Anticancer research
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Anticancer research · Nov 1996
Deoxyadenosine-resistant mouse leukemia L1210 cell lines with alterations in early response genes and p53.
L1210 cell lines selected for resistance to deoxyadenosine exhibit altered steady-state levels of the mRNA for the early response genes and p53. In the deoxyadenosine-resistant cell lines (Y8 and ED2), the levels of the mRNAs for p53 and c-jun were markedly decreased while the steady-state levels for mRNAs for c-myc, c-fos and jun B were elevated in the Y-8 and ED2 cell lines. The levels of the mRNAs for PCNA and c-myb were the same in the wild type and mutant cell lines. ⋯ The Y8 and ED2 cell lines that lack steady-state levels of p53 show decreased sensitivity to cisplatin and increased frequency of gene amplification as measured by PALA resistance in a manner similar to other cell lines lacking p53. On the other hand, the ED2 and Y8 cell lines do not show a G1-block in response to PALA treatment. The cell lines appear to offer an experimental system in which to study the interactions between/among these early response genes and the p53-dependent and independent pathways.
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Anticancer research · Nov 1996
Enhancement of radiation response of prostatic carcinoma by lonidamine.
Potential application of lonidamine (LND) to enhance radiation toxicity in prostate cancer was investigated using human prostate cancer cell lines and a rat tumor model (Dunning MAT LyLu). LND alone was cytotoxic with 50% inhibition concentration (IC50) between 0.5 and 0.8 mM. Preincubation with LND increased clonogenic toxicity of radiation. ⋯ Fractionated irradiation caused a 40% decrease in tumor growth. LND injection (50 mg/kg) before fractionation did not cause any further decrease in tumor growth. Radiation dose fractionation and the combination treatment significantly reduced tumor metastasis in lungs.
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Anticancer research · Sep 1996
Effect of neoadjuvant chemotherapy on Ki67 labelling index, c-erbB-2 expression and steroid hormone receptor status in human breast tumours.
The administration of neoadjuvant chemotherapy to breast cancer (BC) patients with operable disease allowed studies aimed of exploring the interaction between cytotoxic treatment and tumour biology in vivo. 99 patients with T2-4, NO-1, M0 primary BC received a median of 3 cycles of either CMF regimen (cyclophosphamide, methotrexate, 5-fluorouracil) or single agent epirubicin. Endocrine therapy was also concomitantly administered in the first 45 patients with estrogen receptor positive (ER+) BC. 92 ended the treatment plan. Ki67 labelling index, estrogen receptor (ER), progesterone receptor (PgR), and c-erbB-2 oncoprotein expression were evaluated immunohistochemically in tumour biopsies obtained before and after chemotherapy. ⋯ The median Ki67 labelling index, which was 13% in the first biopsy, decreased to 4.5% (p < 0.001) upon mastectomy. No significant differences were observed in steroid hormone receptor and c-erbB-2 expression before and after neoadjuvant treatment. In conclusion, neoadjuvant chemotherapy, whether associated or not to endocrine therapy, leads to a significant decrease in BC proliferation without any appreciable impact on c-erbB-2 and steroid hormone receptor expression.
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Anticancer research · Jul 1996
Determination of serum tumor markers TPS and CA 15-3 during monitoring of treatment in metastatic breast cancer patients.
Serum levels of tissue polypeptide specific antigen (TPS), a cytokeratin 18 marker, and CA 15-3 were determined in 42 patients with metastatic breast cancer during routine treatment follow-up. At the time of proved metastatic disease, 86% of the values for TPS were above the upper reference value as compared to 93% for CA 15-3. The combined use of TPS and CA 15-3 increased the overall sensitivity. ⋯ An increase in the tumor marker level of 25% or more was seen in 60% (TPS) and 52% (CA 15-3), respectively of the studied patients. TPS appeared to indicate changes faster than CA 15-3. The overall results of this study suggest the combined use of TPS and CA 15-3 in the monitoring of breast cancer patients is preferable.
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Anticancer research · Jul 1996
Serum concentrations of type I collagen carboxyterminal telopeptide (ICTP) and type I procollagen carboxy-and aminoterminal propeptides (PICP, PINP) as markers of metastatic bone disease in breast cancer.
The most abundant protein in bone is type I collagen. During type I collagen formation two extension peptides from both ends of the procollagen molecule, carboxy- and aminoterminal propeptides (PICP and PINP), are liberated in equimolar concentrations into the circulation. Type I collagen carboxyterminal telopeptide (ICTP) is formed during bone collagen breakdown and is liberated into the circulation. ⋯ The clinical specifities were 93%, 100%, 98% and 91% respectively. During follow-up the changes in the marker values were parallel to the behaviour of the disease. We conclude that these markers alone are not sensitive enough for diagnosis, but they seem to be of use in detecting bone metastases and monitoring the activity of bone disease.