Abstract：
There is only one report of Barrett\'s esophagus (BE) with mixed neuroendocrine-non-neuroendocrine neoplasm (MiNEN). Herein, for the first time, we present a case with an aggressive esophageal MiNEN, as well as with both primary MiNEN and conventional adenocarcinoma, arising in BE.
A 68-year-old woman had been diagnosed with 0-IIa type adenocarcinoma in the background of long-segment BE, 45 months earlier. She underwent endoscopic submucosal dissection (ESD) and the pathological diagnosis was tubular adenocarcinoma, well-differentiated, with slight submucosal invasion. There was no lymphovascular invasion and the margins were intact. The upper esophagogastroduodenoscopy conducted the year after ESD showed no residual or recurrent cancer. However, she was subsequently followed up at another hospital, and endoscopy was not performed after the second year. She was urgently transported to our hospital due to buttock pain in the ninth month of the fourth year. A computed tomography (CT) of the head showed multiple cerebral metastases and positron emission tomography-CT revealed numerous osseous and nodal involvements. We performed upper endoscopy and detected type 3 esophageal tumor. Multiple biopsy specimens histopathologically contained invasive neoplasm composed of neuroendocrine carcinoma (NEC) and adenocarcinoma, moderately to poorly differentiated. The NEC element showed diffuse proliferation of primitive cancer cells possessing fine-granular cytoplasm and nuclei with prominent nucleoli, whereas the adenocarcinoma component had tubules or nested growth of basophilic cells. Immunohistochemically, the NEC cells were diffusely positive for synaptophysin, with focal expressions of INSM1, chromogranin A and NCAM, whereas the adenocarcinoma cells were mostly negative for these NE markers. The Ki67 index was 90% at the hot spots in both types. The patient died 3.5 months after the biopsy-based histological diagnosis.
Appropriate therapy according to the guidelines and/or meticulous clinical follow-up based on periodic endoscopy as well as a full physical examination are essential, from a proactive perspective, for early diagnosis of secondary aggressive cancers after ESD.
A 68-year-old woman had been diagnosed with 0-IIa type adenocarcinoma in the background of long-segment BE, 45 months earlier. She underwent endoscopic submucosal dissection (ESD) and the pathological diagnosis was tubular adenocarcinoma, well-differentiated, with slight submucosal invasion. There was no lymphovascular invasion and the margins were intact. The upper esophagogastroduodenoscopy conducted the year after ESD showed no residual or recurrent cancer. However, she was subsequently followed up at another hospital, and endoscopy was not performed after the second year. She was urgently transported to our hospital due to buttock pain in the ninth month of the fourth year. A computed tomography (CT) of the head showed multiple cerebral metastases and positron emission tomography-CT revealed numerous osseous and nodal involvements. We performed upper endoscopy and detected type 3 esophageal tumor. Multiple biopsy specimens histopathologically contained invasive neoplasm composed of neuroendocrine carcinoma (NEC) and adenocarcinoma, moderately to poorly differentiated. The NEC element showed diffuse proliferation of primitive cancer cells possessing fine-granular cytoplasm and nuclei with prominent nucleoli, whereas the adenocarcinoma component had tubules or nested growth of basophilic cells. Immunohistochemically, the NEC cells were diffusely positive for synaptophysin, with focal expressions of INSM1, chromogranin A and NCAM, whereas the adenocarcinoma cells were mostly negative for these NE markers. The Ki67 index was 90% at the hot spots in both types. The patient died 3.5 months after the biopsy-based histological diagnosis.
Appropriate therapy according to the guidelines and/or meticulous clinical follow-up based on periodic endoscopy as well as a full physical examination are essential, from a proactive perspective, for early diagnosis of secondary aggressive cancers after ESD.
摘要：
仅有1例Barrett食管（BE）合并神经内分泌-非神经内分泌混合性肿瘤（MiNEN）。在这里，第一次,我们提出一例侵袭性食道MINEN,以及原发性MINEN和常规腺癌，在be中产生。
一名68岁的女性在长段BE的背景下被诊断为0-IIa型腺癌，45个月前她接受了内镜黏膜下剥离术（ESD），病理诊断为管状腺癌，分化良好,有轻微的粘膜下浸润。没有淋巴血管侵犯，边缘完整。ESD后一年进行的上食管胃十二指肠镜检查未显示残留或复发的癌症。然而,她随后在另一家医院接受了随访，第二年后未进行内窥镜检查。在第四年的第九个月，由于臀部疼痛，她被紧急送往我们医院。头部计算机断层扫描（CT）显示多个脑转移瘤，正电子发射断层扫描-CT显示大量骨性和淋巴结受累。我们进行了上内镜检查并检测到3型食管肿瘤。多个活检标本组织病理学包含由神经内分泌癌（NEC）和腺癌组成的浸润性肿瘤，中度到差别化。NEC元件显示原始癌细胞的弥漫性增殖，具有细颗粒细胞质和细胞核，具有突出的核仁，而腺癌成分有小管或嗜碱性细胞的巢式生长。免疫组织化学，NEC细胞对突触素呈弥漫性阳性，具有INSM1、嗜铬粒蛋白A和NCAM的局灶性表达，而腺癌细胞对这些NE标志物大多呈阴性。在这两种类型的热点地区，Ki67指数均为90%。患者在基于活检的组织学诊断后3.5个月死亡。
根据指南进行适当的治疗和/或基于定期内窥镜检查和全面体检的细致临床随访至关重要，从积极主动的角度来看，用于ESD后继发性侵袭性癌症的早期诊断。
一名68岁的女性在长段BE的背景下被诊断为0-IIa型腺癌，45个月前她接受了内镜黏膜下剥离术（ESD），病理诊断为管状腺癌，分化良好,有轻微的粘膜下浸润。没有淋巴血管侵犯，边缘完整。ESD后一年进行的上食管胃十二指肠镜检查未显示残留或复发的癌症。然而,她随后在另一家医院接受了随访，第二年后未进行内窥镜检查。在第四年的第九个月，由于臀部疼痛，她被紧急送往我们医院。头部计算机断层扫描（CT）显示多个脑转移瘤，正电子发射断层扫描-CT显示大量骨性和淋巴结受累。我们进行了上内镜检查并检测到3型食管肿瘤。多个活检标本组织病理学包含由神经内分泌癌（NEC）和腺癌组成的浸润性肿瘤，中度到差别化。NEC元件显示原始癌细胞的弥漫性增殖，具有细颗粒细胞质和细胞核，具有突出的核仁，而腺癌成分有小管或嗜碱性细胞的巢式生长。免疫组织化学，NEC细胞对突触素呈弥漫性阳性，具有INSM1、嗜铬粒蛋白A和NCAM的局灶性表达，而腺癌细胞对这些NE标志物大多呈阴性。在这两种类型的热点地区，Ki67指数均为90%。患者在基于活检的组织学诊断后3.5个月死亡。
根据指南进行适当的治疗和/或基于定期内窥镜检查和全面体检的细致临床随访至关重要，从积极主动的角度来看，用于ESD后继发性侵袭性癌症的早期诊断。
