Synchronous malignancies are rare occurrences for which there may be a genetic link between two cancers or which may be simply coincidental. Although glioblastoma multiforme and esophageal adenocarcinoma have few clinical similarities there are no known biochemical or genetic links between the two malignancies. This case discussion details the synchronous occurrences of these two lesions and highlights possible clinical, biochemical, and genetic commonalities.
Get full access to this article
View all access options for this article.
References
1.
ChenX, YangCS. Esophageal adenocarcinoma: A review and perspectives on the mechanism of carcinogenesis and chemoprevention. Carcinogenesis2001;22:1119–29.
2.
SmithJS, JenkinsRB. Genetic alterations in adult diffuse glioma: Occurrence, significance, and prognostic implications. Front Biosci2000;5:213–31.
3.
NaganeM, ShibuiS, NishikawaR, . Triple primary malignant neoplasms including a malignant brain tumor: Report of two cases and review of the literature. Surg Neurol1996;45:219–29.
4.
UranoY, ItoyamaS, FukushimaT, . Multiple primary cancers in autopsy cases of Tokyo University Hospital (1883–1982) and in Japan Autopsy Annuals (1974–1982). Jpn J Clin Oncol1985;15(Suppl):271–9.
5.
TherrienJP, DrouinR, BarilC, DrobetskyEA. Human cells compromised for p53 function exhibit defective global and transcription-couple nucleotide excision repair, whereas cells compromised for pRb function are defective only in global repair. Proc Natl Acad Sci USA1999;96:15038–43.
6.
MiyakiM, NishioJ, KonishiM, . Drastic genetic instability of tumors and normal tissue in Turcot syndrome. Oncogene1997;15:2877–81.
7.
ShapiroWR, ShapiroJR. Biology and treatment of malignant glioma. Oncology (Huntingt)1998;12:233–40.
8.
HoiSangU, EspirituOD, KelleyPY, . The role of the epidermal growth factor receptor in human gliomas. II. The control of glial process extension and the expression of glial fibrillary acidic protein. J Neurosurg1995;82:847–57.
9.
SmithJS, TachibanaI, PasseSM, . PTEN mutation, EGFR amplification, and outcome in patients with anaplastic astrocytoma and glioblastoma multiforme. J Natl Cancer Inst2001; 93:1246–56.
10.
LouisDN. A molecular genetic model of astrocytoma histopathology. Brain Pathol1997;7:755–64.
11.
YounesM, LebovitzRM, LechagoLB, LechagoJ. p53 protein accumulation in Barrett's metaplasia, dysplasia, and carcinoma: A follow-up study. Gastroenterology1993; 105: 1637–42.
12.
RamelS, ReidBJ, SanchezCA, . Evaluation of p53 protein expression in Barrett's esophagus by two-parameter flow cytometry. Gastroenterology1992;102:1220–8.
13.
Al-KasspoolesM, MooreJH, OrringerMB, BeerDG. Amplification and overexpression of the EGFR and erbB-2 genes in human esophageal adenocarcinomas. Int J Cancer1993;54:213–9.
14.
JankowskiJ, McMeneminR, HopwoodD, PenstonJ, WormsleyKG. Abnormal expression of growth regulatory factors in Barrett's oesophagus. Clin Sci1991;81:663–8.
15.
HirschbergH. Endothelial growth factor production in cultures of human glioma cells. Neuropathol Appl Neurobiol1984; 10:33–42.
16.
MillauerB, ShawverLK, PlateKH, . Glioblastoma growth inhibited in vivo by a dominant-negative flk-1 mutant. Nature1994;367:576–9.
17.
PlateKH, BreierG, MillauerB, . Up-regulation of vascular endothelial growth factor and its cognate receptor in a rat glioma model of tumor angiogenesis. Cancer Res1993;53:5822–7.
18.
CouldwellWT, FraserG, DeVellisG, . Malignant glioma-derived soluble factors regulate proliferation of normal adult human astrocytes. J Neuropathol Exp Neurol1992;51:506–13.
19.
PollackIF, RandallMS, KristofikMP, . Response of low-passage human malignant gliomas in vitro to stimulation and selective inhibition of growth-factor mediated pathways. J Neurosurg1991;75:284–93.
20.
WatanabeK, TachibanaO, SataK, . Overexpression of the EGF receptor and p53 mutations are mutually exclusive in the evolution of primary and secondary glioblastomas. Brain Pathol1996;6:217–24.