The first recognition of a genetic association was with CCBE1, published by its namesake, Raoul Hennekam.[7] The molecular mechanism of the lymphedema phenotype in CCBE1-associated cases was identified as a diminished ability of the mutated CCBE1 to accelerate and focus the activation of the primary lymphangiogenic growth factor VEGF-C.[8] Mutations in the FAT4 gene had previously been only associated with van Maldergem syndrome, but the pathogenetic molecular mechanism and the function of FAT4 within lymphangiogenesis are still unknown.
^Erkan T, Kutlu T, Çullu F; et al. (1998). "Syndrome de hennekamHennekam syndrome" [Hennekam syndrome]. Arch Pediatr (in French). 5 (12): 1344–6. doi:10.1016/S0929-693X(99)80054-2. PMID9885742.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^Van Balkom ID, Alders M, Allanson J, et al. (November 2002). "Lymphedema-lymphangiectasia-mental retardation (Hennekam) syndrome: a review". Am. J. Med. Genet. 112 (4): 412–21. doi:10.1002/ajmg.10707. PMID12376947.
^Alders M, Hogan BM, Gjini E, et al. (December 2009). "Mutations in CCBE1 cause generalized lymph vessel dysplasia in humans". Nat. Genet. 41 (12): 1272–4. doi:10.1038/ng.484. PMID19935664. S2CID205356254.
^Alders M, Al-Gazali L, Cordeiro I, et al. (June 2014). "Hennekam syndrome can be caused by FAT4 mutations and be allelic to Van Maldergem syndrome". Hum. Genet. 133 (9): 1161–7. doi:10.1007/s00439-014-1456-y. PMID24913602. S2CID14414158.
^Hennekam, R. C. M.; Geerdink, R. A.; Hamel, B. C. J.; Hennekam, F. a. M.; Kraus, P.; Rammeloo, J. A.; Tillemans, A. a. W. (1989). "Autosomal recessive intestinal lymphangiectasia and lymphedema, with facial anomalies and mental retardation". American Journal of Medical Genetics. 34 (4): 593–600. doi:10.1002/ajmg.1320340429. PMID2624276.