Mucinous Carcinoma

Morphologic transitions from mucinous cystadenoma to mucinous atypical proliferative tumor (borderline tumor), to mucinous intraepithelial carcinoma and invasive mucinous carcinoma have been recognized for some time, and an increasing frequency of KRAS mutations at codons 12 and 13 has been described in every stage of tumor progression.7,41-44 In addition, the same KRAS mutation has been detected in mucinous carcinoma and in the adjacent mucinous cystadenoma and borderline

Table 2-5. Ovarian Borderline Tumors and Associated Molecular Genetic Changes in Tumor Progression

Summary of Major Molecular

Genetic Alterations Precursor Lesions Progression

Table 2-5. Ovarian Borderline Tumors and Associated Molecular Genetic Changes in Tumor Progression

Summary of Major Molecular

Genetic Alterations Precursor Lesions Progression

Serous Borderline Tumor

BRAF and KRAS mutations (67%)

Serous cystadenoma/ adenofibroma

Invasive low-grade serous carcinoma

Mucinous Borderline Tumor

KRAS mutations (>60%)

Mucinous cystadenoma

Intraepithelial carcinoma then to invasive mucinous carcinoma

Endometrioid Borderline Tumor

LOH or mutations in PTEN (20%)

Endometriosis/ endometrioid

Intraepithelial carcinoma then to invasive endometrioid carcinoma

P-catenin gene mutations (50%)

Microsatellite instability (13-50%) Clear Cell Borderline Tumor

KRAS mutations (5-16%)

Endometriosis/clear cell adenofibroma

Intraepithelial carcinoma then to invasive clear cell carcinoma

Microsatellite instability (13%) Brenner (Transitional Type) Borderline Tumor

Not yet identified

Brenner tumor

Malignant Brenner (transitional cell) carcinoma

LOH, loss of heterozygosity.

LOH, loss of heterozygosity.

tumor.41 In contrast to serous borderline tumor and serous low-grade carcinoma, BRAF mutations are extremely rare in ovarian mucinous tumors. Other than KRAS mutations, molecular genetic changes, including microsatellite instability, have rarely been reported in mucinous borderline tumors.40

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