18 F-FDG and 18 F-AIF-NOTA-Octreotide PET/CT Confirmed a Rare Case of Cutaneous Merkel Cell Carcinoma With a Solitary Local Nodal Metastasis.

ABSTRACT: Cutaneous Merkel cell carcinoma with local nodal metastasis is a rare entity. A 56-year-old man presented with a nontender left inguinal mass, and ultrasound-guided biopsy of this nodal mass confirmed nodal metastasis with strong neuroendocrine differentiation from cutaneous Merkel cell carcinoma. Staging 18 F-FDG PET/CT showed a solitary 3.9 × 6.8-cm hypermetabolic left groin mass with no other suspicious lesions elsewhere. To confirm the patient's eligibility for radical curative treatment, taking into consideration of its neuroendocrine differentiation, a subsequent 18 F-AIF-NOTA-octreotide PET/CT was performed, which demonstrated only solitary somatostatin receptor-positive left inguinal mass. The patient underwent radical treatment.

Linking oxidative DNA lesion 8-OxoG to tumor development and progression.

Cells of the aerobic metabolic organism are inevitably subjected to the damage from reactive oxygen species (ROS). ROS cause multiple forms of DNA damage, among which the oxidation product of guanine G 8-hydroxyguanine (8-oxoG) is the most frequent DNA oxidative damage, recognized by the specific glycosidase OGG1 that initiates the base excision repair pathway. If left unrepaired, 8-oxoG may pair with A instead of C, leading to a mutation of G: C to T: A during replication. Thus, the accumulation of 8-oxoG or the abnormal OGG1 repair is thought to affect gene function, which in turn leads to the development of tumor or aging-related diseases. However, a series of recent studies have shown that 8-oxoG tends to be produced in regulatory regions of the genome. 8-oxoG can be regarded as an epigenetic modification, while OGG1 is a specific reader of this information. Substrate recognition, binding or resection by OGG1 can cause DNA conformation changes or affect histone modifications, causing up-regulation or down-regulation of genes with different properties. Thus, in addition to the potential genotoxicity, the association of guanine oxidative damage with development of tumors is closely related to its aberrant initiation of gene expression through epigenetic mechanisms. In this review, we summarize the underlying mechanism of 8-oxoG and repair enzyme OGG1 in tumor development and progression, with aims to interpret the relationship between DNA oxidative damage and tumor from a new perspective, and provide new ideas and targets for tumor treatment.