(Carboplatin+Paclitaxel) for 6 cycles. Patient 3 had 4 cycles of Carbo/Taxol but was changed to Docetaxel (Docetaxel-Carboplatin) for the last 2 cycles because of a severe allergic reaction.All four patients had recurrence varying from 5 months to 20 months after diagnosis. Patient 1 had confirmed recurrence with omental thickening on CT and a rise in CA125 to 54 at 6 months after staging surgery, which was within 2 weeks after finishing Folfox chemotherapy. Patient 4 had confirmed recurrence at 5 months which was also soon after finishing the 6 cycles of Carbo/Taxol, when CT showed a large cyst on her remaining ovary and a liver nodule. Patient 3 had an elevated CA125 (39) at 8 months and recurrence was confirmed at 9 months after staging surgery, when MRI showed abdominal wall metastasis and tumor nodules in the pelvis. Patient 2 had abdominal pain at 18 months which was thought to be adhesions on CT imaging. Recurrence was not confirmed until 20 months when CT imaging showed abdominal nodules which were confirmed to be metastatic, poorly differentiated MOC on biopsy.Chemotherapy was then used for recurrence in all 4 patients. Patient 1 had hipec cytoreduction with Cisplatin 200 mg/m2. MOC was noted all over the abdomen at surgery (peritoneal carcinoma index of 39 and MOC on the entire gastrointestinal tract). She became bowel-obstructed within 3 weeks after surgery. Since patient 1's tumor showed Her2 mutation, Enhertu was given for 3 cycles, but it failed to reduce tumor burden. After recurrence, patient 2 was given Daraxonrasib, KRAS blocking chemotherapy, for 4 months, but MOC tumor continued to grow and created ascites and blocked gallbladder flow which required a stent. For recurrence, patient 3 was given weekly Nab-Paclitaxel with monthly Bevacizumab infusion for 3 months with Traverinib added later for one month. Since MOC tumor continued to grow, patient 3 was put in an immunotherapy trial where she had weekly infusions of Nivolumab-Etinostat. After recurrence, patient 4 had a salpingo-oophorectomy for a tumor on her other ovary 7 months after staging and was put on Folfox chemotherapy. She developed bowel obstruction and required an ileostomy and colostomy.All four women died of disease ranging from 13 months to 30 months after diagnosis. All had tumor growth in the abdomen that created ascites and intestinal blockage symptoms and inability to eat and drink. MOC also spread to the chest cavity in patient 1 and 2 creating malignant pleural effusion. The young women died of MOC spread and disease.The four young women included in this case series were diagnosed with MOC as teenagers and died of disease within approximately 2 years of diagnosis. Their initial gynecologist or surgeon did not suspect their large cyst to be MOC before the initial surgery, highlighting the need for more awareness in the gynecological community that teenagers can harbor MOC in large ovarian cysts. The four young women had fertility sparing, salpingo-oophorectomy staging surgery and standard chemotherapy for 6 cycles. Despite pathology showing expansile growth pattern, MOC recurred and acted very aggressively. The MOC tumor from three girls with known tumor genetics showed TP and KRAS co-mutations. Zhang et al.'s 2025 study showed that TP53 and KRAS co-mutations are associated with worse outcomes in mucinous ovarian carcinomas. Women with tumors that carried the mutations were more likely to have recurrence and worse prognosis even if they were younger and diagnosed at stage 1. This small case series concurs with Zhang et al.'s study. This highlights the need for targeted treatments, especially in young women that are having fertility sparing surgery. It also demonstrates that tumor biomarkers are important in deciding on treatment strategy since expansile (versus infiltrative) pattern does not guarantee benign behavior.
Lisa Feinstein (Wed,) studied this question.