HAEM5:Plasma cell myeloma / multiple myeloma: Difference between revisions
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<blockquote class= | <blockquote class="blockedit">{{Box-round|title=Content Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition Classification|This page was converted to the new template on 2023-12-07. The original page can be found at [[HAEM4:Plasma Cell Myeloma]]. | ||
Other relevent pages include: [[HAEM4:Plasma Cell Myeloma Variants]] | Other relevent pages include: [[HAEM4:Plasma Cell Myeloma Variants]] | ||
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}}</blockquote> | }}</blockquote> | ||
<span style="color:#0070C0">(General Instructions – The | <span style="color:#0070C0">(General Instructions – The focus of these pages is the clinically significant genetic alterations in each disease type. This is based on up-to-date knowledge from multiple resources such as PubMed and the WHO classification books. The CCGA is meant to be a supplemental resource to the WHO classification books; the CCGA captures in a continually updated wiki-stye manner the current genetics/genomics knowledge of each disease, which evolves more rapidly than books can be revised and published. If the same disease is described in multiple WHO classification books, the genetics-related information for that disease will be consolidated into a single main page that has this template (other pages would only contain a link to this main page). Use [https://www.genenames.org/ <u>HUGO-approved gene names and symbols</u>] (italicized when appropriate), [https://varnomen.hgvs.org/ <u>HGVS-based nomenclature for variants</u>], as well as generic names of drugs and testing platforms or assays if applicable. Please complete tables whenever possible and do not delete them (add N/A if not applicable in the table and delete the examples); to add (or move) a row or column in a table, click nearby within the table and select the > symbol that appears. Please do not delete or alter the section headings. The use of bullet points alongside short blocks of text rather than only large paragraphs is encouraged. Additional instructions below in italicized blue text should not be included in the final page content. Please also see </span><u>[[Author_Instructions]]</u><span style="color:#0070C0"> and [[Frequently Asked Questions (FAQs)|<u>FAQs</u>]] as well as contact your [[Leadership|<u>Associate Editor</u>]] or [mailto:CCGA@cancergenomics.org <u>Technical Support</u>].)</span> | ||
==Primary Author(s)*== | ==Primary Author(s)*== | ||
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The University Of Texas MD Anderson Cancer Center, Department of Hematopathology, Houston, Texas | The University Of Texas MD Anderson Cancer Center, Department of Hematopathology, Houston, Texas | ||
==WHO Classification of Disease== | |||
{| class="wikitable" | |||
!Structure | |||
!Disease | |||
|- | |||
|Book | |||
|Haematolymphoid Tumours (5th ed.) | |||
|- | |||
|Category | |||
|B-cell lymphoid proliferations and lymphomas | |||
|- | |||
|Family | |||
|Plasma cell neoplasms and other diseases with paraproteins | |||
|- | |||
|Type | |||
|Plasma cell neoplasms | |||
|- | |||
|Subtype(s) | |||
|Plasma cell myeloma / multiple myeloma | |||
|} | |||
==Related Terminology== | |||
{| class="wikitable" | {| class="wikitable" | ||
| | |+ | ||
| | |Acceptable | ||
|Myeloma; multiple myeloma (plasma cell myeloma) NOS | |||
|- | |- | ||
| | |Not Recommended | ||
| | |N/A | ||
|} | |} | ||
==Gene Rearrangements== | |||
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.'')</span> | |||
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
|- | |- | ||
! | !Driver Gene!!Fusion(s) and Common Partner Genes!!Molecular Pathogenesis!!Typical Chromosomal Alteration(s) | ||
!Prevalence -Common >20%, Recurrent 5-20% or Rare <5% (Disease) | |||
!Diagnostic, Prognostic, and Therapeutic Significance - D, P, T | |||
!Established Clinical Significance Per Guidelines - Yes or No (Source) | |||
!Clinical Relevance Details/Other Notes | |||
|- | |- | ||
| | |<span class="blue-text">EXAMPLE:</span> ''ABL1''||<span class="blue-text">EXAMPLE:</span> ''BCR::ABL1''||<span class="blue-text">EXAMPLE:</span> The pathogenic derivative is the der(22) resulting in fusion of 5’ BCR and 3’ABL1.||<span class="blue-text">EXAMPLE:</span> t(9;22)(q34;q11.2) | ||
|<span class="blue-text">EXAMPLE:</span> Common (CML) | |||
|<span class="blue-text">EXAMPLE:</span> D, P, T | |||
|<span class="blue-text">EXAMPLE:</span> Yes (WHO, NCCN) | |||
|<span class="blue-text">EXAMPLE:</span> | |||
The t(9;22) is diagnostic of CML in the appropriate morphology and clinical context (add reference). This fusion is responsive to targeted therapy such as Imatinib (Gleevec) (add reference). BCR::ABL1 is generally favorable in CML (add reference). | |||
|- | |- | ||
| | |<span class="blue-text">EXAMPLE:</span> ''CIC'' | ||
|- | |<span class="blue-text">EXAMPLE:</span> ''CIC::DUX4'' | ||
| | |<span class="blue-text">EXAMPLE:</span> Typically, the last exon of ''CIC'' is fused to ''DUX4''. The fusion breakpoint in ''CIC'' is usually intra-exonic and removes an inhibitory sequence, upregulating ''PEA3'' genes downstream of ''CIC'' including ''ETV1'', ''ETV4'', and ''ETV5''. | ||
|<span class="blue-text">EXAMPLE:</span> t(4;19)(q25;q13) | |||
|<span class="blue-text">EXAMPLE:</span> Common (CIC-rearranged sarcoma) | |||
|<span class="blue-text">EXAMPLE:</span> D | |||
| | |||
|<span class="blue-text">EXAMPLE:</span> | |||
''DUX4'' has many homologous genes; an alternate translocation in a minority of cases is t(10;19), but this is usually indistinguishable from t(4;19) by short-read sequencing (add references). | |||
|- | |- | ||
|<span class="blue-text">EXAMPLE:</span> ''ALK'' | |||
| | |<span class="blue-text">EXAMPLE:</span> ''ELM4::ALK'' | ||
Other fusion partners include ''KIF5B, NPM1, STRN, TFG, TPM3, CLTC, KLC1'' | |||
|<span class="blue-text">EXAMPLE:</span> Fusions result in constitutive activation of the ''ALK'' tyrosine kinase. The most common ''ALK'' fusion is ''EML4::ALK'', with breakpoints in intron 19 of ''ALK''. At the transcript level, a variable (5’) partner gene is fused to 3’ ''ALK'' at exon 20. Rarely, ''ALK'' fusions contain exon 19 due to breakpoints in intron 18. | |||
|<span class="blue-text">EXAMPLE:</span> N/A | |||
|<span class="blue-text">EXAMPLE:</span> Rare (Lung adenocarcinoma) | |||
|<span class="blue-text">EXAMPLE:</span> T | |||
| | |||
|<span class="blue-text">EXAMPLE:</span> | |||
</ | |||
Both balanced and unbalanced forms are observed by FISH (add references). | |||
|- | |- | ||
|<span class="blue-text">EXAMPLE:</span> ''ABL1'' | |||
|<span class="blue-text">EXAMPLE:</span> N/A | |||
|<span class="blue-text">EXAMPLE:</span> Intragenic deletion of exons 2–7 in ''EGFR'' removes the ligand-binding domain, resulting in a constitutively active tyrosine kinase with downstream activation of multiple oncogenic pathways. | |||
|<span class="blue-text">EXAMPLE:</span> N/A | |||
|<span class="blue-text">EXAMPLE:</span> Recurrent (IDH-wildtype Glioblastoma) | |||
|<span class="blue-text">EXAMPLE:</span> D, P, T | |||
| | |||
| | |||
|- | |- | ||
| | | | ||
| | |||
| | | | ||
| | | | ||
| | | | ||
| | | | ||
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|} | |||
<blockquote class="blockedit">{{Box-round|title=v4:Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications).|Please incorporate this section into the relevant tables found in: | |||
<blockquote class= | |||
* Chromosomal Rearrangements (Gene Fusions) | * Chromosomal Rearrangements (Gene Fusions) | ||
* Individual Region Genomic Gain/Loss/LOH | * Individual Region Genomic Gain/Loss/LOH | ||
* Characteristic Chromosomal Patterns | * Characteristic Chromosomal Patterns | ||
* Gene Mutations (SNV/INDEL)}} | * Gene Mutations (SNV/INDEL)}}</blockquote> | ||
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'''Gene mutation'''s are also helpful for risk stratification in plasma cell myeloma, e.g., mutations of IRF4 or PRDM1 genes involving plasma cell differentiation are usually indicative for a favorable prognosis, while mutation of ''TP53'', ''ATM'' or ''ATR'' genes involving DNA repair pathway mostly imply for a poor prognosis. <ref name=":11" /> | '''Gene mutation'''s are also helpful for risk stratification in plasma cell myeloma, e.g., mutations of IRF4 or PRDM1 genes involving plasma cell differentiation are usually indicative for a favorable prognosis, while mutation of ''TP53'', ''ATM'' or ''ATR'' genes involving DNA repair pathway mostly imply for a poor prognosis. <ref name=":11" /> | ||
<blockquote class="blockedit"> | |||
<center><span style="color:Maroon">'''End of V4 Section'''</span> | |||
---- | |||
</blockquote> | </blockquote> | ||
==Individual Region Genomic Gain / Loss / LOH== | ==Individual Region Genomic Gain/Loss/LOH== | ||
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Includes aberrations not involving gene rearrangements. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Can refer to CGC workgroup tables as linked on the homepage if applicable. Please include references throughout the table. Do not delete the table.'') </span> | |||
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
|- | |- | ||
!Chr #!!Gain | !Chr #!!Gain, Loss, Amp, LOH!!Minimal Region Cytoband and/or Genomic Coordinates [Genome Build; Size]!!Relevant Gene(s) | ||
!Diagnostic | !Diagnostic, Prognostic, and Therapeutic Significance - D, P, T | ||
!Established Clinical Significance Per Guidelines - Yes or No (Source) | |||
! | !Clinical Relevance Details/Other Notes | ||
!Notes | |||
|- | |- | ||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> | ||
7 | 7 | ||
|<span class="blue-text">EXAMPLE:</span> Loss | |<span class="blue-text">EXAMPLE:</span> Loss | ||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> | ||
chr7 | |||
chr7 | |||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> | ||
Unknown | |||
|<span class="blue-text">EXAMPLE:</span> D, P | |||
|<span class="blue-text">EXAMPLE:</span> No | |||
| | |||
|No | |||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> | ||
Presence of monosomy 7 (or 7q deletion) is sufficient for a diagnosis of AML with MDS-related changes when there is ≥20% blasts and no prior therapy (add reference). Monosomy 7/7q deletion is associated with a poor prognosis in AML (add references). | |||
Presence of monosomy 7 (or 7q deletion) is sufficient for a diagnosis of AML with MDS-related changes when there is ≥20% blasts and no prior therapy (add reference). Monosomy 7/7q deletion is associated with a poor prognosis in AML (add | |||
|- | |- | ||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> | ||
8 | 8 | ||
|<span class="blue-text">EXAMPLE:</span> Gain | |<span class="blue-text">EXAMPLE:</span> Gain | ||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> | ||
chr8 | |||
|<span class="blue-text">EXAMPLE:</span> | |||
Unknown | |||
|<span class="blue-text">EXAMPLE:</span> D, P | |||
| | |||
|<span class="blue-text">EXAMPLE:</span> | |||
Common recurrent secondary finding for t(8;21) (add references). | |||
|- | |||
|<span class="blue-text">EXAMPLE:</span> | |||
17 | |||
|<span class="blue-text">EXAMPLE:</span> Amp | |||
|<span class="blue-text">EXAMPLE:</span> | |||
17q12; chr17:39,700,064-39,728,658 [hg38; 28.6 kb] | |||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> | ||
''ERBB2'' | |||
|<span class="blue-text">EXAMPLE:</span> D, P, T | |||
| | |||
| | |||
| | |||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> | ||
Amplification of ''ERBB2'' is associated with HER2 overexpression in HER2 positive breast cancer (add references). Add criteria for how amplification is defined. | |||
|- | |||
| | |||
| | |||
| | |||
| | |||
| | |||
| | |||
| | |||
|} | |} | ||
==Characteristic Chromosomal Patterns== | ==Characteristic Chromosomal or Other Global Mutational Patterns== | ||
Put your text here and fill in the table <span style="color:#0070C0">(I''nstructions: Included in this category are alterations such as hyperdiploid; gain of odd number chromosomes including typically chromosome 1, 3, 5, 7, 11, and 17; co-deletion of 1p and 19q; complex karyotypes without characteristic genetic findings; chromothripsis; microsatellite instability; homologous recombination deficiency; mutational signature pattern; etc. Details on clinical significance such as prognosis and other important information can be provided in the notes section. Please include references throughout the table. Do not delete the table.'')</span> | |||
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
|- | |- | ||
!Chromosomal Pattern | !Chromosomal Pattern | ||
! | !Molecular Pathogenesis | ||
!Prognostic Significance | !Prevalence - | ||
! | Common >20%, Recurrent 5-20% or Rare <5% (Disease) | ||
!Notes | !Diagnostic, Prognostic, and Therapeutic Significance - D, P, T | ||
!Established Clinical Significance Per Guidelines - Yes or No (Source) | |||
!Clinical Relevance Details/Other Notes | |||
|- | |- | ||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> | ||
Co-deletion of 1p and 18q | Co-deletion of 1p and 18q | ||
| | |<span class="blue-text">EXAMPLE:</span> See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference). | ||
| | |<span class="blue-text">EXAMPLE:</span> Common (Oligodendroglioma) | ||
| | |<span class="blue-text">EXAMPLE:</span> D, P | ||
| | |||
| | |||
|- | |||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> | ||
Microsatellite instability - hypermutated | |||
| | |||
|<span class="blue-text">EXAMPLE:</span> Common (Endometrial carcinoma) | |||
|<span class="blue-text">EXAMPLE:</span> P, T | |||
| | |||
| | |||
|- | |||
| | |||
| | |||
| | |||
| | |||
| | |||
| | |||
|} | |} | ||
<blockquote class= | <blockquote class="blockedit">{{Box-round|title=v4:Characteristic Chromosomal Aberrations / Patterns|The content below was from the old template. Please incorporate above.}}</blockquote> | ||
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<br /> | <br /> | ||
<blockquote class="blockedit"> | |||
<center><span style="color:Maroon">'''End of V4 Section'''</span> | |||
---- | |||
</blockquote> | </blockquote> | ||
==Gene Mutations (SNV / INDEL)== | ==Gene Mutations (SNV/INDEL)== | ||
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: This table is not meant to be an exhaustive list; please include only genes/alterations that are recurrent or common as well either disease defining and/or clinically significant. If a gene has multiple mechanisms depending on the type or site of the alteration, add multiple entries in the table. For clinical significance, denote associations with FDA-approved therapy (not an extensive list of applicable drugs) and NCCN or other national guidelines if applicable; Can also refer to CGC workgroup tables as linked on the homepage if applicable as well as any high impact papers or reviews of gene mutations in this entity. Details on clinical significance such as prognosis and other important information such as concomitant and mutually exclusive mutations can be provided in the notes section. Please include references throughout the table. Do not delete the table.'') </span> | |||
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
|- | |- | ||
!Gene | !Gene!!Genetic Alteration!!Tumor Suppressor Gene, Oncogene, Other!!Prevalence - | ||
! | Common >20%, Recurrent 5-20% or Rare <5% (Disease) | ||
!Diagnostic, Prognostic, and Therapeutic Significance - D, P, T | |||
! | !Established Clinical Significance Per Guidelines - Yes or No (Source) | ||
!Notes | !Clinical Relevance Details/Other Notes | ||
|- | |- | ||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span>''EGFR'' | ||
<span class="blue-text">EXAMPLE:</span> | <br /> | ||
|<span class="blue-text">EXAMPLE:</span> Exon 18-21 activating mutations | |||
|<span class="blue-text">EXAMPLE:</span> Oncogene | |||
|<span class="blue-text">EXAMPLE:</span> Common (lung cancer) | |||
<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> T | ||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> Yes (NCCN) | ||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> Exons 18, 19, and 21 mutations are targetable for therapy. Exon 20 T790M variants cause resistance to first generation TKI therapy and are targetable by second and third generation TKIs (add references). | ||
|- | |||
<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> ''TP53''; Variable LOF mutations | ||
|<span class="blue-text">EXAMPLE:</span> | <br /> | ||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> Variable LOF mutations | ||
|<span class="blue-text">EXAMPLE:</span> Tumor Supressor Gene | |||
|<span class="blue-text">EXAMPLE:</span> Common (breast cancer) | |||
|<span class="blue-text">EXAMPLE:</span> P | |||
| | |||
|<span class="blue-text">EXAMPLE:</span> >90% are somatic; rare germline alterations associated with Li-Fraumeni syndrome (add reference). Denotes a poor prognosis in breast cancer. | |||
|- | |||
|<span class="blue-text">EXAMPLE:</span> ''BRAF''; Activating mutations | |||
|<span class="blue-text">EXAMPLE:</span> Activating mutations | |||
|<span class="blue-text">EXAMPLE:</span> Oncogene | |||
|<span class="blue-text">EXAMPLE:</span> Common (melanoma) | |||
|<span class="blue-text">EXAMPLE:</span> T | |||
| | |||
| | |||
|- | |||
| | |||
| | |||
| | |||
| | |||
| | | | ||
| | | | ||
| | | | ||
|}Note: A more extensive list of mutations can be found in [https://www.cbioportal.org/ <u>cBioportal</u>], [https://cancer.sanger.ac.uk/cosmic <u>COSMIC</u>], and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content. | |||
|} | |||
Note: A more extensive list of mutations can be found in | |||
<blockquote class= | <blockquote class="blockedit">{{Box-round|title=v4:Gene Mutations (SNV/INDEL)|The content below was from the old template. Please incorporate above.}}</blockquote> | ||
'''THIS SECTION NEEDS REFERENCES.''' | '''THIS SECTION NEEDS REFERENCES.''' | ||
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|} | |} | ||
<blockquote class="blockedit"> | |||
<center><span style="color:Maroon">'''End of V4 Section'''</span> | |||
---- | |||
</blockquote> | </blockquote> | ||
==Epigenomic Alterations== | ==Epigenomic Alterations== | ||
| Line 562: | Line 541: | ||
==Genes and Main Pathways Involved== | ==Genes and Main Pathways Involved== | ||
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: | |||
Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Please include references throughout the table. Do not delete the table.)''</span> | |||
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
|- | |- | ||
!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome | !Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome | ||
|- | |- | ||
|<span class="blue-text">EXAMPLE:</span> BRAF and MAP2K1; Activating mutations | |<span class="blue-text">EXAMPLE:</span> ''BRAF'' and ''MAP2K1''; Activating mutations | ||
|<span class="blue-text">EXAMPLE:</span> MAPK signaling | |<span class="blue-text">EXAMPLE:</span> MAPK signaling | ||
|<span class="blue-text">EXAMPLE:</span> Increased cell growth and proliferation | |<span class="blue-text">EXAMPLE:</span> Increased cell growth and proliferation | ||
|- | |- | ||
|<span class="blue-text">EXAMPLE:</span> CDKN2A; Inactivating mutations | |<span class="blue-text">EXAMPLE:</span> ''CDKN2A''; Inactivating mutations | ||
|<span class="blue-text">EXAMPLE:</span> Cell cycle regulation | |<span class="blue-text">EXAMPLE:</span> Cell cycle regulation | ||
|<span class="blue-text">EXAMPLE:</span> Unregulated cell division | |<span class="blue-text">EXAMPLE:</span> Unregulated cell division | ||
|- | |- | ||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> ''KMT2C'' and ''ARID1A''; Inactivating mutations | ||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> Histone modification, chromatin remodeling | ||
|<span class="blue-text">EXAMPLE:</span> | |<span class="blue-text">EXAMPLE:</span> Abnormal gene expression program | ||
|- | |||
| | |||
| | |||
| | |||
|} | |} | ||
<blockquote class= | <blockquote class="blockedit">{{Box-round|title=v4:Genes and Main Pathways Involved|The content below was from the old template. Please incorporate above.}}</blockquote> | ||
Due to the wide spectrum of chromosomal abnormalities and somatic mutations identified in plasma cell myeloma, it’s believed that the oncogenesis and development of plasma cell myeloma may also involve many pathways. Please refer to review articles for more detailed information. <ref name=":9" /><ref name=":11">{{Cite journal|last=Manier|first=Salomon|last2=Salem|first2=Karma Z.|last3=Park|first3=Jihye|last4=Landau|first4=Dan A.|last5=Getz|first5=Gad|last6=Ghobrial|first6=Irene M.|date=02 2017|title=Genomic complexity of multiple myeloma and its clinical implications|url=https://pubmed.ncbi.nlm.nih.gov/27531699|journal=Nature Reviews. Clinical Oncology|volume=14|issue=2|pages=100–113|doi=10.1038/nrclinonc.2016.122|issn=1759-4782|pmid=27531699}}</ref> | Due to the wide spectrum of chromosomal abnormalities and somatic mutations identified in plasma cell myeloma, it’s believed that the oncogenesis and development of plasma cell myeloma may also involve many pathways. Please refer to review articles for more detailed information. <ref name=":9" /><ref name=":11">{{Cite journal|last=Manier|first=Salomon|last2=Salem|first2=Karma Z.|last3=Park|first3=Jihye|last4=Landau|first4=Dan A.|last5=Getz|first5=Gad|last6=Ghobrial|first6=Irene M.|date=02 2017|title=Genomic complexity of multiple myeloma and its clinical implications|url=https://pubmed.ncbi.nlm.nih.gov/27531699|journal=Nature Reviews. Clinical Oncology|volume=14|issue=2|pages=100–113|doi=10.1038/nrclinonc.2016.122|issn=1759-4782|pmid=27531699}}</ref> | ||
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'''MYC activation''': ''MYC'' rearrangement is found in 8% of the newly diagnosed myeloma patient in a Mayo Clinic study. It is associated with high disease burden and is an independent adverse prognostic factor. <ref>{{Cite journal|last=Abdallah|first=Nadine|last2=Baughn|first2=Linda B.|last3=Rajkumar|first3=S. Vincent|last4=Kapoor|first4=Prashant|last5=Gertz|first5=Morie A.|last6=Dispenzieri|first6=Angela|last7=Lacy|first7=Martha Q.|last8=Hayman|first8=Suzanne R.|last9=Buadi|first9=Francis K.|date=2020-12-15|title=Implications of MYC Rearrangements in Newly Diagnosed Multiple Myeloma|url=https://pubmed.ncbi.nlm.nih.gov/33008815|journal=Clinical Cancer Research: An Official Journal of the American Association for Cancer Research|volume=26|issue=24|pages=6581–6588|doi=10.1158/1078-0432.CCR-20-2283|issn=1557-3265|pmid=33008815}}</ref> | '''MYC activation''': ''MYC'' rearrangement is found in 8% of the newly diagnosed myeloma patient in a Mayo Clinic study. It is associated with high disease burden and is an independent adverse prognostic factor. <ref>{{Cite journal|last=Abdallah|first=Nadine|last2=Baughn|first2=Linda B.|last3=Rajkumar|first3=S. Vincent|last4=Kapoor|first4=Prashant|last5=Gertz|first5=Morie A.|last6=Dispenzieri|first6=Angela|last7=Lacy|first7=Martha Q.|last8=Hayman|first8=Suzanne R.|last9=Buadi|first9=Francis K.|date=2020-12-15|title=Implications of MYC Rearrangements in Newly Diagnosed Multiple Myeloma|url=https://pubmed.ncbi.nlm.nih.gov/33008815|journal=Clinical Cancer Research: An Official Journal of the American Association for Cancer Research|volume=26|issue=24|pages=6581–6588|doi=10.1158/1078-0432.CCR-20-2283|issn=1557-3265|pmid=33008815}}</ref> | ||
<blockquote class="blockedit"> | |||
<center><span style="color:Maroon">'''End of V4 Section'''</span> | |||
---- | |||
</blockquote> | </blockquote> | ||
==Genetic Diagnostic Testing Methods== | ==Genetic Diagnostic Testing Methods== | ||
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==References== | ==References== | ||
(use the "Cite" icon at the top of the page) <span style="color:#0070C0">(''Instructions: Add each reference into the text above by clicking | (use the "Cite" icon at the top of the page) <span style="color:#0070C0">(''Instructions: Add each reference into the text above by clicking where you want to insert the reference, selecting the “Cite” icon at the top of the wiki page, and using the “Automatic” tab option to search by PMID to select the reference to insert. If a PMID is not available, such as for a book, please use the “Cite” icon, select “Manual” and then “Basic Form”, and include the entire reference. To insert the same reference again later in the page, select the “Cite” icon and “Re-use” to find the reference; DO NOT insert the same reference twice using the “Automatic” tab as it will be treated as two separate references. The reference list in this section will be automatically generated and sorted''</span><span style="color:#0070C0">''.''</span><span style="color:#0070C0">)</span> <references /> | ||
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==Notes== | ==Notes== | ||
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<nowiki>*</nowiki>''Citation of this Page'': “Plasma cell myeloma / multiple myeloma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/HAEM5:Plasma_cell_myeloma_/_multiple_myeloma</nowiki>. | <nowiki>*</nowiki>''Citation of this Page'': “Plasma cell myeloma / multiple myeloma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/HAEM5:Plasma_cell_myeloma_/_multiple_myeloma</nowiki>. | ||
[[Category:HAEM5]][[Category:DISEASE]][[Category:Diseases P]] | [[Category:HAEM5]] | ||
[[Category:DISEASE]] | |||
[[Category:Diseases P]] | |||