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Query: "author" (Maja Osmak) .

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1.
Cathepsin D and plasminogen activator inhibitor type 1 in normal, benign and alignant ovarian tissues : a preliminary report
Marina Šprem, Damir Babić, Marija Abramić, Duško Miličić, Ivan Vrhovec, Janez Škrk, Maja Osmak, 2000, original scientific article

Abstract: Background. The aim of the present study was to determine the concentration ofcathepsin D (Cath D) and plasminogen activator inhibitor type 1 (PAI-1) in normal ovarian tissues, benign and malignant ovarian tumor tissues, and to asses relationship between Cath D and PAI-1 content, and some clinical and pathohistological parameters. Materials and methods. Cath D contents and PAI-1concentrations were determined (using immunoradiometric ELSA-Cath D assayand commercial IMUDIND R ELISA immunoassay, respectively) in 35 samples: 10 normal ovarii, 10 benign, 10 primary malignant and 5 metastatic ovarian tumors. Results. The concentrations of Cath D were significantly higher in malignant (32.89+-14.26 pmol/mg protein ) and metastatic (31.42+-10.24 pmol/mgprotein), than in normal (13.68+-4.03 pmol/mg protein) and benign (17.89+-13.13 pmol/mg protein) ovarian tissues. There was no statistical differences in the concentrations of PAI-1 between normal, benign, malignant and metastatic tumor specimens. The concentrations of Cath D as well as PAI-1 did not correlate to the age of patients, menopausal status, parity, GOG risk group, clinical stage or pathohistological grading. Conclusion. Concentrationsof Cath D (but not PAI-1) were significantly increased in malignant and metastatic ovarian tumor tissues when compared to normal and benign ovarian tumor samples; they were independent from pathohistological andclinical parameters.
Published in DiRROS: 23.01.2024; Views: 157; Downloads: 56
.pdf Full text (442,49 KB)

2.
Molecular alterations induced in drug-resistant cells
Maja Osmak, 1998, original scientific article

Abstract: The major obstacle to the ultimate success in cancer therapy is the ability oftumor cells to develop resistance to anticancer drugs. Several molecular mechanisms have been suggested to be involved in drugresistance: a) decrease in the intracellular drug accumulation (increased activity of membrane transporters such as P-glycoprotein or multidrug-resistance-associated protein), b) changes in intracellular detoxification system (increased concentrations of glutathione or metallothioneins, or increased activity of related enzymed), c) alteration in nuclear enzymes (enhanced DNA repair and/orbetter tolerance of DNA damage, decreased acitivty of topoisomerases), d) altered expression of oncogenes (inducing increased level of protective molecules in cells or the inhibition of apoptosis). Drug resistance is a multifactorial phenomenon. The complexity of molecular alterations in drug-resistant cells is and will stay the main problem for the successful treatment of cancer.
Published in DiRROS: 19.01.2024; Views: 159; Downloads: 28
.pdf Full text (2,17 MB)
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