Elevated apolipoprotein(A) levels in cancer patients

Wright, Lesley C.; Sullivan, David; Müller, M.; Dyne, Marlen; Tattersall, Martin H. N.; Mountford, Carolyn E.

doi:10.1002/ijc.2910430212

Cited by 59 publications

(21 citation statements)

References 12 publications

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“…Similar to the inverse correlation of Lp(a) and ascorbate in atherosclerosis, a high incidence of cancer is associated with low levels of ascorbate (35) and also high levels of Lp(a) (36). Similar observations were made in diabetes mellitus for ascorbate (37) and Lp(a) (38).…”

Section: Lp(a) and Ascorbate In Cancer And Diabetes Mellitussupporting

confidence: 67%

Hypothesis: lipoprotein(a) is a surrogate for ascorbate.

Rath

Pauling

1990

Proc. Natl. Acad. Sci. U.S.A.

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The concept that lipoprotein (a) [Lp(a)] is a surrogate for ascorbate is suggested by the fact that this lipoprotein is found generally in the blood of primates and the guinea pig, which have lost the ability to synthesize ascorbate, but only rarely in the blood of other animals. Properties of Lp(a) that are shared with ascorbate, in accordance with this hypothesis, are the acceleration of wopnd healing and other cell-repair mechanisms, the strengthening of the extracellular matrix (e.g., in blood vessels), and the prevention of lipid peroxidation. High plasma Lp(a) is associated with coronary heart disease and other forms ofatherosclerosis in humans, and the incidence of cardiovascular disease is decreased by elevated ascorbate. Similar observations have been made in cancer and diabetes. We have formulated the hypothesis that Lp(a) is a surrogate for ascorbate in humans and other species and have marshaled the evidence bearing on this hypothesis.Lipoproteins consist of particles, each of which is a globule of lipid molecules surrounded by an apoprotein shell. Lipoprotein(a) [Lp(a)] was discovered by Blumberg et al. (1) and by Berg (2). It shares with low density lipoprotein (LDL) its lipid and apoprotein composition-mainly apoprotein B-100 (apo B), consisting of a polypeptide chain of 4536 amino acid residues. The unique feature of Lp(a) is an additional glycoprotein, designated apoprotein(a) [apo(a)], which is linked to apo B by disulfide groups. The cDNA sequence of apo(a) (3) shows a striking homology to plasminogen, with multiple repeats of kringle 4, one kringle 5, and a protease domain. The isoforms of apo(a) vary in the range of 300 to 800 kDa and differ mainly in their genetically determined number of kringle 4 structures (3); apo(a) has no plasmin-like protease activity (4), but a serine protease activity has been demonstrated recently (5). Like plasminogen, Lp(a) has been shown to bind to lysine-Sepharose, immobilized fibrin and fibrinogen (6), and the plasminogen receptor on endothelial cells (7)(8)(9). This binding is inhibited by E-aminocaproic acid, certain other amines, and plasminogen.

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Section: Lp(a) and Ascorbate In Cancer And Diabetes Mellitussupporting

confidence: 67%

Hypothesis: lipoprotein(a) is a surrogate for ascorbate.

Rath

Pauling

1990

Proc. Natl. Acad. Sci. U.S.A.

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“…Genetically determined Lp(a) serum levels show broad interindividual differences but seem to be relatively stable intraindividually [I, 7, 18]. However, elevated plasma Lp(a) levels in patients with solid tumours might be an indication for a regulatory mechanism for Lp(a) expression under acquired conditions [20]. Cancer patients frequently have hypocholesterolaemia, which is a consequence rather than the cause of the disease as concluded from large epidemiological studies [8].…”

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confidence: 99%

Elevated lipoprotein(a) levels in patients with acute myeloblastic leukaemia decrease after successful chemotherapeutic treatment

et al. 1992

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Twenty-two patients with acute myeloblastic leukaemia (AML) were studied to investigate disease-associated changes in lipid metabolism. Lipoprotein (a) [Lp(a)] levels were found to be elevated at the time of diagnosis (median 23 mg/dl; 41% of patient group had levels greater than 25 mg/dl) and diminished after successful chemotherapeutic treatment in 9 of 10 cases, with a maximum decrease from 56 to 10 mg/dl. In contrast, reduced levels of total cholesterol, low density lipoprotein (LDL) and high density lipoprotein (HDL) (medians 137, 87 and 20 mg/dl, respectively) were observed at the time of diagnosis. Cholesterol and HDL levels increased in all 10 and LDL in 9 cases in which complete remission was achieved. These data suggest that the catabolism of LDL-cholesterol might be even more enhanced than assumed to date. Furthermore, it indicates that the Lp(a) level in acute myeloblastic leukaemia is influenced either directly or indirectly by the leukaemic blasts.

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“…Interestingly, another lipid lower agent, nicotinic acid in high doses, as well as LDL apheresis and hormone replacement therapy with estrogen, have been shown to lower Lp(a) levels [14]. Lp(a) levels may be increased in the end stage renal disease [15], acute phase response [16], diabetes mellitus [17], cancer [18] and hypothyroidism [19], and in contrary they may be decreased in liver failure [20], hyperthyroidism [21], renal transplantation in patients with the end stage renal disease [15], in patients with severe infections [22][23][24] and after administration of L-carnitine [25], levothyroxine [26] or soy protein [27].…”

Section: Modulation Of Lipoprotein (A) Levelsmentioning

confidence: 99%

Lipoprotein (a) and Stroke: An Overview~!2009-10-29~!2009-12-27~!2010-04-08~!

Christogiannis¹,

Milionis²,

Elisaf³

2012

TOCCHEMJ

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Stroke remains a major cause of mortality and long term severe disability worldwide. Lipoprotein (a) [Lp(a)] is a predictor of many forms of vascular disease, and may serve as a tool in identifying subjects at risk. Despite accumulating evidence from cross sectional and prospective studies, its role in the development of stroke is still in doubt. Methodological issues regarding measurement remain to be resolved. Whether reductions in Lp(a) levels will result in a reduction of vascular events, including stroke, remains to be established. Aggressive management of established cardiovascular risk factors is advocated in subjects exhibiting elevated serum Lp(a) concentrations.

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Elevated apolipoprotein(A) levels in cancer patients

Cited by 59 publications

References 12 publications

Hypothesis: lipoprotein(a) is a surrogate for ascorbate.

Hypothesis: lipoprotein(a) is a surrogate for ascorbate.

Elevated lipoprotein(a) levels in patients with acute myeloblastic leukaemia decrease after successful chemotherapeutic treatment

Lipoprotein (a) and Stroke: An Overview~!2009-10-29~!2009-12-27~!2010-04-08~!

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