Introduction: Following cardiovascular diseases cancer is the second largest cause of death in
the developed countries. Colorectal cancer ranked second among all cancer mortality.
Environmental and genetic factors respectively play an important role in the development
of the disease.
Objective: Our objective was to search for genetic factors which may play a role in the development
of the so called sporadic colorectal cancers in groups that are at risk for colorectal
cancer (e.g. in patients with colorectal polyps)
Patients: Ingested compounds from the environment are metabolized. The majority of the carcinogenic
substances are ingested in a pro-carcinogenic form. These are also going through a
metabolic process following which they become active carcinogens. The carcinogenic
metabolic processes can be divided into two phases. enzymes of the I. phase transform
the pro-carcinogens into electrophile, reactive metabolites, and then the enzymes
of the II. phase contribute to their detoxification and excretion via conjugation
reactions. According to this scheme, enzymes of the II. phase are responsible for
the activation, whereas enzymes of the II. phase are responsible for the inactivation
iof the carcinogenic substances.
We investigated the mutations and polymorphism of the CYP1A1 gene coding for a I.
phase enzyme, and that of the GSTM1, GSTT1, NAT genes coding for II. phase enzymes.
in addition we have investigated the mutations of the p53 gene, which were reported
by several authors to be also responsible for the development of colorectal cancers.
In the current lecture we present the molecular epidemiological results and clinical
chemical tumour markers of 38 patients with colorectal polyps and 30 healthy controls,
which were investigated at the Endoscope Polyclinic and II. Dept. of Medicine of thge
Nyírő Gyula Hospital.
