Molecular and clinicopathological differences by age at the diagnosis of colorectal cancer

Chu Cheng Chang, Pei Ching Lin, Chun Chi Lin, Yuan Tzu Lan, Hung Hsin Lin, Chien Hsing Lin, Shung Haur Yang, Wen Yi Liang, Wei Shone Chen, Jeng Kai Jiang, Jen Kou Lin, Shih Ching Chang*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


We compared the clinicopathological and molecular profiles between different age groups of sporadic colorectal cancer (CRC) patients (age <50, 56–60, 60–70, 70–80, and >80); 1475 CRC patients were enrolled after excluding 30 individuals with Lynch syndrome. The mutation spectra for APC, TP53, KRAS, PIK3CA, FBXW7, BRAF, NRAS, HRAS, TGFbR, Akt1, and PTEN were analyzed using polymerase chain reaction (PCR), followed by MassArray and microsatellite (MSI-high) analysis by performing genotyping. Male patients (74.1%) were significantly predominant to females (25.9%) in the older age group (70–80, >80). There was an insignificantly linear trend between TNM staging and age-onset of CRC diagnosis. Patients aged < 50 had 58.7% diseases in the advanced stages (Stage III: 36.5% and IV: 22.2% respectively), while this decreased to 40.2% (Stage III: 26.2% and IV; 14.0% respectively) in patients >80. The distributions of mutation frequency were similar in majority of the genes studied among different age groups. Additionally, patients aged <50 had significantly higher frequency of MSI-high, PTEN, and HRAS mutations than those of other groups. Age-onset at diagnosis significantly affected overall survival (HR = 1.46; 95% CI: 1.35–1.58), but not cancer-specific survival (HR = 1.08; 95% CI: 0.99–1.18) in multivariate analysis. In conclusion, molecular and clinicopathological differences were not as significant among different age groups of CRC patients as previously suspected.

Original languageEnglish
Article number1441
JournalInternational Journal Of Molecular Sciences
Issue number7
StatePublished - 5 Jul 2017


  • APC
  • Colorectal cancer
  • MSI
  • Mutation
  • PI3K
  • p53


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