Extramedullary Hematopoiesis in Mismatch Repair Deficient Colon Cancer Patient on Adjuvant Chemotherapy.
Extramedullary Hematopoiesis in Mismatch Repair Deficient Colon Cancer Patient on Adjuvant Chemotherapy.
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DOI：
10.7759/cureus.12899
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发表时间：
2021-01-25
期刊：
影响因子：
--
通讯作者：
Parekh H
中科院分区：
文献类型：
--
作者：
De Leo EK;Shah CP;Grajo JR;Liu X;Parekh H
一位59岁男性，因腹痛两个月而就诊，并被发现有阻塞性盲肠肿块。结肠镜检查和活检证实为浸润性腺癌。错配修复（MMR）蛋白的免疫组织化学分析显示，癌细胞核中MLH 1和PMS 2的丢失，这使得肿瘤MMR缺陷。阴性生殖细胞检测MMR蛋白排除了林奇综合征。在对远处转移进行阴性分期计算机断层扫描后，他接受了回结肠切除术和回横结肠吻合术。最终病理学分析显示低分化腺癌伴印戒特征、阴性边缘和3/22个淋巴结阳性，分类为IIIB期（T4 aN 1bM 0）。在未使用任何生长因子支持的情况下，开始使用改良FOLFOX（亚叶酸钙/亚叶酸、氟尿嘧啶和奥沙利铂）进行辅助化疗。在第9/12周期后，患者出现轻度转氨酶升高、癌胚抗原升高，并间隔出现两个不均匀增强的肝脏病变。这两个病变的活检显示髓外造血（EMH），没有转移性疾病的证据。他完成了辅助化疗，没有并发症，这些肝脏病变在近两年的随访期间已经缩小。EMH在结肠癌患者中极为罕见。促成因素包括治疗特异性（生长因子支持）、继发于化疗和放疗的骨髓抑制和肿瘤特异性因子（肿瘤释放的细胞因子和生长因子）。据我们所知，这是第一例在辅助FOLFOX的MMR缺陷结肠癌患者中发生EMH的病例报告。MMR缺陷型肿瘤显示出CD 8+细胞毒性T淋巴细胞以及辅助性T细胞高度浸润的迹象，导致细胞因子如干扰素-γ的产生增加。这可能是一个潜在的病因背后EMH在我们的病人谁是MMR缺陷。MMR缺陷状态在有效市场假说发展中的作用有待进一步探讨。
A 59-year-old male presented with a two-month history of abdominal pain and was found to have an obstructing cecal mass. Colonoscopy and biopsy confirmed invasive adenocarcinoma. Immunohistochemical analyses for mismatch repair (MMR) proteins revealed the loss of MLH1 as well as PMS2 in cancerous nuclei, which makes the tumor MMR deficient. Negative germline testing for MMR proteins ruled out the Lynch syndrome. After negative staging computerized tomography scan for distant metastases, he underwent ileocolectomy with ileotransverse colonic anastomosis. Final pathological analysis revealed poorly differentiated adenocarcinoma with signet ring features, negative margins, and 3/22 lymph nodes positive, classified as stage IIIB (T4aN1bM0). Adjuvant chemotherapy with modified FOLFOX (leucovorin calcium/folinic acid, fluorouracil, and oxaliplatin) was started without the use of any growth factor support. After cycle 9 of 12, he developed mild transaminitis, carcinoembryonic antigen elevation, and interval development of two heterogeneously enhancing hepatic lesions. Biopsy of both of these lesions revealed extramedullary hematopoiesis (EMH), with no evidence of metastatic disease. He completed adjuvant chemotherapy without complication, and these liver lesions have decreased in size during the follow-up period of almost two years thus far. EMH is extremely rare in patients with colon cancer. Contributing factors include therapy-specific (growth factor support), bone marrow suppression secondary to chemotherapy and radiation therapy, and tumor-specific factors (cytokine and growth factors released by the tumor). To the best of our knowledge, this is the first case report of EMH in an MMR deficient colon cancer patient on adjuvant FOLFOX. MMR-deficient tumors show signs of a high degree of infiltration with CD8+ cytotoxic T lymphocytes as well as helper T cells, leading to increased production of cytokines, such as interferon-γ. This could be a potential etiology behind EMH in our patient who was MMR deficient. The role of the MMR-deficient state in the development of EMH should be explored further.
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