Serous tumor of low malignant potential (SLMP) and low-grade serous carcinoma (LGSC) are part of one biological continuum, whereby SLMP can transform into LGSC. It has been suggested that some nodal SLMPs arise from nodal endosalpingiosis and evolve independently in lymph nodes (rather than being related to the ovarian primary). In this article, we present the clinicopathologic features of 5 cases of nodal LGSC presenting in association with ovarian SLMP. Clinical information was obtained from the patients' charts. Pathologic features of the nodal LGSC, including lymph node location, size of and extent of involvement of tumor, architectural pattern, degree of cytologic atypia, mitotic index, and presence of psammoma bodies, were recorded. Ovarian SLMPs were noted for laterality, size, presence of surface excrescences, microinvasion, and micropapillary/cribriform pattern and for presence of autoimplants, invasive, and noninvasive implants. The distribution of any lymph nodes with nodal endosalpingiosis or SLMPs was also recorded. Patients ranged in age from 28 to 68 years (median, 32 y). In 4 cases, the diagnosis of nodal LGSC occurred at a different time from that of the ovarian SLMPs, ranging from 7 months before to 5 months after the ovarian tumor diagnosis. Nodal LGSC was detected in supraclavicular (2 cases), cervical, intramammary, and periaortic lymph nodes (1 case each). The gross lymph node size ranged from 0.9 to 2.5 cm (median, 1.3 cm). The tumors either replaced the entire lymph node or were found diffusely involving subcapsular and medullary sinuses or lymph node cortices. Tumor cells showed typical cytologic features of LGSC and no mitotic activity. In 2 cases, however, focal pleomorphic cells and 1 mitosis per 10 HPF were noted. Psammoma bodies were identified in all cases. When immunohistochemical analysis was performed, all tumors exhibited a profile in keeping with Müllerian origin. All ovarian tumors were well sampled and ranged in size from 0.1 to 13 cm (median, 2.5 cm). No ovarian SLMP tumors showed the micropapillary/cribriform pattern, whereas only focal microinvasion was detected in 3 cases. Four tumors had surface excrescences. All cases had noninvasive implants, and a single case also had invasive implants. Lymph node dissection was performed in 2 cases, revealing extensive endosalpingiosis in pelvic and periaortic lymph nodes and SLMP in pelvic lymph nodes. In 1 additional case, a single lymph node was sampled, revealing a nodal SLMP. Clinical follow-up ranged from 2 to 14 years (median, 9 y). All patients received postoperative chemotherapy. None of the patients experienced recurrence in pelvic or abdominal soft tissue. Two patients are free of disease. However, 2 patients, one with cervical and another with supraclavicular nodal LGSC, had recurrences at these sites and subsequently succumbed to metastatic disease. Both of these patients had pelvic and periaortic nodal SLMP and extensive nodal endosalpingiosis. Another patient, originally with supraclavicular LGSC, developed pelvic and abdominal lymphadenopathy, and is currently alive with disease. For the first time, we present a case series of patients with ovarian SLMP who, despite any evidence of LGSC in the pelvis or any pelvic recurrences, developed extrapelvic/extra-abdominal nodal LGSC. These patients also had endosalpingiosis and SLMP in pelvic and periaortic lymph nodes, suggesting that SLMP/LGSC tumors in lymph nodes may arise independently of the ovarian primary, progress along their own timeline, and undergo metastatic spread. Therefore, in patients with ovarian SLMP and extensive pelvic/periaortic nodal endosalpingiosis and/or SLMP, examination and follow-up of extrapelvic lymph nodes are warranted, even if the ovarian tumor lacks high-risk features of recurrence.