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{{DISPLAYTITLE:ALK-positive large B-cell lymphoma}} | {{DISPLAYTITLE:ALK-positive large B-cell lymphoma}} | ||
| − | [[HAEM5:Table_of_Contents|Haematolymphoid Tumours (5th ed.)]] | + | [[HAEM5:Table_of_Contents|Haematolymphoid Tumours (WHO Classification, 5th ed.)]] |
{{Under Construction}} | {{Under Construction}} | ||
| − | <blockquote class='blockedit'>{{Box-round|title= | + | <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:ALK-Positive Large B-cell Lymphoma]]. |
}}</blockquote> | }}</blockquote> | ||
| − | <span style="color:#0070C0">(General Instructions – The main focus of these pages is the clinically significant genetic alterations in each disease type. Use [https://www.genenames.org/ <u>HUGO-approved gene names and symbols</u>] (italicized when appropriate), [https://varnomen.hgvs.org/ HGVS-based nomenclature for variants], 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). 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> | + | <span style="color:#0070C0">(General Instructions – The main focus of these pages is the clinically significant genetic alterations in each disease type. Use [https://www.genenames.org/ <u>HUGO-approved gene names and symbols</u>] (italicized when appropriate), [https://varnomen.hgvs.org/ HGVS-based nomenclature for variants], 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 to a table, click within the table and select the > symbol that appears to be given options. 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)*== | ||
| Line 17: | Line 17: | ||
__TOC__ | __TOC__ | ||
| − | == | + | ==WHO Classification of Disease== |
| − | Mature B cell | + | {| class="wikitable" |
| − | + | !Structure | |
| − | + | !Disease | |
| − | + | |- | |
| − | Large B-cell lymphomas | + | |Book |
| + | |Haematolymphoid Tumours (5th ed.) | ||
| + | |- | ||
| + | |Category | ||
| + | |B-cell lymphoid proliferations and lymphomas | ||
| + | |- | ||
| + | |Family | ||
| + | |Mature B-cell neoplasms | ||
| + | |- | ||
| + | |Type | ||
| + | |Large B-cell lymphomas | ||
| + | |- | ||
| + | |Subtype(s) | ||
| + | |ALK-positive large B-cell lymphoma | ||
| + | |} | ||
==Definition / Description of Disease== | ==Definition / Description of Disease== | ||
| Line 88: | Line 102: | ||
!Notes | !Notes | ||
|- | |- | ||
| − | |EXAMPLE t(9;22)(q34;q11.2)||EXAMPLE 3'ABL1 / 5'BCR||EXAMPLE der(22)||EXAMPLE 20% (COSMIC) | + | |<span class="blue-text">EXAMPLE:</span> t(9;22)(q34;q11.2)||<span class="blue-text">EXAMPLE:</span> 3'ABL1 / 5'BCR||<span class="blue-text">EXAMPLE:</span> der(22)||<span class="blue-text">EXAMPLE:</span> 20% (COSMIC) |
| − | EXAMPLE 30% (add reference) | + | <span class="blue-text">EXAMPLE:</span> 30% (add reference) |
|Yes | |Yes | ||
|No | |No | ||
|Yes | |Yes | ||
| − | |EXAMPLE | + | |<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). | 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). | ||
| Line 151: | Line 165: | ||
==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 fusions. Can include references in the table. Can refer to CGC workgroup tables as linked on the homepage if applicable.'') </span> | + | Put your text here and fill in the table <span style="color:#0070C0">(''Instructions: Includes aberrations not involving gene fusions. Can include references in the table. Can refer to CGC workgroup tables as linked on the homepage if applicable. Do not delete table.'') </span> |
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
| Line 161: | Line 175: | ||
!Notes | !Notes | ||
|- | |- | ||
| − | |EXAMPLE | + | |<span class="blue-text">EXAMPLE:</span> |
7 | 7 | ||
| − | |EXAMPLE Loss | + | |<span class="blue-text">EXAMPLE:</span> Loss |
| − | |EXAMPLE | + | |<span class="blue-text">EXAMPLE:</span> |
chr7:1- 159,335,973 [hg38] | chr7:1- 159,335,973 [hg38] | ||
| − | |EXAMPLE | + | |<span class="blue-text">EXAMPLE:</span> |
chr7 | chr7 | ||
| Line 174: | Line 188: | ||
|Yes | |Yes | ||
|No | |No | ||
| − | |EXAMPLE | + | |<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 reference). | 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 reference). | ||
|- | |- | ||
| − | |EXAMPLE | + | |<span class="blue-text">EXAMPLE:</span> |
8 | 8 | ||
| − | |EXAMPLE Gain | + | |<span class="blue-text">EXAMPLE:</span> Gain |
| − | |EXAMPLE | + | |<span class="blue-text">EXAMPLE:</span> |
chr8:1-145,138,636 [hg38] | chr8:1-145,138,636 [hg38] | ||
| − | |EXAMPLE | + | |<span class="blue-text">EXAMPLE:</span> |
chr8 | chr8 | ||
| Line 191: | Line 205: | ||
|No | |No | ||
|No | |No | ||
| − | |EXAMPLE | + | |<span class="blue-text">EXAMPLE:</span> |
Common recurrent secondary finding for t(8;21) (add reference). | Common recurrent secondary finding for t(8;21) (add reference). | ||
| Line 202: | Line 216: | ||
==Characteristic Chromosomal Patterns== | ==Characteristic Chromosomal Patterns== | ||
| − | Put your text here <span style="color:#0070C0">(''EXAMPLE PATTERNS: 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'')</span> | + | Put your text here <span style="color:#0070C0">(''EXAMPLE PATTERNS: 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. Do not delete table.'')</span> |
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
| Line 212: | Line 226: | ||
!Notes | !Notes | ||
|- | |- | ||
| − | |EXAMPLE | + | |<span class="blue-text">EXAMPLE:</span> |
Co-deletion of 1p and 18q | Co-deletion of 1p and 18q | ||
| Line 218: | Line 232: | ||
|No | |No | ||
|No | |No | ||
| − | |EXAMPLE: | + | |<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). | See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference). | ||
| Line 229: | Line 243: | ||
==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 and common as well either disease defining and/or clinically significant. Can include references 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 | + | 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 and common as well as either disease defining and/or clinically significant. Can include references 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. Do not delete table.'') </span> |
{| class="wikitable sortable" | {| class="wikitable sortable" | ||
| Line 239: | Line 253: | ||
!Notes | !Notes | ||
|- | |- | ||
| − | |EXAMPLE: TP53; Variable LOF mutations | + | |<span class="blue-text">EXAMPLE:</span> TP53; Variable LOF mutations |
| − | EXAMPLE: | + | <span class="blue-text">EXAMPLE:</span> |
EGFR; Exon 20 mutations | EGFR; Exon 20 mutations | ||
| − | EXAMPLE: BRAF; Activating mutations | + | <span class="blue-text">EXAMPLE:</span> BRAF; Activating mutations |
| − | |EXAMPLE: TSG | + | |<span class="blue-text">EXAMPLE:</span> TSG |
| − | |EXAMPLE: 20% (COSMIC) | + | |<span class="blue-text">EXAMPLE:</span> 20% (COSMIC) |
| − | EXAMPLE: 30% (add Reference) | + | <span class="blue-text">EXAMPLE:</span> 30% (add Reference) |
| − | |EXAMPLE: IDH1 R123H | + | |<span class="blue-text">EXAMPLE:</span> IDH1 R123H |
| − | |EXAMPLE: EGFR amplification | + | |<span class="blue-text">EXAMPLE:</span> EGFR amplification |
| | | | ||
| | | | ||
| | | | ||
| − | |EXAMPLE: Excludes hairy cell leukemia (HCL) (add reference). | + | |<span class="blue-text">EXAMPLE:</span> Excludes hairy cell leukemia (HCL) (add reference). |
<br /> | <br /> | ||
|} | |} | ||
Latest revision as of 17:29, 6 September 2024
Haematolymphoid Tumours (WHO Classification, 5th ed.)
 | This page is under construction |
editContent Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition ClassificationThis page was converted to the new template on 2023-12-07. The original page can be found at HAEM4:ALK-Positive Large B-cell Lymphoma.
(General Instructions – The main focus of these pages is the clinically significant genetic alterations in each disease type. Use HUGO-approved gene names and symbols (italicized when appropriate), HGVS-based nomenclature for variants, 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 to a table, click within the table and select the > symbol that appears to be given options. 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 Author_Instructions and FAQs as well as contact your Associate Editor or Technical Support)
Primary Author(s)*
Manando Nakasaki, MD, PhD (University of California, Irvine)
Fabiola Quintero-Rivera, MD, FACMG (University of California, Irvine)
WHO Classification of Disease
| Structure | Disease |
|---|---|
| Book | Haematolymphoid Tumours (5th ed.) |
| Category | B-cell lymphoid proliferations and lymphomas |
| Family | Mature B-cell neoplasms |
| Type | Large B-cell lymphomas |
| Subtype(s) | ALK-positive large B-cell lymphoma |
Definition / Description of Disease
Diffuse, monomorphic neoplasm of large B-cells with a plasmablastic immunophenotype and ALK expression due to ALK rearrangement
Synonyms / Terminology
Not recommended: ALK-positive plasmablastic B-cell lymphoma; ALK-positive diffuse large B-cell lymphoma
Epidemiology / Prevalence
- <1% of large B-cell lymphomas
- ~ 200 cases reported in literature to date[1]
Clinical Features
| Signs and Symptoms | Asymptomatic lymphadenopathy
B-symptoms |
| Laboratory Findings | Serum LDH elevation |
Sites of Involvement
- Lymph nodes are most commonly involved (~ 75%)
- Extranodal sites: bone marrow, GI tract, liver, epidural space, ovaries, skeletal system, nasopharyngeal/nasal area, tongue, and brain[6][7][8]
Morphologic Features
- Partial or diffuse effacement of lymph node architecture
- Lymphoma cells infiltrate sinusoids[9][10]
- Monomorphic infiltrate of large cells with abundant amphophilic or eosinophilic cytoplasm
Immunophenotype
| Finding | Marker |
|---|---|
| Positive (universal) | ALK, CD138, VS38, IRF4/MUM1, BLIMP1, XBP1 |
| Positive (subset) | EMA (90%), Cytoplasmic Ig (90%), IgA (80%), CD45 (90%), CD30 (15%), CD4 (50%), CD57 (10%), CD43, Cytokeratin (10%) |
| Negative (universal) | Pan-T cell antigens, CD8, B-cell antigens, CD10, BCL-6, Cyclin-D1, HHV8 |
Chromosomal Rearrangements (Gene Fusions)
Put your text here and fill in the table
| Chromosomal Rearrangement | Genes in Fusion (5’ or 3’ Segments) | Pathogenic Derivative | Prevalence | Diagnostic Significance (Yes, No or Unknown) | Prognostic Significance (Yes, No or Unknown) | Therapeutic Significance (Yes, No or Unknown) | Notes |
|---|---|---|---|---|---|---|---|
| EXAMPLE: t(9;22)(q34;q11.2) | EXAMPLE: 3'ABL1 / 5'BCR | EXAMPLE: der(22) | EXAMPLE: 20% (COSMIC)
EXAMPLE: 30% (add reference) |
Yes | No | Yes | EXAMPLE:
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). |
editv4:Chromosomal Rearrangements (Gene Fusions)The content below was from the previous version of the page. Please incorporate above.
Chromosomal Rearrangement Genes in Fusion (5’ or 3’ Segments) ALK Immunostain Pattern Prevalence Notes t(2;17)(p23;q23) CLTC::ALK Cytoplasmic; granular Most common [11] t(2;5)(p23;q35) NPM::ALK Nuclear and cytoplasmic [12] t(2;5)(p23;q35.3) SQSTM1::ALK Cytoplasmic; diffuse [13] inv(2)(p23q13) or t(2;2)(p23;q13) RANBP2::ALK Nuclear membrane and perinuclear punctate [14] inv(2)(p21p23) EML4::ALK Cytoplasmic; diffuse [15] inv(2)(p21q31.1) or t(2;2)(p23;q31.1) GORASP2::ALK Cytoplasmic; diffuse [16] Cryptic SEC31A::ALK Cytoplasmic; granular [17]
Individual Region Genomic Gain / Loss / LOH
Put your text here and fill in the table (Instructions: Includes aberrations not involving gene fusions. Can include references in the table. Can refer to CGC workgroup tables as linked on the homepage if applicable. Do not delete table.)
| Chr # | Gain / Loss / Amp / LOH | Minimal Region Genomic Coordinates [Genome Build] | Minimal Region Cytoband | Diagnostic Significance (Yes, No or Unknown) | Prognostic Significance (Yes, No or Unknown) | Therapeutic Significance (Yes, No or Unknown) | Notes |
|---|---|---|---|---|---|---|---|
| EXAMPLE:
7 |
EXAMPLE: Loss | EXAMPLE:
chr7:1- 159,335,973 [hg38] |
EXAMPLE:
chr7 |
Yes | Yes | No | EXAMPLE:
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 reference). |
| EXAMPLE:
8 |
EXAMPLE: Gain | EXAMPLE:
chr8:1-145,138,636 [hg38] |
EXAMPLE:
chr8 |
No | No | No | EXAMPLE:
Common recurrent secondary finding for t(8;21) (add reference). |
editv4:Individual Region Genomic Gain / Loss / LOHThe content below was from the previous version of the page. Please incorporate above.Gains or amplifications of MYC (~50% of cases)[18]
Characteristic Chromosomal Patterns
Put your text here (EXAMPLE PATTERNS: 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. Do not delete table.)
| Chromosomal Pattern | Diagnostic Significance (Yes, No or Unknown) | Prognostic Significance (Yes, No or Unknown) | Therapeutic Significance (Yes, No or Unknown) | Notes |
|---|---|---|---|---|
| EXAMPLE:
Co-deletion of 1p and 18q |
Yes | No | No | EXAMPLE:
See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference). |
editv4:Characteristic Chromosomal PatternsThe content below was from the previous version of the page. Please incorporate above.N/A
Gene Mutations (SNV / INDEL)
Put your text here and fill in the table (Instructions: This table is not meant to be an exhaustive list; please include only genes/alterations that are recurrent and common as well as either disease defining and/or clinically significant. Can include references 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. Do not delete table.)
| Gene; Genetic Alteration | Presumed Mechanism (Tumor Suppressor Gene [TSG] / Oncogene / Other) | Prevalence (COSMIC / TCGA / Other) | Concomitant Mutations | Mutually Exclusive Mutations | Diagnostic Significance (Yes, No or Unknown) | Prognostic Significance (Yes, No or Unknown) | Therapeutic Significance (Yes, No or Unknown) | Notes |
|---|---|---|---|---|---|---|---|---|
| EXAMPLE: TP53; Variable LOF mutations
EXAMPLE: EGFR; Exon 20 mutations EXAMPLE: BRAF; Activating mutations |
EXAMPLE: TSG | EXAMPLE: 20% (COSMIC)
EXAMPLE: 30% (add Reference) |
EXAMPLE: IDH1 R123H | EXAMPLE: EGFR amplification | EXAMPLE: Excludes hairy cell leukemia (HCL) (add reference).
|
Note: A more extensive list of mutations can be found in cBioportal (https://www.cbioportal.org/), COSMIC (https://cancer.sanger.ac.uk/cosmic), ICGC (https://dcc.icgc.org/) and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.
editv4:Gene Mutations (SNV / INDEL)The content below was from the previous version of the page. Please incorporate above.N/A
Epigenomic Alterations
N/A
Genes and Main Pathways Involved
| Gene; Genetic Alteration | Pathway | Pathophysiologic Outcome |
|---|---|---|
| ALK rearrangement; Activating fusions | JAK/STAT, PI3K/AKT, MAPK/ERK and phospholipase C gamma 2 (PLCG2) pathways | Transformation, increased growth and inhibition of apoptosis |
Genetic Diagnostic Testing Methods
- Detection of ALK rearrangement by NGS or FISH
- Monoclonal IGH rearrangements by PCR
Familial Forms
N/A
Additional Information
N/A
Links
N/A
References
- ↑ Castillo, Jorge J.; et al. (2021-12). "Anaplastic lymphoma kinase-positive large B-cell lymphoma (ALK + LBCL): a systematic review of clinicopathological features and management". Leukemia & Lymphoma. 62 (12): 2845–2853. doi:10.1080/10428194.2021.1941929. ISSN 1029-2403. PMID 34151703 Check
|pmid=value (help). Check date values in:|date=(help) - ↑ Pan, Zenggang; et al. (2017-01). "ALK-positive Large B-cell Lymphoma: A Clinicopathologic Study of 26 Cases With Review of Additional 108 Cases in the Literature". The American Journal of Surgical Pathology. 41 (1): 25–38. doi:10.1097/PAS.0000000000000753. ISSN 1532-0979. PMID 27740969. Check date values in:
|date=(help) - ↑ Castillo, Jorge J.; et al. (2021-12). "Anaplastic lymphoma kinase-positive large B-cell lymphoma (ALK + LBCL): a systematic review of clinicopathological features and management". Leukemia & Lymphoma. 62 (12): 2845–2853. doi:10.1080/10428194.2021.1941929. ISSN 1029-2403. PMID 34151703 Check
|pmid=value (help). Check date values in:|date=(help) - ↑ Sukswai, Narittee; et al. (2020-01). "Diffuse large B-cell lymphoma variants: an update". Pathology. 52 (1): 53–67. doi:10.1016/j.pathol.2019.08.013. ISSN 1465-3931. PMID 31735345. Check date values in:
|date=(help) - ↑ Castillo, Jorge J.; et al. (2021-12). "Anaplastic lymphoma kinase-positive large B-cell lymphoma (ALK + LBCL): a systematic review of clinicopathological features and management". Leukemia & Lymphoma. 62 (12): 2845–2853. doi:10.1080/10428194.2021.1941929. ISSN 1029-2403. PMID 34151703 Check
|pmid=value (help). Check date values in:|date=(help) - ↑ Morgan, Elizabeth A.; et al. (2012). "Anaplastic lymphoma kinase-positive large B-cell lymphoma: an underrecognized aggressive lymphoma". Advances in Hematology. 2012: 529572. doi:10.1155/2012/529572. ISSN 1687-9112. PMC 3299366. PMID 22474449.
- ↑ Pan, Zenggang; et al. (2017-01). "ALK-positive Large B-cell Lymphoma: A Clinicopathologic Study of 26 Cases With Review of Additional 108 Cases in the Literature". The American Journal of Surgical Pathology. 41 (1): 25–38. doi:10.1097/PAS.0000000000000753. ISSN 1532-0979. PMID 27740969. Check date values in:
|date=(help) - ↑ Laurent, Camille; et al. (2009-09-01). "Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma: a rare clinicopathologic entity with poor prognosis". Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology. 27 (25): 4211–4216. doi:10.1200/JCO.2008.21.5020. ISSN 1527-7755. PMID 19636007.
- ↑ Pan, Zenggang; et al. (2017-01). "ALK-positive Large B-cell Lymphoma: A Clinicopathologic Study of 26 Cases With Review of Additional 108 Cases in the Literature". The American Journal of Surgical Pathology. 41 (1): 25–38. doi:10.1097/PAS.0000000000000753. ISSN 1532-0979. PMID 27740969. Check date values in:
|date=(help) - ↑ Sukswai, Narittee; et al. (2020-01). "Diffuse large B-cell lymphoma variants: an update". Pathology. 52 (1): 53–67. doi:10.1016/j.pathol.2019.08.013. ISSN 1465-3931. PMID 31735345. Check date values in:
|date=(help) - ↑ Gascoyne, Randy D.; et al. (2003-10-01). "ALK-positive diffuse large B-cell lymphoma is associated with Clathrin-ALK rearrangements: report of 6 cases". Blood. 102 (7): 2568–2573. doi:10.1182/blood-2003-03-0786. ISSN 0006-4971. PMID 12763927.
- ↑ Onciu, Mihaela; et al. (2003-10-01). "ALK-positive plasmablastic B-cell lymphoma with expression of the NPM-ALK fusion transcript: report of 2 cases". Blood. 102 (7): 2642–2644. doi:10.1182/blood-2003-04-1095. ISSN 0006-4971. PMID 12816858.
- ↑ Takeuchi, Kengo; et al. (2011-03). "Identification of a novel fusion, SQSTM1-ALK, in ALK-positive large B-cell lymphoma". Haematologica. 96 (3): 464–467. doi:10.3324/haematol.2010.033514. ISSN 1592-8721. PMC 3046280. PMID 21134980. Check date values in:
|date=(help) - ↑ Lee, Seung Eun; et al. (2014-12). "Identification of RANBP2-ALK fusion in ALK positive diffuse large B-cell lymphoma". Hematological Oncology. 32 (4): 221–224. doi:10.1002/hon.2125. ISSN 1099-1069. PMID 24470379. Check date values in:
|date=(help) - ↑ Sakamoto, Kana; et al. (2016-04). "ALK-positive large B-cell lymphoma: identification of EML4-ALK and a review of the literature focusing on the ALK immunohistochemical staining pattern". International Journal of Hematology. 103 (4): 399–408. doi:10.1007/s12185-016-1934-1. ISSN 1865-3774. PMID 26781614. Check date values in:
|date=(help) - ↑ Ise, Mikiko; et al. (2019-02). "Identification of a novel GORASP2-ALK fusion in an ALK-positive large B-cell lymphoma". Leukemia & Lymphoma. 60 (2): 493–497. doi:10.1080/10428194.2018.1493731. ISSN 1029-2403. PMID 30187817. Check date values in:
|date=(help) - ↑ Bedwell, Clare; et al. (2011-02). "Cytogenetically complex SEC31A-ALK fusions are recurrent in ALK-positive large B-cell lymphomas". Haematologica. 96 (2): 343–346. doi:10.3324/haematol.2010.031484. ISSN 1592-8721. PMC 3031708. PMID 21109691. Check date values in:
|date=(help) - ↑ Valera, Alexandra; et al. (2013-10). "ALK-positive large B-cell lymphomas express a terminal B-cell differentiation program and activated STAT3 but lack MYC rearrangements". Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc. 26 (10): 1329–1337. doi:10.1038/modpathol.2013.73. ISSN 1530-0285. PMC 6368829. PMID 23599149. Check date values in:
|date=(help)
Notes
*Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.
*Citation of this Page: “ALK-positive large B-cell lymphoma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 09/6/2024, https://ccga.io/index.php/HAEM5:ALK-positive_large_B-cell_lymphoma.