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. 2021:151:197-229.
doi: 10.1016/bs.acr.2021.02.007. Epub 2021 May 5.

Racial and ethnic disparities in colorectal cancer incidence and mortality

John M Carethers  1
Affiliations

Racial and ethnic disparities in colorectal cancer incidence and mortality

John M Carethers. Adv Cancer Res. 2021.

Abstract

The occurrence of colorectal cancer (CRC) shows a large disparity among recognized races and ethnicities in the U.S., with Black Americans demonstrating the highest incidence and mortality from this disease. Contributors for the observed CRC disparity appear to be multifactorial and consequential that may be initiated by structured societal issues (e.g., low socioeconomic status and lack of adequate health insurance) that facilitate abnormal environmental factors (through use of tobacco and alcohol, and poor diet composition that modifies one's metabolism, microbiome and local immune microenvironment) and trigger cancer-specific immune and genetic changes (e.g., localized inflammation and somatic driver gene mutations). Mitigating the disparity by prevention through CRC screening has been demonstrated; this has not been adequately shown once CRC has developed. Acquiring additional knowledge into the science behind the observed disparity will inform approaches towards abating both the incidence and mortality of CRC between U.S. racial and ethnic groups.

Keywords: African American; Colon cancer disparity; Colon cancer genetics; Colon cancer risk; Colon cancer screening; Colon cancer survival; Ethnicity; Family history; Inherited colon cancer syndrome; Race.

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Conflict of interest statement

Disclosure of Potential Conflicts of Interest: No potential conflicts of interest are disclosed.

Figures

Figure 1.
Figure 1.
Trends in SEER age-adjusted colorectal cancer incidence and mortality per 100,000 (adjusted to the 2000 U.S. standard population), by race/ethnicity. (A) Trends for SEER age-adjusted colorectal cancer incidence, 2000-2017. (B) Trends for SEER age-adjusted colorectal cancer mortality, 2000-2018. Data obtained from seer.cancer.gov.
Figure 2.
Figure 2.
Trends in SEER relative survival rates per 100,000 (adjusted to the 2000 U.S. standard population), 2000-2016, by race/ethnicity. (A) Trends for SEER relative survival rates for all stages of colorectal cancer. (B) Trends for SEER relative survival rates for localized stage of colorectal cancer. (C) Trends for SEER relative survival rates for regional stage of colorectal cancer. (D) Trends for SEER relative survival rates for distant stage of colorectal cancer. Data obtained from seer.cancer.gov.
Figure 2.
Figure 2.
Trends in SEER relative survival rates per 100,000 (adjusted to the 2000 U.S. standard population), 2000-2016, by race/ethnicity. (A) Trends for SEER relative survival rates for all stages of colorectal cancer. (B) Trends for SEER relative survival rates for localized stage of colorectal cancer. (C) Trends for SEER relative survival rates for regional stage of colorectal cancer. (D) Trends for SEER relative survival rates for distant stage of colorectal cancer. Data obtained from seer.cancer.gov.
Figure 3.
Figure 3.
Non-modifiable and modifiable patient risk factors associated with the development of colorectal cancer. Green box includes elements that make up family history, and the blue box contains elements that make up race/ethnicity. NSAID, non-steroidal anti-inflammatory drug; HRT, hormone replacement therapy; CRC, colorectal cancer
Figure 4.
Figure 4.
Connections and consequences initiated by socioeconomic disparities for ultimate risk and development of colorectal cancer.
Figure 5.
Figure 5.
Adenoma-to-carcinoma sequence in the human colon for sporadic, familial adenomatous polyposis (FAP) and Lynch colorectal cancers, with potential environmental modifiers and ultimate population risk of cancer. Note that sporadic colorectal cancer has a dwell time of up to 5 decades for tumor initiation and up to 2 additional decades for tumor progression; tumor initiation is greatly accelerated in FAP while tumor progression is greatly accelerated in Lynch syndrome. Environmental influences that modify the local microbiome and inflammatory microenvironment may modify the rate of progression of the adenoma-to-carcinoma sequence at any step.
Figure 6.
Figure 6.
Summary of patient associations and outcomes from colorectal cancer genomic instability genotypes. EMAST, elevated microsatellite alterations at selected tetranucleotide repeats; MSI-H, microsatellite instability-high; MSS, microsatellite stable; PD-L1, programmed death ligand-1; NSAID, non-steroidal anti-inflammatory drug
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References

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