 2015;29:1928-38.[https://www.ncbi.nlm.nih.gov/pubmed/25943179]</ref><ref name=":9" /><ref name=":5" /><ref name=":15" /><ref name=":16" /><ref name=":17" /><ref name=":18" />
|-
|-
|5
|5
|D, P (Good when isolated)
|D, P (Good when isolated)
|1
|1
|<ref name=":3" /><ref name=":19" /><ref name=":14" /><ref name=":23" />19<ref name=":8" /><ref name=":0" /><ref name=":9" /><ref name=":20" /><ref name=":30" /><ref name=":1" /><ref name=":25" />43<ref name=":16" /><ref name=":2" /><ref name=":31" /><ref name=":21" /><ref name=":17" /><ref name=":32" /><ref name=":27" /><ref name=":7" /><ref name=":22" />116]
|<ref name=":3" /><ref name=":19" /><ref name=":14" /><ref name=":23" /><ref name=":43" /><ref name=":8" /><ref name=":0" /><ref name=":9" /><ref name=":20" /><ref name=":30" /><ref name=":1" /><ref name=":25" /><ref name=":45">Bajaj R, Xu F, Xiang B, Wilcox K, Diadamo AJ, Kumar R, et al. Evidence-based genomic diagnosis characterized chromosomal and cryptic imbalances in 30 elderly patients with myelodysplastic syndrome and acute myeloid leukemia. Mol Cytogenet 2011;4:3.[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031273/]</ref><ref name=":16" /><ref name=":2" /><ref name=":31" /><ref name=":21" /><ref name=":17" /><ref name=":32" /><ref name=":27" /><ref name=":7" /><ref name=":22" /><ref name=":46">Noronha TR, Rohr SS, Chauffaille Mde L. Identifying the similarities and differences between single nucleotide polymorphism array (SNPa) analysis and karyotyping in acute myeloid leukemia and myelodysplastic syndromes. Rev Bras Hematol Hemoter 2015;37:48-54. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4318843/]</ref>
|-
|-
|7
|7
|D, P (Intermediate)
|D, P (Intermediate)
|1
|1
|<ref name=":3" /><ref name=":19" /><ref name=":23" />19,<ref name=":0" /><ref name=":9" /><ref name=":24" /><ref name=":30" /><ref name=":25" /><ref name=":16" /><ref name=":2" /><ref name=":6" /><ref name=":26" /><ref name=":27" /><ref name=":7" /><ref name=":22" />
|<ref name=":3" /><ref name=":19" /><ref name=":23" /><ref name=":43" /><ref name=":0" /><ref name=":9" /><ref name=":24" /><ref name=":30" /><ref name=":25" /><ref name=":16" /><ref name=":2" /><ref name=":6" /><ref name=":26" /><ref name=":27" /><ref name=":7" /><ref name=":22" />
|-
|-
|7
|7
|Recurrent
|Recurrent
|2
|2
|<ref name=":13" /><ref name=":3" /><ref name=":14" />19<ref name=":8" /><ref name=":4" /><ref name=":9" /><ref name=":5" /><ref name=":2" /><ref name=":29" /><ref name=":18" />
|<ref name=":13" /><ref name=":3" /><ref name=":14" /><ref name=":43" /><ref name=":8" /><ref name=":4" /><ref name=":9" /><ref name=":5" /><ref name=":2" /><ref name=":29" /><ref name=":18" />
|-
|-
|7
|7
|P (Intermediate)**
|P (Intermediate)**
|1
|1
|<ref name=":3" /><ref name=":8" /><ref name=":9" /><ref name=":30" /><ref name=":12" /><ref name=":2" /><ref name=":6" /><ref name=":31" />74<ref name=":26" /><ref name=":27" /><ref name=":22" />
|<ref name=":3" /><ref name=":8" /><ref name=":9" /><ref name=":30" /><ref name=":12" /><ref name=":2" /><ref name=":6" /><ref name=":31" /><ref>Paulsson K, Heidenblad M, Strombeck B, Staaf J, Jonsson G, Borg A, et al. High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in AML and MDS cases with trisomy 8 as the sole cytogenetic aberration. Leukemia 2006;20:840-6. [https://www.ncbi.nlm.nih.gov/pubmed/16498392]</ref><ref name=":26" /><ref name=":27" /><ref name=":22" />
|-
|-
|9
|9
|Recurrent
|Recurrent
|2
|2
|<ref name=":3" />31,<ref name=":1" />
|<ref name=":3" /><ref name=":36" /><ref name=":1" />
|-
|-
|11
|11
|Recurrent
|Recurrent
|2
|2
|<ref name=":13" /><ref name=":3" /><ref name=":19" />25,<ref name=":1" /><ref name=":5" /><ref name=":17" /><ref name=":7" /><ref name=":28" />
|<ref name=":13" /><ref name=":3" /><ref name=":19" /><ref name=":4" /><ref name=":1" /><ref name=":5" /><ref name=":17" /><ref name=":7" /><ref name=":28" />
|-
|-
|11
|11
|Recurrent
|Recurrent
|3
|3
|<ref name=":3" /><ref name=":19" /> 25, 29<ref name=":5" />
|<ref name=":3" /><ref name=":19" /><ref name=":4" /><ref name=":44" /><ref name=":5" />
|-
|-
|16
|16
|P (Poor)
|P (Poor)
|1
|1
|<ref name=":3" /><ref name=":9" /><ref name=":30" />43<ref name=":12" /><ref name=":2" /><ref name=":27" />
|<ref name=":3" /><ref name=":9" /><ref name=":30" /><ref name=":45" /><ref name=":12" /><ref name=":2" /><ref name=":27" />
|-
|-
|17
|17
|Recurrent
|Recurrent
|2
|2
|<ref name=":3" />19, 25]
|<ref name=":3" /><ref name=":43" /><ref name=":4" />
|-
|-
|19
|19
|P (Good)**
|P (Good)**
|1
|1
|<ref name=":3" /><ref name=":8" /><ref name=":0" /> 43,<ref name=":2" /><ref name=":6" /><ref name=":31" />65<ref name=":29" /><ref name=":27" /><ref name=":28" />112<ref name=":19" /> 30<ref name=":16" />114, 117]
|<ref name=":3" /><ref name=":8" /><ref name=":0" /><ref name=":45" /><ref name=":2" /><ref name=":6" /><ref name=":31" /><ref name=":32" /><ref name=":29" /><ref name=":27" /><ref name=":28" /><ref name=":22" /><ref name=":19" /><ref name=":9" /><ref name=":16" /><ref name=":40" /><ref>Bacher U, Haferlach T, Schnittger S, Zenger M, Meggendorfer M, Jeromin S, et al. Investigation of 305 patients with myelodysplastic syndromes and 20q deletion for associated cytogenetic and molecular genetic lesions and their prognostic impact. Br J Haematol 2014;164:822-33.[https://www.ncbi.nlm.nih.gov/pubmed/24372512]</ref>
|-
|-
|20
|20
|D, P (Poor)
|D, P (Poor)
|2
|2
|<ref name=":3" /><ref name=":14" /><ref name=":23" />21<ref name=":24" /><ref name=":30" /><ref name=":12" />
|<ref name=":3" /><ref name=":14" /><ref name=":23" /><ref name=":8" /><ref name=":24" /><ref name=":30" /><ref name=":12" />
|-
|-
|21
|21
|Recurrent
|Recurrent
|2
|2
|<ref name=":3" /> 25, <ref name=":2" /><ref name=":18" />116]
|<ref name=":3" /><ref name=":4" /><ref name=":2" /><ref name=":18" /><ref name=":46" />
|-
|-
|21
|21
|Recurrent
|Recurrent
|2
|2
|[37]
|<ref name=":5" />
|-
|-
|4
|4
|P (Intermediate)
|P (Intermediate)
|1
|1
|[23, 28<ref name=":20" /><ref name=":34" />56<ref name=":21" />
|<ref name=":10" /><ref name=":47">Slovak ML, Smith DD, Bedell V, Hsu YH, O'Donnell M, Forman SJ, et al. Assessing karyotype precision by microarray-based comparative genomic hybridization in the myelodysplastic/myeloproliferative syndromes. Mol Cytogenet 2010;3:23. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3000833/]</ref><ref name=":20" /><ref name=":34" /><ref name=":37" /><ref name=":21" />
|-
|-
|7
|7
|P (Poor)
|P (Poor)
|1
|1
|[56<ref name=":17" />
|<ref name=":37" /><ref name=":17" />
|-
|-
|9
|9
|P (Intermediate)
|P (Intermediate)
|1
|1
|<ref name=":33" />28]
|<ref name=":33" /><ref name=":47" />
|-
|-
|13
|13
|P (Intermediate)
|P (Intermediate)
|1
|1
|<ref name=":34" />56]
|<ref name=":34" /><ref name=":37" />
|-
|-
|14
|14
|P (Poor)***
|P (Poor)***
|1
|1
|[56]
|<ref name=":37" />
|-
|-
|20
|20
|Recurrent
|Recurrent
|2
|2
|<ref name=":35" /><ref name=":35" />56]
|<ref name=":35" /><ref name=":35" /><ref name=":37" />
|-
|-
|4
|4
|Recurrent
|Recurrent
|2
|2
|<ref name=":11" />58]
|<ref name=":11" /><ref name=":38" />
|-
|-
|5
|5
|Recurrent
|Recurrent
|3
|3
|[56, 60]
|<ref name=":37" /><ref>Puda A, Milosevic JD, Berg T, Klampfl T, Harutyunyan AS, Gisslinger B, et al. Frequent deletions of JARID2 in leukemic transformation of chronic myeloid malignancies. Am J Hematol 2012;87:245-50. [https://www.ncbi.nlm.nih.gov/pubmed/22190018]</ref>
|-
|-
|7
|7
|Recurrent
|Recurrent
|2
|2
|[52]
|<ref name=":42" />
|-
|-
|8
|8
|P (Poor)
|P (Poor)
|1
|1
|[51]
|<ref name=":41" />
|-
|-
|9
|9
|Recurrent
|Recurrent
|2
|2
|<ref name=":35" /><ref name=":35" />56]
|<ref name=":35" /><ref name=":35" /><ref name=":37" />
|-
|-
|9
|9
|Recurrent
|Recurrent
|2
|2
|<ref name=":35" /><ref name=":34" /><ref name=":35" />56, 113]
|<ref name=":35" /><ref name=":34" /><ref name=":35" /><ref name=":37" /><ref name=":39" />
|-
|-
|9
|9
|Recurrent
|Recurrent
|3
|3
|[50, 51]
|<ref name=":48">Huh J, Jung CW, Kim JW, Kim HJ, Kim SH, Shin MG, et al. Genome-wide high density single-nucleotide polymorphism array-based karyotyping improves detection of clonal aberrations including der(9) deletion, but does not predict treatment outcomes after imatinib therapy in chronic myeloid leukemia. Ann Hematol 2011;90:1255-64. [https://www.ncbi.nlm.nih.gov/pubmed/21384125]</ref><ref name=":41" />
|-
|-
|9
|9
|Recurrent
|Recurrent
|1
|1
|[51]
|<ref name=":41" />
|-
|-
|11
|11
|P (Poor)
|P (Poor)
|1
|1
|[52]
|<ref name=":42" />
|-
|-
|13
|13
|Recurrent
|Recurrent
|3
|3
|<ref name=":35" /><ref name=":35" />56<ref name=":6" />
|<ref name=":35" /><ref name=":35" /><ref name=":37" /><ref name=":6" />
|-
|-
|17
|17
|P (Poor)
|P (Poor)
|1
|1
|[51, 52<ref name=":35" />
|<ref name=":41" /><ref name=":42" /><ref name=":35" />
|-
|-
|20
|20
|Recurrent
|Recurrent
|1
|1
|<ref name=":35" />114]
|<ref name=":35" /><ref name=":40" />
|-
|-
|22
|22
|Recurrent
|Recurrent
|3
|3
|[50, 51]
|<ref name=":48" /><ref name=":41" />
|-
|-
|22
|22
|Recurrent
|Recurrent
|1
|1
|[51]
|<ref name=":41" />
|}
|}
<references />
<references />