Abstract
In a previous study of α-L-fucosidase (ALF) activities in plasma samples from three ovarian cancer-prone kindreds, we observed a significant inverse correlation of cancer susceptibility and enzyme activity. Because a low level of plasma ALF activity is an inherited characteristic that has been termed the "fucosidase variant," the above demonstration has provoked great interest in the fucosidase variant relative to the genetic transmission of ovarian cancer susceptibility. We have now observed in these same plasma samples that the concentrations of lipid-associated sialic acid (LAS) are also inversely correlated with the ALF activities and, therefore, directly correlated with ovarian cancer susceptibility. In the fucosidase variant individual, the ALF is modified intracellularly, but the modified enzyme only exhibits decreased activity in the plasma. For this reason, ALF cannot be involved in tumorigenesis. Rather, the factor that modifies ALF is probably involved and is the inherited character. Therefore, we hypothesize that this modifier is responsible not only for the "fucosidase variant" but also for the elevated concentration of LAS and plays a role in hereditary ovarian cancer.
| Original language | English |
|---|---|
| Pages (from-to) | 247-251 |
| Number of pages | 5 |
| Journal | Cancer Genetics and Cytogenetics |
| Volume | 25 |
| Issue number | 2 |
| DOIs | |
| State | Published - 1987 |
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All Science Journal Classification (ASJC) codes
- Cancer Research
- Genetics
- Molecular Biology
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α-L-fucosidase variant and lipid-associated sialic acid in hereditary ovarian cancer. / Wells, Ibert C.; Lynch, Henry T.; Lynch, Jane F.
In: Cancer Genetics and Cytogenetics, Vol. 25, No. 2, 1987, p. 247-251.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - α-L-fucosidase variant and lipid-associated sialic acid in hereditary ovarian cancer
AU - Wells, Ibert C.
AU - Lynch, Henry T.
AU - Lynch, Jane F.
PY - 1987
Y1 - 1987
N2 - In a previous study of α-L-fucosidase (ALF) activities in plasma samples from three ovarian cancer-prone kindreds, we observed a significant inverse correlation of cancer susceptibility and enzyme activity. Because a low level of plasma ALF activity is an inherited characteristic that has been termed the "fucosidase variant," the above demonstration has provoked great interest in the fucosidase variant relative to the genetic transmission of ovarian cancer susceptibility. We have now observed in these same plasma samples that the concentrations of lipid-associated sialic acid (LAS) are also inversely correlated with the ALF activities and, therefore, directly correlated with ovarian cancer susceptibility. In the fucosidase variant individual, the ALF is modified intracellularly, but the modified enzyme only exhibits decreased activity in the plasma. For this reason, ALF cannot be involved in tumorigenesis. Rather, the factor that modifies ALF is probably involved and is the inherited character. Therefore, we hypothesize that this modifier is responsible not only for the "fucosidase variant" but also for the elevated concentration of LAS and plays a role in hereditary ovarian cancer.
AB - In a previous study of α-L-fucosidase (ALF) activities in plasma samples from three ovarian cancer-prone kindreds, we observed a significant inverse correlation of cancer susceptibility and enzyme activity. Because a low level of plasma ALF activity is an inherited characteristic that has been termed the "fucosidase variant," the above demonstration has provoked great interest in the fucosidase variant relative to the genetic transmission of ovarian cancer susceptibility. We have now observed in these same plasma samples that the concentrations of lipid-associated sialic acid (LAS) are also inversely correlated with the ALF activities and, therefore, directly correlated with ovarian cancer susceptibility. In the fucosidase variant individual, the ALF is modified intracellularly, but the modified enzyme only exhibits decreased activity in the plasma. For this reason, ALF cannot be involved in tumorigenesis. Rather, the factor that modifies ALF is probably involved and is the inherited character. Therefore, we hypothesize that this modifier is responsible not only for the "fucosidase variant" but also for the elevated concentration of LAS and plays a role in hereditary ovarian cancer.
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U2 - 10.1016/0165-4608(87)90184-1
DO - 10.1016/0165-4608(87)90184-1
M3 - Article
VL - 25
SP - 247
EP - 251
JO - Cancer Genetics and Cytogenetics
JF - Cancer Genetics and Cytogenetics
SN - 0165-4608
IS - 2
ER -