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Abnormal vascular network complexity: a new phenotypic marker in hereditary non-polyposis colorectal cancer syndrome
  1. C De Felice1,
  2. G Latini2,
  3. G Bianciardi3,
  4. S Parrini4,
  5. G M Fadda4,
  6. M Marini5,
  7. R N Laurini6,
  8. R J Kopotic7
  1. 1Neonatal Intensive Care Unit, Azienda Ospedaliera Universitaria Senese, Siena, Italy
  2. 2Clinical Physiology Institute, National Research Council of Italy (IFC-CNR), Lecce Section, Italy
  3. 3Department of Human Pathology and Oncology, University of Siena, Siena, Italy
  4. 4Department of Odontostomatologic Sciences, University of Siena, Siena, Italy
  5. 5Gastroenterology and Digestive Endoscopy Unit, Azienda Ospedaliera Universitaria Senese, Siena, Italy
  6. 6Department of Obstetrics and Gynaecology, University Hospital San Joao, Porto, Portugal
  7. 7Imagyn Medical Technologies, Irvine, CA, USA
  1. Correspondence to:
    Dr C De Felice
    Neonatal Intensive Care Unit, Azienda Ospedaliera Universitaria Senese, Policlinico “Le Scotte”, Viale M Bracci 16, I-53100 Siena, Italy; defelice.claudiolibero.it

Abstract

Background: Hereditary non-polyposis colorectal cancer (HNPCC) (Lynch cancer family syndrome I (LCFS1) and II (LCFS2)) is one of the most common hereditary cancer disorders. HNPCC results from dominantly inherited germline mutations in mismatch repair (MMR) genes, leading to genomic instability and cancer. No predictive physical signs of HNPCC are available to date.

Aims: Increased complexity in tumour associated vascular growth has been reported. Here, we tested the hypothesis that an increased vascular network complexity is a phenotypic marker for LCFS2.

Methods: Fourteen subjects from an LCFS2 kindred (gene carriers, n = 5; non-carriers, n = 9) and 30 controls were examined. Fractal dimension (D) at two scales (D (1–46), and D (1–15), tortuosity (minimum path dimension, Dmin), and relative Lempel-Ziev complexity (L-Z) of the vascular networks from the lower gingival and vestibular oral mucosa were measured.

Results: LCFS2 networks exhibited a significantly increased overall complexity at both larger (D (1–46): 1.82 (0.04) v 1.68 (0.08); p<0.0001) and smaller (D (1–15): 1.51 (0.11) v 1.20 (0.09); p<0.0001) scales, increased destructured randomness (L-Z: 0.77 (0.09) v 0.56 (0.03); p<0.0001), and decreased vessel tortuosity (Dmin: 1.02 (0.03) v 1.07 (0.04); p = 0.0005) compared with control patterns. The vascular networks of LCFS2 gene carriers showed higher complexity at the smaller scale (D (1–15): 1.59 (0.12) v 1.47 (0.07); p = 0.034), and higher destructured randomness (L-Z: 0.85 (0.11) v 0.73 (0.05); p = 0.013) than those of non-carriers.

Conclusions: Increased oral vascular network complexity is a previously unrecognised phenotypic marker for LCFS2, and is related to gene mutation carrier status.

  • colorectal neoplasms
  • hereditary non-polyposis/diagnosis
  • blood vessels
  • population surveillance
  • colorectal cancer
  • HNPCC, hereditary non-polyposis colorectal cancer
  • LCFS1, Lynch cancer family syndrome I
  • LCFS2, Lynch cancer family syndrome II
  • MMR, mismatch repair
  • CRC, colorectal carcinoma
  • D, fractal dimension
  • Dmin, minimum path fractal dimension
  • L-Z, relative Lempel-Ziv complexity

https://doi.org/10.1136/gut.52.12.1764

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