Hcy is a non essential sulfur containing amino acid derivedfrom methionine (an essential amino acid). In normal metabolism, the amino acid Hcy is very toxic; it is immediately converted intocysteine or remethylated into methionine. It is found in plasma asprotein bound (mostly bound to albumin) and free forms.Normally, very slight concentrations of it could be found in bloodand urine of healthy people. Its normal values reach about 5-14μmol /L in plasma. Its plasma concentrations depend on twometabolic steps. These involve the demethylation of Hcy tocysteine and remethylation back to methionine. The key enzymesin these two steps are cystathionine β synthase and methylenetetrahydrofolate reductase , respectively. Vitamin B6 acts as acofactor for the demethylation of Hcy, and Vitamin B12 and folateare cofactors involved in the remethylation pathway back tomethionine. There is also another pathway, which is betainedependent methylation of Hcy.Numerous studies have shown that moderately elevatedblood levels of plasma total Hcy increase the risk of cardiovasculardisorders. Patients with homocysteinuria, a rare genetic inbornerror of Hcy metabolism , have extremely high levels of total Hcyin plasma with high incidence of cardiovascular disease in earlyadolescence and even in childhood. The data available so far showsthat Hcy is an independent risk factor in atherosclerosis .The study was done on 30 subjects (10 controls &20 cases). All the subjects were females. Serum Hcy had beenmeasured in the control group and in cases group before and afterchemotherapy associated with other investigationsOur results demonstrated the following results :1. Plasma Hcy level was higher in cases group than in the controlgroup but it was not significant but the level of serum Hcy in casesgroup was higher enough to increase the risk of thrombosis.2-Plasma Hcy level was significantly dropped in cases afterchemotherapy compared to before chemotherapy but still higherenough to increase the risk of thrombosis.Conclusions :- Elevated plasma Hcy may be an independent risk factor forcardiovascular disease , its correlation with major components ofthe cardiovascular risk profile j.e. old age, smoking, hypertension,elevated cholesterol level and lack of exercise requires furtherstudy and this confounding factors has been encountered in ourstudy and they were non significant.-A detailed discussion of the prevention and treatment ofthromboembolism in cancer is beyond the scope of this review.However, primary prevention of venous thrombosis, possibly byoral anticoagulants, should be considered for ‘high-risk’ cancerpatients during and immediately after chemotherapy, when long termindwelling central venous catheters are placed, during longspells of immobilisation from any cause, and after surgicalinterventions. For example, in cancer patients going for generalsurgery without prophylaxis, the frequency of DVT is about 29%,compared with 19% in patients who do not have cancer-Another possibility for the prevention of venousthromboembolism in high-risk patients undergoing surgery oradjuvant chemotherapy may be the use of long-term, low-intensityanticoagulation . One trial of low-dose warfarin (1 mg daily for 6weeks, then adjusted to maintain an international normalised ratioof 1.3–1.9) resulted in a relative thromboembolic risk reduction of85%, with a low bleeding rate.-The initial treatment of acute venous thromboembolismin cancer patients does not differ from that used for other patients .Initial hospital treatment includes unfractionated heparin or low molecular-weight heparin, to be continued for at least 5 days.Warfarin is started at the same time and should overlap heparintherapy for at least 4–5 days. Heparin can be stopped once theinternational normalised ratio has been above 2 for 2 consecutivedays. Warfarin should be continued for at least 6 months in patientswith a first episode of idiopathic DVT, but patients with cancer andwith recurrent thromboembolism require long-term anticoagulationtherapy. The rates of recurrent thrombosis (suggesting some‘warfarin resistance’) in patients with malignant disease who havebeen treated with oral anticoagulants are greater than would beexpected. In recurrent pulmonary thromboembolism, despitewarfarin, other measures such as placement of a filter onthe inferior vena cava should be considered.-The treatment of hyperhomocysteinemia varies with theunderlying causes however , vitamin supplementation (with folicacid, pyrixodine , and vitamin B12) is generally effective inreducing Hcy concentrations- Further study is needed to document the effect ofdifferent types of chemotherapy giving to the cancer patients andtheir effect on serum Hcy levels.