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. Author manuscript; available in PMC: 2016 Sep 19.
Published in final edited form as: Histopathology. 2016 Jan;68(1):5–21. doi: 10.1111/his.12876

Table 2.

Summary of studies evaluating the relationship between fibroadenomas and phyllodes tumours

Study, year Summary of findings
Noguchi et al.,36 1993 Epithelial and stromal cells were polyclonal in all of 10 fibroadenomas, whereas stromal cells were monoclonal in all of five phyllodes tumours
Noguchi et al.,37 1995 The same allele of the androgen receptor gene was inactivated in fibroadenomas and phyllodes tumours in each of three patients with both tumours
Kasami et al.,38 1998 5% (1/20) of ‘complex’ fibroadenomas and 1% (1/25) of ‘simple’ fibroadenomas showed stromal monoclonality. The one ‘simple’ fibroadenoma coexisted with a phyllodes tumour component, which showed similar stromal monoclonality
Kuijper et al.,39 2002 Areas of ‘stromal expansion’ in three of 25 fibroadenomas were monoclonal. In addition, nine of 12 phyllodes tumours showed stromal monoclonality
Wang et al.,40 2006 Phyllodes tumours harboured a subset of LOH loci, which were absent in fibroadenomas. Primary and recurrent phyllodes tumours shared common regions of LOH
Hodges et al.,41 2009 A single, laser-microdissected fibroadenoma and phyllodes tumour (synchronous) showed similar allelic loss (D7S522) in both components, wheras the phyllodes component showed additional losses at TP53 and D22S264
Abe et al.,42 2011 Eleven of 36 cases of malignant phyllodes tumours were associated with prior diagnoses of fibroadenomas
Foucar et al.,43 2012 A recent report of benign phyllodes tumours that developed in a mother and daughter pair raised the possibility of a genetic predisposition for phyllodes tumour development
Lim et al.,44 2014 Recurrent somatic mutations in exon 2 of MED12 were discovered in 59% of 98 fibroadenomas on exome sequencing, with 71% of mutations occurring in codon 44
Cani et al.,45 2015 MED12 mutations were found in phyllodes tumours of all histological grades on next-generation sequencing. Additional mutations in p53, RB1 and NF1, as well as high-level copy number alterations, such as amplifications in EGFR and IGF1R, were features of malignant tumours
Yoshida et al.,46 2015 All grades of phyllodes tumours showed MED12 mutations. Microdissection analysis confirmed MED12 mutations to be stroma-confined in fibroadenomas and phyllodes tumours
Piscuoglio et al.,47 2015 Malignant phyllodes tumours were significantly less likely to harbour MED12 mutations than fibroadenomas, and benign and borderline phyllodes tumours
Nagasawa et al.,48 2015 MED12 mutations were found in 67% of fibroadenomas (6/9) and in 45% of phyllodes tumours (5/11)
Pfarr et al.,49 2015 60% of all fibroepithelial breast lesions (fibroadenomas and phyllodes tumours) showed MED12 mutations. Intracanalicular fibroadenomas showed the highest frequency of mutations (82%), whereas malignant phyllodes tumours were least likely to contain the mutations (20%)
Ng et al.,50 2015 62.5% (70/112) of phyllodes tumours showed MED12 mutations. Tumours with MED12 mutations were associated with longer disease-free survival, whereas absence of MED12 mutations was correlated with a higher likelihood of recurrence

LOH, loss of heterozygosity.