BRST5:Secretory carcinoma: Difference between revisions

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Created page with " ==Primary Author(s)*== __TOC__ ==Cancer Category/Type== Breast cancer ==Cancer Sub-Classification / Subtype== Put your text here ==Definition / Description of Disease==..."
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==Primary Author(s)*==
==Primary Author(s)*==
Hui Chen, MD, PhD, The University of Texas MD Anderson Cancer Center
Morteza Seifi, PhD, University of Wisconsin


__TOC__
__TOC__
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==Cancer Category/Type==
==Cancer Category/Type==


Breast Tumours /  Epithelial tumours of the breast
Breast cancer


==Cancer Sub-Classification / Subtype==
==Cancer Sub-Classification / Subtype==


Rare and salivary gland-type tumours / Secretory carcinoma
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==Definition / Description of Disease==
==Definition / Description of Disease==


Secretory carcinoma is a low-grade tumor displaying pushing borders and areas of unequivocal stromal invasion. Tumors may show combinations of microcystic, solid and tubular patterns. The microcystic pattern is composed of irregular shaped small cysts lined with single layer of tumor cells and filled with eosinophilic secretions. The tubular pattern shows luminal eosinophil secretions. The microcystic and tubular patterns can mimic thyroid follicles and can merge into solid islands. Tumor cells are polygonal with granular eosinophilic to foamy cytoplasm. Tumor nuclei are slightly enlarged and regular in shape with inconspicuous nucleoli. Mitotic activity is rare.
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==Synonyms / Terminology==
==Synonyms / Terminology==


Synonyms: Juvenile breast carcinoma (historical)
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==Epidemiology / Prevalence==
==Epidemiology / Prevalence==


Rare, < 0.02% of all breast cancers<ref name=":0">{{Cite journal|last=Horowitz|first=David P.|last2=Sharma|first2=Charu S.|last3=Connolly|first3=Eileen|last4=Gidea-Addeo|first4=Daniela|last5=Deutsch|first5=Israel|date=2012-06|title=Secretory carcinoma of the breast: results from the survival, epidemiology and end results database|url=https://pubmed.ncbi.nlm.nih.gov/22494666|journal=Breast (Edinburgh, Scotland)|volume=21|issue=3|pages=350–353|doi=10.1016/j.breast.2012.02.013|issn=1532-3080|pmid=22494666}}</ref><ref>{{Cite journal|last=Jacob|first=John Doromal|last2=Hodge|first2=Caitlin|last3=Franko|first3=Jan|last4=Pezzi|first4=Christopher M.|last5=Goldman|first5=Charles D.|last6=Klimberg|first6=Vicki Suzanne|date=2016-06|title=Rare breast cancer: 246 invasive secretory carcinomas from the National Cancer Data Base|url=https://pubmed.ncbi.nlm.nih.gov/27040042|journal=Journal of Surgical Oncology|volume=113|issue=7|pages=721–725|doi=10.1002/jso.24241|issn=1096-9098|pmid=27040042}}</ref> (Breast 2012;21:350 PMID: 22494666, J Surg Oncol 2016;113:721 PMID: 27040042)
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Initially described in children; most common childhood breast cancer<ref>{{Cite journal|last=McDivitt|first=R. W.|last2=Stewart|first2=F. W.|date=1966-01-31|title=Breast carcinoma in children|url=https://pubmed.ncbi.nlm.nih.gov/4285563|journal=JAMA|volume=195|issue=5|pages=388–390|issn=0098-7484|pmid=4285563}}</ref> (JAMA 1966;195:388 PMID: 4285563)
 
Wide age range, bimodal age distribution with peaks in second and seventh decades<ref name=":0" /> (Breast 2012;21:350 PMID: 22494666, Diagn Histopathol 2020;26:51[C1] )
 
M:F = 1:6 to 1:31 (World J Surg Oncol 2005;3:35 PMID: 15963235, Mod Pathol 2012;25:567 PMID: 22157932, J Surg Oncol 2016;113:721 PMID: 27040042 , Ann Oncol 2000;11:1343 PMID: 11106125 )


==Clinical Features==
==Clinical Features==


Put your text here and fill in the table
Put your text here
{| class="wikitable"
|'''Signs and Symptoms'''
|Well-circumscribed mobile masses
|-
|'''Laboratory Findings'''
|Not applicable
|}


==Sites of Involvement==
==Sites of Involvement==


The tumors are commonly seen in sub-areolar area.
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==Morphologic Features==
==Morphologic Features==


Microcystic, solid and tubular patterns
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==Immunophenotype==
==Immunophenotype==


Put your text here and fill in the table
Put your text here and/or fill in the table


{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Finding!!Marker
! Finding   !! Marker
|-
|-
|Positive (universal)||S100, EMA, TRK
|Positive (universal) || EXAMPLE CD1
|-
|-
|Positive (subset)||CEA (polyclonal), mammaglobin, SOX10
|Positive (subset) || EXAMPLE CD2
|-
|-
|Negative (universal)||ER, PR, and HER2
|Negative (universal) || EXAMPLE CD3
|-
|-
|Negative (subset)||
|Negative (subset) || EXAMPLE CD4
|}
|}


==Chromosomal Rearrangements (Gene Fusions)==
==Chromosomal Rearrangements (Gene Fusions)==


Put your text here and fill in the table
Put your text here and/or fill in the table


{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Chromosomal Rearrangement!!Genes in Fusion (5’ or 3’ Segments)!!Pathogenic Derivative!!Prevalence
! 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
|-
|-
|t(12;15)(p13;q25)||''ETV6::NTRK3''||der(15)||92% (PMID: 12450792)
|EXAMPLE t(9;22)(q34;q11.2) || EXAMPLE 3'ABL1 / 5'BCR || EXAMPLE der(22) || EXAMPLE 5%
|Yes
|-
|Yes
|EXAMPLE t(8;21)(q22;q22) || EXAMPLE 5'RUNX1 / 3'RUNXT1 || EXAMPLE der(8) || EXAMPLE 5%
|Yes
|The ''ETV6::NTRK3'' fusion is diagnostic of secretory carcinoma of breast in the appropriate morphology and clinical context (Cancer Cell. 2002 Nov;2(5):367-76. PMID: 12450792). This fusion is responsive to targeted therapy such as larotrectinib (Vitrakvi) and  entrectinib (Rozlytrek) (ESMO Open
. 2021 Apr;6(2):100072 <nowiki>PMID 33676294</nowiki>).
|}
|}
==Individual Region Genomic Gain/Loss/LOH==
==Characteristic Chromosomal Aberrations / Patterns==


Put your text here and fill in the table
Put your text here
 
==Genomic Gain/Loss/LOH==
 
Put your text here and/or fill in the table


{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Chr #!!Gain / Loss / Amp / LOH!!Minimal Region Genomic Coordinates [Genome Build]!!Minimal Region Cytoband
! Chromosome Number !! Gain/Loss/Amp/LOH !! Region
!Diagnostic Significance (Yes, No or Unknown)
!Prognostic Significance (Yes, No or Unknown)
!Therapeutic Significance (Yes, No or Unknown)
!Notes
|-
|-
|N/A
|EXAMPLE 8 || EXAMPLE Gain || EXAMPLE chr8:0-1000000
|N/A
|N/A
|N/A
|N/A
|N/A
|N/A
|N/A
|-
|-
|
|EXAMPLE 7 || EXAMPLE Loss || EXAMPLE chr7:0-1000000
|
|}
|
|
==Gene Mutations (SNV/INDEL)==
|
|
|
|
|}
==Characteristic Chromosomal Patterns==


Put your text here
Put your text here and/or fill in the tables


{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Chromosomal Pattern
! Gene !! Mutation !! Oncogene/Tumor Suppressor/Other !! Presumed Mechanism (LOF/GOF/Other; Driver/Passenger) !! Prevalence (COSMIC/TCGA/Other)
!Diagnostic Significance (Yes, No or Unknown)
!Prognostic Significance (Yes, No or Unknown)
!Therapeutic Significance (Yes, No or Unknown)
!Notes
|-
|-
|N/A
| EXAMPLE TP53 || EXAMPLE R273H || EXAMPLE Tumor Suppressor || EXAMPLE LOF || EXAMPLE 20%
|N/A
|}
|N/A
|N/A
===Other Mutations===
|
|}
==Gene Mutations (SNV/INDEL)==
 
Put your text here and fill in the table
 
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Gene; Genetic Alteration!!'''Presumed Mechanism (Tumor Suppressor Gene [TSG] / Oncogene / Other)'''!!'''Prevalence (COSMIC /  TCGA / Other)'''!!'''Concomitant Mutations'''!!'''Mutually Exclusive Mutations'''
! Type !! Gene/Region/Other
!'''Diagnostic Significance (Yes, No or Unknown)'''
!Prognostic Significance (Yes, No or Unknown)
!Therapeutic Significance (Yes, No or Unknown)
!Notes
|-
|-
|N/A
| Concomitant Mutations || EXAMPLE IDH1 R123H
|N/A
|-
|N/A
| Secondary Mutations || EXAMPLE Trisomy 7
|N/A
|-
|N/A
|Mutually Exclusive || EXAMPLE EGFR Amplification
|N/A
|N/A
|N/A
|
|}
|}
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.


==Epigenomic Alterations==
==Epigenomics (Methylation)==


N/A
Put your text here


==Genes and Main Pathways Involved==
==Genes and Main Pathways Involved==


<br />
Put your text here
{| class="wikitable sortable"
 
|-
==Diagnostic Testing Methods==
!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
 
|-
Put your text here
|NTRK3 fusion; Activating mutations
 
|Ras-Mek1 and PI3K-Akt pathways
==Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications)==
|Increased cell growth and proliferation
|-
|
|
|
|-
|
|
|
|}
==Genetic Diagnostic Testing Methods==


FISH, RT-PCR, RNAseq
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==Familial Forms==
==Familial Forms==


None
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==Additional Information==
==Other Information==


Put your text here
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==Links==
==Links==


Put your text placeholder here (use "Link" icon at top of page)
Put your links here


==References==
==References==
<references />
(use "Cite" icon at top of page)
===EXAMPLE Book===


#Arce, C; et al. (2005-06) Secretory carcinoma of the breast containing the ETV6-NTRK3 fusion gene in a male: case report and review of the literature. ''World J Surg Oncol.'' '''17''':3:35. doi: 10.1186/1477-7819-3-35. doi: 10.1186/1477-7819-3-35. PMC PMC1184104 <nowiki>PMID 15963235</nowiki> Krings G, et al., (2019). Secretory carcinoma, in World Health Organization Classification of Tumours of Breast Tumours, Revised 5th edition. Allison KH, Brogi E, Ellis IO, Fox SB, Morris EA, Sahin A, Salgado R, Sapino A, Sasano H, Schnitt SJ, Sotiriou C, van Diest PJ, Editorial board expert members. IARC Press: Lyon, France, p146-148.
=== EXAMPLE Book ===
#Arber DA, et al., (2008). Acute myeloid leukaemia with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, 4thedition.Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Vardiman JW, Editors. IARC Press: Lyon, France, p117-118.
 
=== EXAMPLE Journal Article ===
#Li Y, et al., (2001). Fusion of two novel genes, RBM15 and MKL1, in the t(1;22)(p13;q13) of acute megakaryoblastic leukemia. Nat Genet 28:220-221, PMID 11431691.


==Notes==
== Notes ==
<nowiki>*</nowiki>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.
<nowiki>*</nowiki>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.

Revision as of 11:39, 26 July 2017

Primary Author(s)*

Cancer Category/Type

Breast cancer

Cancer Sub-Classification / Subtype

Put your text here

Definition / Description of Disease

Put your text here

Synonyms / Terminology

Put your text here

Epidemiology / Prevalence

Put your text here

Clinical Features

Put your text here

Sites of Involvement

Put your text here

Morphologic Features

Put your text here

Immunophenotype

Put your text here and/or fill in the table

Finding Marker
Positive (universal) EXAMPLE CD1
Positive (subset) EXAMPLE CD2
Negative (universal) EXAMPLE CD3
Negative (subset) EXAMPLE CD4

Chromosomal Rearrangements (Gene Fusions)

Put your text here and/or fill in the table

Chromosomal Rearrangement Genes in Fusion (5’ or 3’ Segments) Pathogenic Derivative Prevalence
EXAMPLE t(9;22)(q34;q11.2) EXAMPLE 3'ABL1 / 5'BCR EXAMPLE der(22) EXAMPLE 5%
EXAMPLE t(8;21)(q22;q22) EXAMPLE 5'RUNX1 / 3'RUNXT1 EXAMPLE der(8) EXAMPLE 5%

Characteristic Chromosomal Aberrations / Patterns

Put your text here

Genomic Gain/Loss/LOH

Put your text here and/or fill in the table

Chromosome Number Gain/Loss/Amp/LOH Region
EXAMPLE 8 EXAMPLE Gain EXAMPLE chr8:0-1000000
EXAMPLE 7 EXAMPLE Loss EXAMPLE chr7:0-1000000

Gene Mutations (SNV/INDEL)

Put your text here and/or fill in the tables

Gene Mutation Oncogene/Tumor Suppressor/Other Presumed Mechanism (LOF/GOF/Other; Driver/Passenger) Prevalence (COSMIC/TCGA/Other)
EXAMPLE TP53 EXAMPLE R273H EXAMPLE Tumor Suppressor EXAMPLE LOF EXAMPLE 20%

Other Mutations

Type Gene/Region/Other
Concomitant Mutations EXAMPLE IDH1 R123H
Secondary Mutations EXAMPLE Trisomy 7
Mutually Exclusive EXAMPLE EGFR Amplification

Epigenomics (Methylation)

Put your text here

Genes and Main Pathways Involved

Put your text here

Diagnostic Testing Methods

Put your text here

Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications)

Put your text here

Familial Forms

Put your text here

Other Information

Put your text here

Links

Put your links here

References

EXAMPLE Book

  1. Arber DA, et al., (2008). Acute myeloid leukaemia with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, 4thedition.Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Vardiman JW, Editors. IARC Press: Lyon, France, p117-118.

EXAMPLE Journal Article

  1. Li Y, et al., (2001). Fusion of two novel genes, RBM15 and MKL1, in the t(1;22)(p13;q13) of acute megakaryoblastic leukemia. Nat Genet 28:220-221, PMID 11431691.

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.

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