Can my metastatic colon cancer be controlled?

Hello,​

Welcome to icliniq.com.

​I read your query and can understand your concern.

​Based on the information provided, you have developed vomiting and constipation during the third trimester of pregnancy, leading to the diagnosis of early-onset colorectal cancer. Imaging (attachments removed to protect the patient’s identity) suggested a bowel obstruction in the descending colon, and you underwent an urgent left colectomy with preservation of the pregnancy. A colostomy was created. The pathology report showed a well-differentiated adenocarcinoma with three of 12 lymph nodes positive for metastasis, staged as pT3N1b. You have received total parenteral nutrition (TPN) after surgery, and the baby was delivered preterm by cesarean section.

Following recovery, started adjuvant chemotherapy with Capecitabine and Oxaliplatin. Baseline imaging was not performed before initiating treatment. Carcinoembryonic antigen (CEA) level was elevated before chemotherapy. Four cycles of treatment were completed. Therapy was interrupted due to thrombocytopenia.

Molecular testing showed wild-type KRAS (Kirsten rat sarcoma viral oncogene homolog), NRAS (Neuroblastoma RAS viral oncogene homolog), BRAF (B-Raf proto-oncogene), and HER2/ERBB2 (human epidermal growth factor receptor 2/Erb-B2 receptor tyrosine kinase 2) were not amplified.

Evaluation thereafter revealed a rising level of CEA (carcinoembryonic antigen), and the PET-CT (Positron emission tomography-Computed tomography) scan showed a para-aortic lymphadenopathy that was FDG (Fluorodeoxyglucose) avid with suspicion of possible peritoneal metastasis. But there was no biopsy of the suspected peritoneal mass, and further radiological review indicated that it may be benign. The biopsy of the para-aortic lymph node revealed metastatic adenocarcinoma in keeping with the colonic primary.

​Next-generation sequencing identified alterations in APC (adenomatous polyposis coli) and TP53 (tumor protein p53), with amplification of PMS2 (postmeiotic segregation increased 2) and MSH6 (mutS homolog 6). The tumor was microsatellite stable (MSS), and mismatch repair (MMR) protein expression was reported as intact. The clinical significance of the reported PMS2 and MSH6 amplification should be clarified.

​Treatment was changed to FOLFIRI (Folinic acid, Fluorouracil, and Irinotecan) plus Cetuximab. Serial CEA (carcinoembryonic antigen) levels subsequently decreased, and follow-up PET-CT (positron emission tomography-computed tomography) imaging demonstrated a reduction in both the size and metabolic activity of the metastatic lesion, indicating a favorable response to treatment. The Cetuximab-related skin toxicity was present initially but improved significantly without specific treatment.

​The next-generation sequencing report also indicated that germline genetic testing did not identify any pathogenic inherited mutations associated with an increased risk of early-onset colorectal cancer. Plasma circulating tumor DNA (ctDNA) testing has not yet been performed.

The available medical records do not indicate a history of inflammatory bowel disease or any identified hereditary cancer syndrome that would explain the early onset of colorectal cancer.

​I hope this helps you.

​Take care.