BACKGROUND: The histogeneses of fibroadenoma and phyllodes tumor of the breast appear to be closely related, but it is still unclear whether fibroadenoma can progress directly to phyllodes tumor. METHODS: This issue was studied by conducting clonal analysis of fibroadenoma and phyllodes tumors that were obtained sequentially from the same patient. One patient developed local recurrence of phyllodes tumor twice, and the other two patients each developed a phyllodes tumor after excision of a primary fibroadenoma. The method for clonal analysis was based on trinucleotide repeat polymorphism of the X chromosome-linked androgen receptor (AR) gene and on random inactivation of the gene by methylation. RESULTS: Clonal analysis revealed that all the three primary fibroadenomas were monoclonal and all four recurrent phyllodes tumors were also monoclonal in origin. In addition, the same allele of the AR gene was inactivated in fibroadenoma and phyllodes tumor(s) in each patient. The probability that phyllodes tumors of different origin happen to inactivate the same allele of the AR gene as fibroadenomas in every case is quite low. Rather, it is more reasonable to assume that the phyllodes tumor has the same origin as fibroadenoma. CONCLUSIONS: These results identified monoclonal fibroadenomas that can progress to phyllodes tumors.
BACKGROUND: The histogeneses of fibroadenoma and phyllodestumor of the breast appear to be closely related, but it is still unclear whether fibroadenoma can progress directly to phyllodestumor. METHODS: This issue was studied by conducting clonal analysis of fibroadenoma and phyllodestumors that were obtained sequentially from the same patient. One patient developed local recurrence of phyllodestumor twice, and the other two patients each developed a phyllodestumor after excision of a primary fibroadenoma. The method for clonal analysis was based on trinucleotide repeat polymorphism of the X chromosome-linked androgen receptor (AR) gene and on random inactivation of the gene by methylation. RESULTS: Clonal analysis revealed that all the three primary fibroadenomas were monoclonal and all four recurrent phyllodestumors were also monoclonal in origin. In addition, the same allele of the AR gene was inactivated in fibroadenoma and phyllodestumor(s) in each patient. The probability that phyllodestumors of different origin happen to inactivate the same allele of the AR gene as fibroadenomas in every case is quite low. Rather, it is more reasonable to assume that the phyllodestumor has the same origin as fibroadenoma. CONCLUSIONS: These results identified monoclonal fibroadenomas that can progress to phyllodestumors.
Authors: Salvatore Piscuoglio; Melissa Murray; Nicola Fusco; Caterina Marchiò; Florence L Loo; Luciano G Martelotto; Anne M Schultheis; Muzaffar Akram; Britta Weigelt; Edi Brogi; Jorge S Reis-Filho Journal: Histopathology Date: 2015-05-24 Impact factor: 5.087
Authors: Jing Tan; Choon Kiat Ong; Weng Khong Lim; Cedric Chuan Young Ng; Aye Aye Thike; Ley Moy Ng; Vikneswari Rajasegaran; Swe Swe Myint; Sanjanaa Nagarajan; Saranya Thangaraju; Sucharita Dey; Nur Diyana Md Nasir; Giovani Claresta Wijaya; Jing Quan Lim; Dachuan Huang; Zhimei Li; Bernice Huimin Wong; Jason Yong Sheng Chan; John R McPherson; Ioana Cutcutache; Gregory Poore; Su Ting Tay; Wai Jin Tan; Thomas Choudary Putti; Buhari Shaik Ahmad; Philip Iau; Ching Wan Chan; Anthony P H Tang; Wei Sean Yong; Preetha Madhukumar; Gay Hui Ho; Veronique Kiak Mien Tan; Chow Yin Wong; Mikael Hartman; Kong Wee Ong; Benita K T Tan; Steven G Rozen; Patrick Tan; Puay Hoon Tan; Bin Tean Teh Journal: Nat Genet Date: 2015-10-05 Impact factor: 38.330