Computational modelling suggests that Barrett's oesophagus may be the precursor of all oesophageal adenocarcinomas.
Computational modelling suggests that Barrett's oesophagus may be the precursor of all oesophageal adenocarcinomas.
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DOI：
10.1136/gutjnl-2020-321598
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发表时间：
2020-11-24
期刊：
影响因子：
24.5
通讯作者：
Inadomi JM
中科院分区：
文献类型：
--
作者：
Curtius K;Rubenstein JH;Chak A;Inadomi JM
Barrett氏食道癌(BE)是已知的食管腺癌(OAC)的先兆，但目前的临床数据尚未得到证实，以确定BE是否是所有OAC的起因，这将加强BE筛查工作的证据。我们的目标是回答是否所有预期的流行的BE，诊断的和未诊断的，可以解释美国癌症登记数据中的所有事件OAC。我们使用了一个多尺度的OAC计算模型，该模型包括了从正常食道到BE在美国人群中的进化过程。该模型先前经过了校准，以适应监测、流行病学和最终结果癌症发病率曲线。在这里，我们还使用了特定年龄和特定性别的美国人口普查数据，以了解高危人数。模型验证的主要结果是给定日历年的OAC病例的预期数量。次要结果包括模型预测的BE和BE-to-OAC进展的患病率与观察的患病率和进展率的比较。该模型估计2010年BE的OAC病例总数为9970例(95%CI：9140至11980)，这概括了人口数据中几乎所有的OAC病例。该模型同时预测45-55岁高危男性BE患病率为8%-9%，男性非发育异常BE-to-OAC年进展为0.1%-0.2%，与临床研究一致。除了预期来自BE患者的病例外，美国人口中可能很少会出现额外的OAC病例。对高危患者的有效筛查可以捕捉到大多数OAC进展的人群，并可能通过在监测期间及早发现和根治性地切除小(前)癌来降低死亡率。
Barrett’s oesophagus (BE) is a known precursor to oesophageal adenocarcinoma (OAC) but current clinical data have not been consolidated to address whether BE is the origin of all incident OAC, which would reinforce evidence for BE screening efforts. We aimed to answer whether all expected prevalent BE, diagnosed and undiagnosed, could account for all incident OACs in the US cancer registry data. We used a multiscale computational model of OAC that includes the evolutionary process from normal oesophagus through BE in individuals from the US population. The model was previously calibrated to fit Surveillance, Epidemiology and End Results cancer incidence curves. Here, we also utilised age-specific and sex-specific US census data for numbers at-risk. The primary outcome for model validation was the expected number of OAC cases for a given calendar year. Secondary outcomes included the comparisons of resulting model-predicted prevalence of BE and BE-to-OAC progression to the observed prevalence and progression rates. The model estimated the total number of OAC cases from BE in 2010 was 9970 (95% CI: 9140 to 11 980), which recapitulates nearly all OAC cases from population data. The model simultaneously predicted 8%–9% BE prevalence in high-risk males age 45–55, and 0.1%–0.2% non-dysplastic BE-to-OAC annual progression in males, consistent with clinical studies. There are likely few additional OAC cases arising in the US population outside those expected from individuals with BE. Effective screening of high-risk patients could capture the majority of population destined for OAC progression and potentially decrease mortality through early detection and curative removal of small (pre)cancers during surveillance.
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