This report describes an extremely rare case of large laterally-spreading EGC of the distal stomach. LSTs are considered non-polypoid lesions with specified clinic-pathologic features. They are characterized by lateral progression along the intra-luminal wall, where they form broad-based granular or non-granular flat-type lesions [2]. EGCs progress slowly, although the speed of their progression is accelerated according to the downward invasion by the cancer. Most patients with EGC are usually asymptomatic or they present with the earliest signs and symptoms of indigestion, loss of appetite, heartburn, epigastric pain, and anaemia.
The aetiology of gastric cancer is multifactorial and involves both hereditary predilection and environmental aspects. Family history, genetic risk factors, H. pylori and Epstein–Barr virus infection [4], pernicious anaemia, chronic atrophic gastritis, Ménétrier’s disease, smoking and dietary factors, such as the consumption of processed foods and pickled vegetables, as well as obesity are risk factors for gastric cancer. Elevated expression rates of tumour markers such as CEA and CA 19–9, and recently, cancer-testis antigens have been reported in gastric cancer; which include Kita-kyushu lung cancer antigen 1, which is expressed in; 79.5%; MAGE-A1 at; 32.5%, MAGE-A3 at; 39.8%, and NY-ESO-1 at; 15.7% [5]. According to Futawatari et al. [5] Kita-kyushu lung cancer antigen 1 is tumour-specific and can be frequently detected even in the early stages of the disease. In addition, the assessment of cancer-testis antigens expression in gastric mucosa infected with H. pylori may be helpful for the identification of patients with a high risk of gastric cancer.
The present case is unique and suggestive. This was the first gastric LST of the distal stomach that extended into the entire duodenal bulb; this was also the second gastric LST to be reported after a laterally-spreading gastric mucosal cancer was reported by Nunobe et al. [6]. Nunobe demonstrated surgical techniques for safe lesion removal, but the case report lacked genuine images of the lesion as well as detailed information on the lesion. In contrast, this case presents serial endoscopic and histopathological images that demonstrate not only the gross-morphological changes of the lesion but also a thorough examination of the pit patterns and surface patterns of the lesion, respectively. In this case, the circumferential-type laterally spreading tumour in the antrum adjacent to the pyloric mucosa exhibited roughness and granulation, and macroscopically, the nodules were confined to the pylorus and duodenal bulb. In addition, oedematous villi with a white opaque substance were prominent in the antral and duodenal bulb regions of the lesion which indicates EGC. According to Um et al. [7] clinical behaviors of EGC vary by the endoscopic gross appearance. Endoscopic gross appearance associated with histological differentiation and clinical behavior of EGC. In order to characterize tumour burden of EGC, usually the longest diameter of tumour and maximal longitudinal diameter of tumour, the tumour burden is important to predict clinical behaviors of cancer. In contrast, the clinicopathologic characteristics of LST are also dependent on the endoscopic appearance of the lesion surface, that is, LST-granular or granular nodular mixed as compared with LST-non granular, and the risk of malignant transformation is significantly higher for the mixed nodular or pseudo-depressed subtypes and lesion of larger size [8]. According to Ohara et al. [1] endoscopic treatment for superficial elevated and depressed type EGC has a high potential to result in non-curative resection. Based on the classification of colorectal LSTs, LST- non-granular and LST- granular-nodular mixed with larger size exhibit a high risk of submucosal invasion and malignancy [2, 3]. Thus, these subtypes of tumours are suggestive to undergo surgery rather than incomplete endoscopic resection [8]. A summary of the clinical and aetiological factors as well as the management of EGC lesions is presented in (Fig. 3) [1, 4, 5].
Detection of early neoplasia, precise characterization of the lesion, and decision-making as to the ultimate treatment are crucial for better outcomes [9]. Therefore, EGC has driven the development of novel imaging technologies such as NBI and high-definition chromoendoscopy using indigo to detect early lesions [9]. A methodical approach to describe and report superficial lesions so that the appropriate resection approach is performed includes the location of the lesion, its size, morphology, surface pattern, as well as other gross morphological features [2].
Considering that ESD is broadly recognized as a less invasive method for the treatment of EGC [9], it is still a complicated procedure and is accompanied by a negligible risk of lymph node metastasis, bleeding, perforation, and longer operation times [6]. Moreover, ESD may result in incomplete or non-curative resection in EGC patients, which may necessitate additional gastrectomy [1, 10]. According to Ohara et al. [1] ESD may be curative in (a) differentiated-type mucosal cancers that are negative for ulceration (UL (−)) and without lymphovascular invasion irrespective of tumour size; (b) differentiated-type UL(+) mucosal cancers without lymphovascular invasion and a size ≤ 30 mm; (c) undifferentiated-type UL(−) mucosal cancers without lymphovascular invasion and a size ≤ 20 mm; (d) differentiated-type submucosal cancers ≤ 500 μm without lymphovascular invasion and those ≤ 30 mm. ESD is non-curative for undifferentiated-type lesions > 20 mm and superficial elevated and depressed-type 0-IIa + IIc or 0-IIc + IIa, and UL(+) lesions. Thus, endoscopic resection of these tumours is considered an investigational treatment as in our case, and additional surgical treatment should be performed [10, 11].
According to the 2010 Japanese gastric cancer treatment guidelines (ver. 3), gastrectomy with lymph -node dissection is the standard treatment for EGC [11]. Recently, laparoscopic surgery, particularly laparoscopic-assisted distal gastrectomy for EGC, has gained an advantage to some extent over open surgery in terms of minimal invasiveness, decreased morbidity and better postoperative short and long-term patient outcomes with excellent 5-year overall survival [9, 12,13,14,15]. More recently, laparoscopic and endoscopic cooperative surgery for benign gastric tumours and EGC lesions has been promising in terms of minimal invasiveness, precise lesion localization, safe excision, minimal margins, restoration and reduction in hospital stay [6, 16]. We remain confident that, commercialization of the knowledge of EGC lesions may improve their primary detection rate and thus the treatment outcome.
This case is a new indication for the gastroenterologist as well as for researchers. Early identification and curative management of EGC lesions are crucial for better patient outcomes. Lesions, particularly those of a larger size or with granules and nodules, should be removed surgically rather than by endoscopic resection because these tumours are highly invasive and carry a significant risk of malignancy. Many clinicians and researchers hope that our knowledge will be improved based on new scientific findings, which will lead to the evolution of gastric cancer diagnosis and treatment.