Lymph node involvement is seen in approximately one quarter of women with surgically staged ovarian serous tumors of low malignant potential (serous borderline tumors), and this finding apparently does not adversely impact their overall survival. To help illuminate some of the pathomechanisms underlying this novel phenomenon, in which a largely noninvasive epithelial neoplasm is able to exit its primary site and be transported to lymph nodes with such a substantial frequency, we investigated whether significant differences in lymphatic vessel density exist between ovarian serous borderline tumors that show lymph node involvement and those that do not. The lymphatic vessel density of 13 conventional ovarian serous borderline tumors (i.e. tumors without stromal microinvasion, micropapillary/cribriform areas, or invasive implants) with at least 1 positive lymph node (study group) was compared with the lymphatic vessel density of an age- and disease extent–matched control group of 13 similarly selected lymph node–negative ovarian serous borderline tumors. Lymphatic vessel density was determined by counting the total number of vascular spaces immunohistochemically stained by the lymphatic endothelium marker D2-40 in 5 consecutive microscopic fields (×20 objective, field area of 1 microscopic field, 0.95 mm2) in the most vessel-dense areas and calculating the average value per microscopic field. The peritumoral lymphatic vessel density was significantly higher than the intratumoral lymphatic vessel density in both groups. However, no statistically significant differences were found between the study and control groups regarding intratumoral lymphatic vessel density (8.0 vs. 7.61; P=0.77), peritumoral lymphatic vessel density (20.33 vs. 21.0; P=0.79), or combined, that is, peritumoral plus intratumoral lymphatic vessel density (27.81 vs. 28.62; P=0.83). Our findings, in conjunction with others in the medical literature, do not support a role for tumor lymphatics in nodal metastasis in this neoplasm. We discuss the possibility that nodal deposits may represent metastatic disease from secondary tumor implants.
Department of Pathology (O.F., M.P.O.), Wilford Hall Medical Center, Lackland AFB, San Antonio, Texas
Department of Pathology (O.F.), University of Texas Health Science Center at San Antonio, Texas
Pathology Program (M.P.O.), San Antonio Uniformed Services Health Education Consortium, San Antonio, Texas
Department of Pathology & Laboratory Services, Brooke Army Medical Center, Ft Sam Houston, Texas (M.P.O.)
Department of Pathology, Virginia Commonwealth University, Richmond, Virginia (R.J.)
Department of Pathology, Beth Israel Deaconess Medical Center (M.R.M., J.L.H.)
Department of Pathology, Harvard Medical School (M.R.M., J.L.H.)
Division of Matrix Biology, Beth Israel Deaconess Medical Center, Boston, Massachusetts (M.R.M.)
Vanguard Pathology Associates, Austin, Texas (I.L.R.)
Department of Pathology, McMaster University, Hamilton, Ontario, Canada (D.H.)
Department of Pathology, University of Massachusetts Medical School, Worcester, Massachusetts (S.A.W.)
Department of Pathology, Southwest Washington Medical Center, Vancouver, Washington (M.G.)
Department of Pathology, Stony Brook University Medical Center, Stony Brook, New York (S.X.L.)
The authors Mohiedean Ghofrani and Sharon X. Liang equally contributed to this article.
The views expressed in this article are those of the authors and do not reflect the official policy of the Department of Defense or other Departments of the United States Government.
Address correspondence and reprint requests to Oluwole Fadare, MD, Department of Pathology, Wilford Hall Medical Center, 2200 Bergquist Dr., Ste 1, Lackland AFB, TX 78236. E-mail: email@example.com