Oesophagogastric junction adenocarcinoma: which therapeutic approach?

Mariette, C.; Piessen, Guillaume; Briez, Nicolas; Gronnier, Caroline; Triboulet, Jean

doi:10.1016/s1470-2045(10)70125-x

Cited by 163 publications

(109 citation statements)

References 53 publications

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“…As surgical findings showed a higher incomplete tumor resection in locallyadvanced T3/T4 gastroesophageal junction adenocarcinomas, the evaluation of the effects of pre operative chemoradiotherapy is urgently needed in this setting [45] . One ongoing phase III clinical trial is focusing on this question.…”

Section: Questionsmentioning

confidence: 99%

Neoadjuvant therapy for gastroesophageal adenocarcinoma

Samalin

Ychou

2016

WJCO

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Gastric and esophageal adenocarcinomas are one of the main causes of cancer-related death worldwide. While the incidence of gastric adenocarcinoma is decreasing, the incidence of gastroesophageal junction adenocarcinoma is rising rapidly in Western countries. Considering that surgical resection is currently the major curative treatment, and that the 5-year survival rate highly depends on the pTNM stage at diagnosis, gastroesophageal adenocarcinoma management is very challenging for oncologists. Several treatment strategies are being evaluated, and among them systemic chemotherapy, to decrease recurrences and improve overall survival. The MAGIC and FNCLCC-FFCD trials showed a survival benefit of perioperative chemotherapy in patients with operable gastric and lower esophageal cancer, and these results had an impact on the European clinical practice. New strategies, including induction chemotherapy followed by preoperative chemoradiotherapy, targeted therapies in combination with perioperative chemotherapy and the new cytotoxic regimens, are currently assessed to improve current standards and help developing patienttailored therapeutic interventions. Core tip: Gastric and esophageal adenocarcinomas are one of the main causes of cancer-related death worldwide. The incidence of gastroesophageal junction adenocarcinoma is rapidly rising in Western countries. Surgical resection is currently the major curative treatment. As the 5-year survival rate highly depends on the pTNM stage, the treatment strategy is very challenging for oncologists. Several treatments, including systemic chemotherapy, are being assessed to prevent recurrences and improve overall survival. New strategies, such as induction chemotherapy followed by preoperative chemoradiotherapy, targeted therapies and new cytotoxic regimens in perioperative chemotherapy, are currently assessed to improve current standards and develop more tailored therapeutic interventions.

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Section: Questionsmentioning

confidence: 99%

Neoadjuvant therapy for gastroesophageal adenocarcinoma

Samalin

Ychou

2016

WJCO

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“…Since the 1990s the (2002), whereas in the current, seventh, edition (2010), a cardia cancer is defined by (1) the midpoint of the tumor lying more than 5 cm from the gastroesophageal junction and extending across it, or (2) a tumor arising within 5 cm of but not extending into the gastroesophageal junction. As an example, the tumor shown here (broken red lines) would be classified as gastric cardia according to sixth edition of the AJCC staging system but as an esophageal lesion according to the seventh edition of the AJCC staging system Siewert classification system for gastroesophageal junction tumors has been in common use by surgeons and pathologists throughout the world [14]. In this schema, type 1 tumors are those that have their epicenter in the lower esophagus, type 2 tumors arise from an area 1 cm proximal to 2 cm distal to the gastroesophageal junction, and type 3 tumors originate 2-5 cm distally.…”

Section: The Gastric Cardia and Gca: Anatomy And Definitional Issuesmentioning

confidence: 99%

Obesity and related risk factors in gastric cardia adenocarcinoma

Olefson

Moss

2014

Gastric Cancer

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Over recent decades, the incidence of cancers of the gastroesophageal junction, including gastric cardia tumors, has increased markedly. This is a trend that has been well documented, especially in studies from the USA and northern Europe that have also demonstrated a concomitant rise in the ratio of cardia to distal gastric cancers. The rise in the prevalence of gastric cardia adenocarcinoma has been paralleled by the worldwide obesity epidemic, with almost all epidemiological studies reporting increased body mass index and obesity increase the risk of cardia cancer development. However, the strength of this association is less marked than the link between obesity and esophageal adenocarcinoma, and the mechanisms remain poorly understood. Other possible confounders of the relationship between obesity and cardia cancer include the decline in Helicobacter pylori infection and the widespread use of proton pump inhibitors, although these have rarely been controlled for in case-control and cohort studies investigating associations between obesity and cardia cancer. We review these epidemiological trends and discuss proposed mechanisms for the association, drawing attention to controversies over the difficulty of defining cardia cancer. The relative paucity of high-quality epidemiological studies from other regions of the world should prompt further investigation of this issue, especially in populations undergoing rapid socioeconomic change.

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“…Most notably, survival curves for these two procedures were identical in patients with type II AEG. Meanwhile, though not statistically significant, there is a non-negligible trend favoring better survival with the transthoracic esophagectomy in two subgroups; patients with type I AEG and those with a limited number of metastatic nodes [1][2][3][4][5][6][7][8]. Therefore, there is a possibility that selected patients would benefit from the transthoracic procedure based on better local control, as evidenced by longer locoregional disease free survival, as the authors described.…”

Section: Commentarymentioning

confidence: 99%

“…It is generally classified into three subtypes according to the Siewert system based on where the tumor center is located (1); type I, 1-5 cm above the EGJ; type II, 1 cm above to 2 cm below the EGJ; type III, 2-5 cm below the EGJ. Therefore, tumor burden is essentially esophageal in type I and gastric in type III, and in general the former is thus treated as an esophageal carcinoma and the latter as a gastric carcinoma (2). Type I AEG, usually arising from premalignant Barrett epithelium, is closely associated with increased body weight and gastroesophageal reflux disease (GERD).…”

mentioning

confidence: 99%