Age effects and temporal trends in adenocarcinoma of the esophagus and gastric cardia (United States)

Jeon, Jihyoun; Luebeck, E. Georg; Moolgavkar, Suresh H.

doi:10.1007/s10552-006-0037-3

Cited by 58 publications

(53 citation statements)

References 51 publications

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“…Whether the similarity of the estimated sojourn times in colon and pancreas is a general feature of epithelial cancers or mere coincidence for the two particular cancers studied here remains to be seen. However, estimates of α − β in lung (45,46), breast (W. D. Hazelton, personal communication), and Barrett's esophagus (47) suggest that clonal expansion of the earliest epithelial neoplasms is uniformly slow, ensuing with rates not too different from those found here (between 0.1 and 0.2 per year).…”

Section: Discussioncontrasting

confidence: 51%

Age-specific incidence of cancer: Phases, transitions, and biological implications

Meza

Jeon

Moolgavkar

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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140

183

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The observation that the age-specific incidence curve of many carcinomas is approximately linear on a double logarithmic plot has led to much speculation regarding the number and nature of the critical events involved in carcinogenesis. By a consideration of colorectal and pancreatic cancers in the Surveillance Epidemiology and End Results (SEER) registry we show that the log-log model provides a poor description of the data, and that a much better description is provided by a multistage model that predicts two basic phases in the age-specific incidence curves, a first exponential phase until the age of ≈60 followed by a linear phase after that age. These two phases in the incidence curve reflect two phases in the process of carcinogenesis. Paradoxically, the early-exponential phase reflects events between the formation (initiation) of premalignant clones in a tissue and the clinical detection of a malignant tumor, whereas the linear phase reflects events leading to initiated cells that give rise to premalignant lesions because of abrogated growth/differentiation control. This model is consistent with Knudson's idea that renewal tissue, such as the colon, is converted into growing tissue before malignant transformation. The linear phase of the age-specific incidence curve represents this conversion, which is the result of recessive inactivation of a gatekeeper gene, such as the APC gene in the colon and the CDKN2A gene in the pancreas.colorectal | pancreatic | multistage carcinogenesis | neoplastic progression | Knudson's "two-hit" hypothesis T he precise shape of the age-specific incidence of various cancers, especially of nonembryonal solid tumors, and what information can be gleaned from their behavior, is still subject to scientific debate. A widely held view, put forward independently by Muller (1) and Nordling (2) and which reflects the basis of the Armitage-Doll model (3), conceives the stepwise progression of normal cells to cancer as a multistage process involving a number of rate-limiting (epi)genetic events. When viewed at the population level, this assumption uniquely defines the mathematical shape of the age-specific incidence of a cancer, also reflecting the assumed number of rate-limiting events. Indeed, at some level of mathematical approximation (see, e.g., ref. 4), the sequential nature of such a multistep process imposes a power-law behavior, that is, the age-specific incidence of cancers that arise as a consequence of several rate-limiting genomic alterations is predicted to increase with a power of age that is one less than the number of events necessary for malignant transformation. Although it is generally recognized that the carcinogenic process is more complicated and possibly punctuated by selection of advantageous mutations and clonal expansions (5), the qualitative power-law behavior of the age-specific cancer incidence is still considered a reasonable approximation for many cancers and continues to be invoked to argue for or against the importance of specific biological events in car...

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Section: Discussioncontrasting

confidence: 51%

Age-specific incidence of cancer: Phases, transitions, and biological implications

Meza

Jeon

Moolgavkar

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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140

183

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“…For all years combined, a total of 6,017 male cases (5,562 pleural, 455 peritoneal) and 1,673 female cases (1,291 pleural, 382 peritoneal) were available for the analyses. 1 We have previously presented likelihood-based analyses of the incidence of different cancers in the SEER registry using hazard functions derived from multistage models to replace the non-specific effects of age in the traditional APC models, while secular trends, i.e., period and cohort effects, were modeled in the usual fashion (see [12][13][14]). Briefly, we model the age-specific incidence (age a) occurring in calendar year j as…”

Section: Methodsmentioning

confidence: 99%

“…We discuss this model below. We also considered the two-stage clonal expansion (TSCE) model proposed by Moolgavkar and Venzon [18] and Moolgavkar and Knudson [19] and a three-stage extension of it as described in earlier papers [12][13][14]. 1 Incidence data for the same tumor can be downloaded using different coding schemes from the SEER registry.…”

Section: Methodsmentioning

confidence: 99%

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Pleural and peritoneal mesotheliomas in SEER: age effects and temporal trends, 1973–2005

Moolgavkar

Meza

Turim

2009

Cancer Causes Control

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177

152

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We analyzed mesothelioma incidence in the Surveillance, Epidemiology, and End Results (SEER) database over the period 1973-2005 using extensions of the age-period-cohort (APC) models. In these analyses, the usual non-specific age effects of the conventional APC models were replaced by hazard functions derived from two multistage models of carcinogenesis, the Armitage-Doll model and the two-stage clonal expansion (TSCE) model. The extended APC models described the incidence data on pleural and peritoneal mesotheliomas well. After adjustment for temporal trends, the data suggest that the age-specific incidence rates of both pleural and peritoneal mesotheliomas are identical in men and women. Driven largely by birth cohort effects, age-adjusted rates of pleural mesothelioma among men rose from about 7.5 per million person-years in 1973 to about 20 per million person-years in the early 1990s and appear to be stable or declining thereafter. Age-adjusted rates of pleural mesothelioma among women have remained more or less constant at about 2.5 per million person-years over the period 1973-2005. Age-adjusted rates for peritoneal mesothelioma in both men (1.2 per million person-years) and women (0.8 per million person-years) exhibit no temporal trends over the period of the study. We estimate that approximately 94,000 cases of pleural and 15,000 cases of peritoneal mesothelioma will occur in the US over the period 2005-2050.

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“…Other prospective studies, mendelian randomization studies and meta-analyses confirmed the association between overweight/obesity and esophageal inflammation, metaplasia, and adenocarcinoma (17)(18)(19), according to tumorigenic mechanisms that are either dependent or independent from other risk factors, including gastroesophageal reflux and Barrett's esophagus diseases (20,21). These findings have led to speculation that obesity may represent a novel pathogenic factor involved in esophageal adenocarcinoma, so that the increase in obesity prevalence may partially explain the increase in esophageal adenocarcinoma incidence (22,23). The mechanistic link between obesity and esophageal adenocarcinoma appears to be the IGF-1 axis, together with adipocyte-secreted cytokines.…”

Section: Esophageal Cancermentioning

confidence: 87%

Obesity and gastrointestinal malignancies

Vangapandu¹

2015

rghn

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SummaryObesity is an important risk factor of death worldwide, with increasing rates in adults and children. Convincing evidences underline that body fatness is also a key risk factor for several types of tumors, in particular those of the gastrointestinal tract; among them, oesophageal, liver, pancreatic and colon rectal cancers show the strongest link with obesity. Unbalance in specific biological pathways (including adipokine secretion, insulin-like growth factor-1 pathway, redox state and inflammation), often accompanying obesity, contribute to cancer onset and progression. By acting on specific lifestyle and cancer risk factors, including food, nutrition, physical activity and body composition, cancer incidence may be effectively decreased. In this review, we summarize the most convincing evidence on the relationship between obesity and gastrointestinal tumors, underling the potential mechanisms of action, as well as strategies that may be useful for cancer prevention.

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Age effects and temporal trends in adenocarcinoma of the esophagus and gastric cardia (United States)

Cited by 58 publications

References 51 publications

Age-specific incidence of cancer: Phases, transitions, and biological implications

Age-specific incidence of cancer: Phases, transitions, and biological implications

Pleural and peritoneal mesotheliomas in SEER: age effects and temporal trends, 1973–2005

Obesity and gastrointestinal malignancies

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