**10. Conclusions**

Various epidemiological studies have found that between blood lipids and various neoplastic diseases there are some correlations.

Some authors found that in patients with newly diagnosed NHL the blood levels of CH, phospholipids and HDL-cholesterol had lower values than those of controls and the values of CH increased progressively after chemotherapy if the disease reached complete remission or was stationary, unlike those with disease progression, that their blood lipid levels were even lower.

Nearly all the children with ALL when diagnosed and during chemotherapy revealed a predictable model of serum dyslipidemia that consisted of very low levels of HDLcholesterol, and elevated TG, and LDL-cholesterol, that regained normal values during the remission period.

In children with ALL, treated with asparaginase, hypertriglyceridemia was frequently observed and it can be cause of acute pancreatitis and thrombosis.

Imatinib mesylate, used for the treatment of patients with chronic myeloid leukemia, led to a diminishing of serum CH and TG values and CH depletion can inhibit cell proliferation.

The young survivors of ALL, disease which they had in their childhood, especially those who received cranial radiotherapy, are likely to develop hyperlipidemia, insulin resistance, obesity, arterial hypertension and even MS soon after the treatment.

Cranial irradiation favors more the appearance of MS by GH deficiency, lower level of insulin-like growth factor 1, fasting hyperinsulinemia, abdominal obesity and hyperlipidemia, especially in women.

It is believed that CH is important for cell proliferation, because low serum CH values may be the result of high cellular CH need of cancerous cells. Low serum CH values correlate with elevated levels of CH in lymphocytes. Malignant, proliferative cells have an intense metabolism of CH, while decreased intake of CH is responsible for decreasing cell proliferation.

An increase of lipoprotein lipase mRNA levels is present in CLL patients with shorter survival.

CD5 antigen is responsible for CH synthesis and even for adipogenesis. It is known that malignant cells from CLL are undergoing a process of continuous stimulation due to CD5 activation and cell survival.

The loss of CH is responsible for the decrease in the number of sites that can fix some monoclonal antibodies, including CD20. Statins interfere with the detection of CD20 antigen as well as the antilymphomatous function of the rituximab, but this effect was not showed in some clinical studies.

Statins reduce cellular proliferation and stimulate apoptosis of cancerous cells. By their pleiotropic effects, statins can be useful in the treatment of different diseases, like NHL, CLL, multiple myeloma and AML, as adjuvant therapy.

The association of simvastatin with fludarabine or cladribine synergistically induces DNA damages, and these lead to apoptosis.

Statins are active also in acute promyelocytic leukemia cells, where they augment the antileukemic response that depends on all-trans retinoic acid.

The ATP-ase activity of P-gp, frequently involved in the emergence of multidrug resistance during chemotherapy, is controlled linearly by CH of the membrane structure. The changes of the membrane CH quantity may be responsible for P-gp inhibition.

This drug efflux pump can be inhibited by statins and verapamil. By their pleiotropic effects, statins are useful not only for dyslipidemia treatment, but also in antineoplastic therapy.
