Bargellini, Annalisa

Borella, Paola

Piccinini, Lino

English

PICCININI, Lino

BORELLA, Paola

BARGELLINI, Annalisa

Archivio istituzionale della ricerca - Università di Modena e Reggio Emilia

letters to the editorHaematologica 1997; 82:123-128Selenium status in the body and proliferative activity ofmalignant cellsSir,Avanzini and co-workers recently reported the results oftheir study on serum selenium concentrations in patients withnewly diagnosed lymphoid malignancies.1 Interestingly, ascompared to controls, selenium (Se) levels were significantlylower in patients with non-Hodgkin’s lymphoma (in a repre-sentative sample) in IV stage and/or in those with high gradedisease. However, literature reports of serum Se levels inpatients with lymphoid malignancy or solid tumors are discor-dant.2-4 These discrepancies may be due to case series that arenot directly comparable among themselves or with healthycontrol cohorts.It must be borne in mind that the elevated variability ofserum Se may be due to factors other than cancer such as age,sex, body mass, dietary habits, life style (alcohol, smoking),intercurrent disease and medications.When considering the various biological roles of Se (prolifer-ation and expression of oncogenes by both normal and malig-nant cells, carcinogen metabolism, cellular immune response,prevention of oxidative stress, apoptosis) and when addressingthe topic of whether Se is a risk factor or a protection againstcancer,5 one must evaluate selenium levels both in serum andin biological material that integrates selenium intake andreflects its status over the medium and long term (4 monthsfor red blood cells, 12 months or longer nails and hair). Thesestudies are however methodologically complex, and at presentvarious types of investigations (prospective, environmental,epidemiological, ecological) have failed to provide conclusiveresults.Several factors may influence Se exchanges between labilepools, deposits and cancer tissue, and we wish to point out oneimportant factor which has so far received little attention butwhich might influence selenium profiles, namely the prolifera-tive activity of cancer cells. Of particular interest along this lineof thought is the finding by Avanzini and co-workers of aninverse relationship between serum selenium and b2-microglobulin, an important index of the turnover of neoplasticcells.In an ongoing study on Se levels in the serum and hair ofwomen with breast cancer (unpublished data), we observedthat patients recruited at an early clinical stage had lowerserum Se and higher Se hair content with respect to patients ata more advanced stage or to healthy controls:Stage 0-I (n=42): serum Se mean value 76.2±21.7 µg/L, hair Secontent geometric mean 416.5 µg/gStage II-IV (n=44): serum Se mean value 81.5±22.4 µg/L, hairSe content geometric mean 335.2 µg/gControls (n=86): serum Se mean value 88.6±26.4 µg/L, hair Secontent geometric mean 370.5 µg/gThough our data fell short of statistical significance, due inpart to the wide spread of values in the series, the findings aresuggestive in light of the kinetic properties of tumor cells.6Indeed the relationship between Se and cellular growthemerged from our in vitro studies that showed different Se accu-mulation and effect according to cell density in the lymphocytecultures used in our experiments.7 Breast cancer shows a Gom-pertz-type growth curve with an exponential increase in theearly proliferative phases. These events, whose underlyingmechanisms also require further investigation in terms of host-tumor interactions, might influence different aspects of Se dis-tribution in various body districts.In conclusion, further experimental and epidemiologicalstudies are warranted to better elucidate the relationshipsbetween Se status and carcinogenesis; however, determinationof Se levels in subjects with malignancies will only contributedata useful for the clinician when it is performed across severalbody districts (blood, depots, healthy and diseased tissue) andinterpreted in the light of the proliferative characteristics of thetumor and of the intricate tumor host relationships.LINO PICCININI* PAOLA BORELLA°ANNALISA BARGELLINI°*Dipartimento di Scienze Mediche, Oncologiche e Radiologiche; °Dipartimento diScienze Biomediche; Università degli Studi di Modena, ItalyReferences1. Avanzini P, Vinceti M, Ilariucci F, et al. Selenium status in the bodyand proliferative activity of malignant cells. Haematologica 1995;80:505-11.2. Stampfer MJ, Colditz GA, Willett WC. The epidemiology of seleni-um and cancer. Cancer Surv 1987; 6:623-33.3. Deffuant C, Celerier P, Boiteau HL, Litoux P, Dreno B. Serum seleni-um in melanoma and epidermotropic cutaneous T-cell lymphoma.Acta Derm Venereol 1994; 74:90-2.4. Piccinini L, Borella P, Bargellini A, Incerti Medici C, Zoboli A. Acase-control study on selenium, zinc and copper in plasma and hairof subjects affected by breast and lung cancer. Biol Trace Elem Res1996; 51:23-30.5. Clark LC, Alberts DS. Selenium and cancer: risk or protection? JNatl Cancer Inst 1995; 87:4735.6. Orfao A, Ruiz-Arguelles A, Lacombe F, Ault K, Basso G, Danova M.Flow cytometry: its applications in hematology. Haematologica1995; 80:69-81.7. Borella P, Bargellini A, Incerti Medici C. Chemical form of seleniumgreatly influences metal uptake and effects on cultured human lym-phocytes. Biol Trace Elem Res 1996; 51:43-54.Correspondence: Prof. Lino Piccinini, Divisione Oncologia Medica,Policlinico, via del Pozzo 71, 41100 Modena, ItalySelenium and lymphoid malignancies (Reply)Sir,Piccinini et al.’s hypothesis that the proliferative activity ofmalignant lymphoid cells and of cancer cells in general mightinfluence selenium status is interesting and is partially support-ed by prior data, including our own.1 However, due to the lim-ited evidence available on this topic, further data are needed toconfirm that enhanced selenium uptake by neoplastic tissuemay vary according to the mitotic activity of the cancer cells.Piccinini and colleagues also addressed a fundamental issuein epidemiologic and clinical research on the health effects ofselenium: the methodology for exposure assessment and, inparticular, the use of biomarkers as surrogate measures of sele-nium exposure (represented in most individuals by dietaryintake). Selenium content of serum, plasma, erythrocytes,whole blood, hair, toenails, and urine are among the biomark-ers most frequently used in epidemiologic and clinical studies.Serum, plasma and urine selenium are short-term markers ofexposure, whereas the remaining indicators tend to reflect long-term selenium intake. The limitations of these indicators as sur-rogate measures of intake have been reviewed.2 Selenium-dependent glutathione peroxidase activity has also been evalu-ated as a possible biomarker of exposure, but it does notappear to be a reliable indicator of selenium intake since thecorrelation between the two parameters is not linear2 and, whatis more, glutathione peroxidase activity may be induced by oxi-dizing agents3 (including selenium itself).4,5In our clinical studies1,6 we evaluated selenium exposurethrough determination of serum selenium content, a sensitiveshort-term selenium marker,2 because we were interested in apossible relationship between the clinical characteristics of lym-phoid malignancies and recent changes in selenium status.Obviously the characteristic that makes serum selenium contentof interest in clinical research, i.e. its ability to reflect short-termselenium intake, also represents a limitation in an epidemiolog-ic setting, particularly in retrospective studies where seleniumstatus is likely to be affected by the disease, at least in somebody tissues. This is why we did not consider our results to becontradictory to the prior hypothesis of a direct associationbetween selenium exposure and the risk of lymphoid malignan-cies,7 though they did not add any evidence to support thishypothesis.Biomarkers, however, may not adequately reflect seleniumintake due to factors such as gender, body mass, medical

Selenium status in the body of proliferative activity of malignant cells

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Selenium status in the body of proliferative activity of malignant cells

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