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{{DISPLAYTITLE:Fibroadenoma}}
[[BRST5:Table_of_Contents|Breast Tumours (WHO Classification, 5th ed.)]]
==Primary Author(s)*==
==Primary Author(s)*==
H. Evin Gulbahce, MD and Katherine Geiersbach, MD
==WHO Classification of Disease==


Put your text here
__TOC__
==Cancer Category/Type==
Put your text here
==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 and fill in the table
{| class="wikitable"
{| class="wikitable"
|'''Signs and Symptoms'''
!Structure
|EXAMPLE Asymptomatic (incidental finding on complete blood counts)
!Disease
 
EXAMPLE B-symptoms (weight loss, fever, night sweats)
 
EXAMPLE Fatigue
 
EXAMPLE Lymphadenopathy (uncommon)
|-
|'''Laboratory Findings'''
|EXAMPLE Cytopenias
 
EXAMPLE Lymphocytosis (low level)
|}
 
==Sites of Involvement==
 
Put your text here
 
==Morphologic Features==
 
Put your text here
 
==Immunophenotype==
 
Put your text here and fill in the table
 
{| class="wikitable sortable"
|-
|-
!Finding!!Marker
|Book
|Breast Tumours (5th ed.)
|-
|-
|Positive (universal)||EXAMPLE CD1
|Category
|Fibroepithelial tumours and hamartomas of the breast
|-
|-
|Positive (subset)||EXAMPLE CD2
|Family
|Fibroepithelial tumours and hamartomas of the breast: Introduction
|-
|-
|Negative (universal)||EXAMPLE CD3
|Type
|Fibroadenoma
|-
|-
|Negative (subset)||EXAMPLE CD4
|Subtype(s)
|N/A
|}
|}


==Chromosomal Rearrangements (Gene Fusions)==
==Related Terminology==


Put your text here and fill in the table
{| class="wikitable"
|+
|Acceptable
|N/A
|-
|Not Recommended
|Adenofibroma
|}


==Gene Rearrangements==
<br />
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Chromosomal Rearrangement!!Genes in Fusion (5’ or 3’ Segments)!!Pathogenic Derivative!!Prevalence
!Driver Gene!!Fusion(s) and Common Partner Genes!!Molecular Pathogenesis!!Typical Chromosomal Alteration(s)
!Diagnostic Significance (Yes, No or Unknown)
!Prevalence -Common >20%, Recurrent 5-20% or Rare <5% (Disease)
!Prognostic Significance (Yes, No or Unknown)
!Diagnostic, Prognostic, and Therapeutic Significance - D, P, T
!Therapeutic Significance (Yes, No or Unknown)
!Established Clinical Significance Per Guidelines - Yes or No (Source)
!Notes
!Clinical Relevance Details/Other 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).
|
|}
|}
==Individual Region Genomic Gain/Loss/LOH==
==Individual Region Genomic Gain/Loss/LOH==
 
<br />
Put your text here and fill in the table
 
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Chr #!!Gain / Loss / Amp / LOH!!Minimal Region Genomic Coordinates [Genome Build]!!Minimal Region Cytoband
!Chr #!!Gain, Loss, Amp, LOH!!Minimal Region Cytoband and/or Genomic Coordinates [Genome Build; Size]!!Relevant Gene(s)
!Diagnostic Significance (Yes, No or Unknown)
!Diagnostic, Prognostic, and Therapeutic Significance - D, P, T
!Prognostic Significance (Yes, No or Unknown)
!Established Clinical Significance Per Guidelines - Yes or No (Source)
!Therapeutic Significance (Yes, No or Unknown)
!Clinical Relevance Details/Other Notes
!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).
|}
|}
==Characteristic Chromosomal Patterns==
==Characteristic Chromosomal or Other Global Mutational Patterns==
 
<br />
Put your text here
 
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Chromosomal Pattern
!Chromosomal Pattern
!Diagnostic Significance (Yes, No or Unknown)
!Molecular Pathogenesis
!Prognostic Significance (Yes, No or Unknown)
!Prevalence -
!Therapeutic Significance (Yes, No or Unknown)
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
|-
|-
|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).
|}
|}
==Gene Mutations (SNV/INDEL)==
==Gene Mutations (SNV/INDEL)==
 
<br />
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'''
!Gene!!Genetic Alteration!!Tumor Suppressor Gene, Oncogene, Other!!Prevalence -
!'''Diagnostic Significance (Yes, No or Unknown)'''
Common >20%, Recurrent 5-20% or Rare <5% (Disease)
!Prognostic Significance (Yes, No or Unknown)
!Diagnostic, Prognostic, and Therapeutic Significance - D, P, T  
!Therapeutic Significance (Yes, No or Unknown)
!Established Clinical Significance Per Guidelines - Yes or No (Source)
!Notes
!Clinical Relevance Details/Other Notes
|-
|''MED12''
|
|Oncogene
|Common
|D
|
|G44 hotspot mutations<ref>{{Cite journal|last=Tan|first=Jing|last2=Ong|first2=Choon Kiat|last3=Lim|first3=Weng Khong|last4=Ng|first4=Cedric Chuan Young|last5=Thike|first5=Aye Aye|last6=Ng|first6=Ley Moy|last7=Rajasegaran|first7=Vikneswari|last8=Myint|first8=Swe Swe|last9=Nagarajan|first9=Sanjanaa|date=2015-11|title=Genomic landscapes of breast fibroepithelial tumors|url=https://pubmed.ncbi.nlm.nih.gov/26437033|journal=Nature Genetics|volume=47|issue=11|pages=1341–1345|doi=10.1038/ng.3409|issn=1546-1718|pmid=26437033}}</ref><ref>{{Cite journal|last=Sim|first=Yirong|last2=Ng|first2=Gwendolene Xin Pei|last3=Ng|first3=Cedric Chuan Young|last4=Rajasegaran|first4=Vikneswari|last5=Wong|first5=Suet Far|last6=Liu|first6=Wei|last7=Guan|first7=Peiyong|last8=Nagarajan|first8=Sanjanaa|last9=Ng|first9=Wai Yee|date=2019-10-23|title=A novel genomic panel as an adjunctive diagnostic tool for the characterization and profiling of breast Fibroepithelial lesions|url=https://pubmed.ncbi.nlm.nih.gov/31647027|journal=BMC medical genomics|volume=12|issue=1|pages=142|doi=10.1186/s12920-019-0588-2|issn=1755-8794|pmc=6813086|pmid=31647027}}</ref>
|-
|''TERT''
|
|Oncogene
|Recurrent
|
|
|Associated with juvenile fibroadenoma<ref name=":0">{{Cite journal|last=Jorns|first=Julie M.|last2=Farooq|first2=Ayesha|last3=Puzyrenko|first3=Andrii|last4=Jarzembowski|first4=Jason|last5=Thike|first5=Aye Aye|last6=Nasir|first6=Nur Diyana Md|last7=Ng|first7=Cedric Chuan Young|last8=Liu|first8=Wei|last9=Lee|first9=Jing Yi|date=2023-09|title=Giant juvenile fibroadenomas with and without prominent pseudoangiomatous stromal hyperplasia (PASH)-like change: clinicopathological and molecular characteristics|url=https://pubmed.ncbi.nlm.nih.gov/37140543|journal=Histopathology|volume=83|issue=3|pages=357–365|doi=10.1111/his.14935|issn=1365-2559|pmid=37140543}}</ref>
|-
|''RARA''
|
|Oncogene
|Recurrent
|
|
|Frequently co-mutated with MED12<ref>{{Cite journal|last=Tan|first=Jing|last2=Ong|first2=Choon Kiat|last3=Lim|first3=Weng Khong|last4=Ng|first4=Cedric Chuan Young|last5=Thike|first5=Aye Aye|last6=Ng|first6=Ley Moy|last7=Rajasegaran|first7=Vikneswari|last8=Myint|first8=Swe Swe|last9=Nagarajan|first9=Sanjanaa|date=2015-11|title=Genomic landscapes of breast fibroepithelial tumors|url=https://pubmed.ncbi.nlm.nih.gov/26437033|journal=Nature Genetics|volume=47|issue=11|pages=1341–1345|doi=10.1038/ng.3409|issn=1546-1718|pmid=26437033}}</ref>
|-
|''EGFR''
|
|Oncogene
|Rare
|
|
|
|-
|-
|EXAMPLE: TP53; Variable LOF mutations
|''TP53''
 
|
EXAMPLE:
|Tumor Suppressor Gene
 
|Common
EGFR; Exon 20 mutations
|
 
|
EXAMPLE: BRAF; Activating mutations
|Associated with juvenile fibroadenoma and stromal PASH-like changes<ref name=":0" />
|EXAMPLE: TSG
|-
|EXAMPLE: 20% (COSMIC)
|''PIK3CA''
 
|
EXAMPLE: 30% (add Reference)
|Oncogene
|EXAMPLE: IDH1 R123H
|Rare
|EXAMPLE: EGFR amplification
|
|
|
|-
|''KMT2D''
|
|Tumor Suppressor Gene
|Recurrent
|
|
|
|-
|''NF1''
|
|Tumor Suppressor Gene
|Rare
|
|
|
|-
|''SETD2''
|
|Other
|Common
|D
|
|Associated with juvenile fibroadenoma and PASH-like changes<ref name=":0" />
|-
|''FLNA''
|
|Oncogene
|Common
|D
|
|Associated with juvenile fibroadenoma<ref name=":0" />
|-
|
|
|
|
|
|
|
|
|
|
|EXAMPLE:  Excludes hairy cell leukemia (HCL) (add reference).
|}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.
==Epigenomic Alterations==
<br />
<br />
|}
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==
Put your text here
==Genes and Main Pathways Involved==
==Genes and Main Pathways Involved==
 
<br />
Put your text here and fill in the table
{| class="wikitable sortable"
{| class="wikitable sortable"
|-
|-
!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome
|-
|-
|EXAMPLE: BRAF and MAP2K1; Activating mutations
|
|EXAMPLE: MAPK signaling
|
|EXAMPLE: Increased cell growth and proliferation
|
|-
|EXAMPLE: CDKN2A; Inactivating mutations
|EXAMPLE: Cell cycle regulation
|EXAMPLE: Unregulated cell division
|-
|EXAMPLE:  KMT2C and ARID1A; Inactivating mutations
|EXAMPLE:  Histone modification, chromatin remodeling
|EXAMPLE:  Abnormal gene expression program
|}
|}
==Genetic Diagnostic Testing Methods==
==Genetic Diagnostic Testing Methods==
 
Next generation sequencing, PCR based testing with Sanger sequencing.<br />
Put your text here
 
==Familial Forms==
==Familial Forms==
 
Women with Carney complex due to an inherited pathogenic variant in PRKAR1A can develop myxoid fibroadenomas, which appear genetically distinct from conventional fibroadenomas.<ref>{{Cite journal|last=Carney|first=J. A.|last2=Toorkey|first2=B. C.|date=1991-08|title=Myxoid fibroadenoma and allied conditions (myxomatosis) of the breast. A heritable disorder with special associations including cardiac and cutaneous myxomas|url=https://pubmed.ncbi.nlm.nih.gov/2069209|journal=The American Journal of Surgical Pathology|volume=15|issue=8|pages=713–721|doi=10.1097/00000478-199108000-00001|issn=0147-5185|pmid=2069209}}</ref><ref>{{Cite journal|last=Lozada|first=John R.|last2=Burke|first2=Kathleen A.|last3=Maguire|first3=Aoife|last4=Pareja|first4=Fresia|last5=Lim|first5=Raymond S.|last6=Kim|first6=Jisun|last7=Gularte-Merida|first7=Rodrigo|last8=Murray|first8=Melissa P.|last9=Brogi|first9=Edi|date=2017-10|title=Myxoid fibroadenomas differ from conventional fibroadenomas: a hypothesis-generating study|url=https://pubmed.ncbi.nlm.nih.gov/28513873|journal=Histopathology|volume=71|issue=4|pages=626–634|doi=10.1111/his.13258|issn=1365-2559|pmc=5597459|pmid=28513873}}</ref> Beckwith-Wiedemann syndrome has been associated with the development of fibroadenomas in young patients.<ref>{{Cite journal|last=Poh|first=Melissa M.|last2=Ballard|first2=Tiffany N.|last3=Wendel|first3=J. Jason|date=2010-06|title=Beckwith-Wiedemann syndrome and juvenile fibroadenoma: a case report|url=https://pubmed.ncbi.nlm.nih.gov/20506580|journal=Annals of Plastic Surgery|volume=64|issue=6|pages=803–806|doi=10.1097/sap.0b013e3181b025f6|issn=1536-3708|pmid=20506580}}</ref><ref>{{Cite journal|last=Raine|first=P. A.|last2=Noblett|first2=H. R.|last3=Houghton-Allen|first3=B. W.|last4=Campbell|first4=P. E.|date=1979-04|title=Breast fibroadenoma and cardiac anomaly associated with EMG (Beckwith-Wiedemann) syndrome|url=https://pubmed.ncbi.nlm.nih.gov/430311|journal=The Journal of Pediatrics|volume=94|issue=4|pages=633–634|doi=10.1016/s0022-3476(79)80039-6|issn=0022-3476|pmid=430311}}</ref><br />
Put your text here
 
==Additional Information==
==Additional Information==
 
<br />
Put your text here
 
==Links==
==Links==
 
https://www.pathologyoutlines.com/topic/breastfibroadenoma.html
Put your text placeholder here (use "Link" icon at top of page)
 
==References==
==References==
<references />
<br /><references />
(use "Cite" icon at top of page)


'''EXAMPLE Book'''
==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 [[Leadership|''<u>Associate Editor</u>'']] or other CCGA representative.  When pages have a major update, the new author will be acknowledged at the beginning of the page, and those who contributed previously will be acknowledged below as a prior author.


#Arber DA, et al., (2017). Acute myeloid leukaemia with recurrent genetic abnormalities, in World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J, Arber DA, Hasserjian RP, Le Beau MM, Orazi A, and Siebert R, Editors. IARC Press: Lyon, France, p129-171.
Prior Author(s):
 
<nowiki>*</nowiki>''Citation of this Page'': “Fibroadenoma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/BRST5:Fibroadenoma</nowiki>.
==Notes==
[[Category:BRST5]]
<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.
[[Category:DISEASE]]
[[Category:Diseases F]]

Latest revision as of 17:31, 11 December 2025


Breast Tumours (WHO Classification, 5th ed.)

Primary Author(s)*

H. Evin Gulbahce, MD and Katherine Geiersbach, MD

WHO Classification of Disease

Structure Disease
Book Breast Tumours (5th ed.)
Category Fibroepithelial tumours and hamartomas of the breast
Family Fibroepithelial tumours and hamartomas of the breast: Introduction
Type Fibroadenoma
Subtype(s) N/A

Related Terminology

Acceptable N/A
Not Recommended Adenofibroma

Gene Rearrangements


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

Individual Region Genomic Gain/Loss/LOH


Chr # Gain, Loss, Amp, LOH Minimal Region Cytoband and/or Genomic Coordinates [Genome Build; Size] Relevant Gene(s) Diagnostic, Prognostic, and Therapeutic Significance - D, P, T Established Clinical Significance Per Guidelines - Yes or No (Source) Clinical Relevance Details/Other Notes

Characteristic Chromosomal or Other Global Mutational Patterns


Chromosomal Pattern Molecular Pathogenesis 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

Gene Mutations (SNV/INDEL)


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) Clinical Relevance Details/Other Notes
MED12 Oncogene Common D G44 hotspot mutations[1][2]
TERT Oncogene Recurrent Associated with juvenile fibroadenoma[3]
RARA Oncogene Recurrent Frequently co-mutated with MED12[4]
EGFR Oncogene Rare
TP53 Tumor Suppressor Gene Common Associated with juvenile fibroadenoma and stromal PASH-like changes[3]
PIK3CA Oncogene Rare
KMT2D Tumor Suppressor Gene Recurrent
NF1 Tumor Suppressor Gene Rare
SETD2 Other Common D Associated with juvenile fibroadenoma and PASH-like changes[3]
FLNA Oncogene Common D Associated with juvenile fibroadenoma[3]

Note: A more extensive list of mutations can be found in cBioportal, COSMIC, and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.

Epigenomic Alterations


Genes and Main Pathways Involved


Gene; Genetic Alteration Pathway Pathophysiologic Outcome

Genetic Diagnostic Testing Methods

Next generation sequencing, PCR based testing with Sanger sequencing.

Familial Forms

Women with Carney complex due to an inherited pathogenic variant in PRKAR1A can develop myxoid fibroadenomas, which appear genetically distinct from conventional fibroadenomas.[5][6] Beckwith-Wiedemann syndrome has been associated with the development of fibroadenomas in young patients.[7][8]

Additional Information


Links

https://www.pathologyoutlines.com/topic/breastfibroadenoma.html

References


  1. ↑ Tan, Jing; et al. (2015-11). "Genomic landscapes of breast fibroepithelial tumors". Nature Genetics. 47 (11): 1341–1345. doi:10.1038/ng.3409. ISSN 1546-1718. PMID 26437033. Check date values in: |date= (help)
  2. ↑ Sim, Yirong; et al. (2019-10-23). "A novel genomic panel as an adjunctive diagnostic tool for the characterization and profiling of breast Fibroepithelial lesions". BMC medical genomics. 12 (1): 142. doi:10.1186/s12920-019-0588-2. ISSN 1755-8794. PMC 6813086. PMID 31647027.
  3. ↑ 3.0 3.1 3.2 3.3 Jorns, Julie M.; et al. (2023-09). "Giant juvenile fibroadenomas with and without prominent pseudoangiomatous stromal hyperplasia (PASH)-like change: clinicopathological and molecular characteristics". Histopathology. 83 (3): 357–365. doi:10.1111/his.14935. ISSN 1365-2559. PMID 37140543 Check |pmid= value (help). Check date values in: |date= (help)
  4. ↑ Tan, Jing; et al. (2015-11). "Genomic landscapes of breast fibroepithelial tumors". Nature Genetics. 47 (11): 1341–1345. doi:10.1038/ng.3409. ISSN 1546-1718. PMID 26437033. Check date values in: |date= (help)
  5. ↑ Carney, J. A.; et al. (1991-08). "Myxoid fibroadenoma and allied conditions (myxomatosis) of the breast. A heritable disorder with special associations including cardiac and cutaneous myxomas". The American Journal of Surgical Pathology. 15 (8): 713–721. doi:10.1097/00000478-199108000-00001. ISSN 0147-5185. PMID 2069209. Check date values in: |date= (help)
  6. ↑ Lozada, John R.; et al. (2017-10). "Myxoid fibroadenomas differ from conventional fibroadenomas: a hypothesis-generating study". Histopathology. 71 (4): 626–634. doi:10.1111/his.13258. ISSN 1365-2559. PMC 5597459. PMID 28513873. Check date values in: |date= (help)
  7. ↑ Poh, Melissa M.; et al. (2010-06). "Beckwith-Wiedemann syndrome and juvenile fibroadenoma: a case report". Annals of Plastic Surgery. 64 (6): 803–806. doi:10.1097/sap.0b013e3181b025f6. ISSN 1536-3708. PMID 20506580. Check date values in: |date= (help)
  8. ↑ Raine, P. A.; et al. (1979-04). "Breast fibroadenoma and cardiac anomaly associated with EMG (Beckwith-Wiedemann) syndrome". The Journal of Pediatrics. 94 (4): 633–634. doi:10.1016/s0022-3476(79)80039-6. ISSN 0022-3476. PMID 430311. 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 Associate Editor or other CCGA representative.  When pages have a major update, the new author will be acknowledged at the beginning of the page, and those who contributed previously will be acknowledged below as a prior author.

Prior Author(s): *Citation of this Page: “Fibroadenoma”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated 12/11/2025, https://ccga.io/index.php/BRST5:Fibroadenoma.

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