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The pulmonary embolism after switching from letrozole to tamoxifen in a patient with breast cancer. A case report and literature review

100%
Tomaszewska A., Żach-Muzolf M., Grabysa R.
OncoReview
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2020
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vol. 10
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issue 1
31-36
EN
Women with breast cancer are affected by deep venous thrombosis and/or pulmonary embolism 3 times more often than the group of healthy women in the same age. Thrombosis can be the first manifestation of a malignant disease, but it can also result from hormonal therapy with aromatase inhibitors or tamoxifen which is used in cancer treatment. The necessary clinical problem to solve in this population is the issue of prophylactic antithrombotic treatment. In this paper we present a case of pulmonary embolism in the course of the breast cancer, which was associated with tamoxifen hormone therapy and inadequate thromboprophylaxis.
2
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Can transforming growth factor-β1 and retinoids modify the activity of estradiol and antiestrogens in MCF-7 breast cancer cells?

75%
Czeczuga-Semeniuk E., Anchim T., Dzięcioł J., Dąbrowska M., Wołczyński S.
Acta Biochimica Polonica
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2004
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vol. 51
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issue 3
733-745
EN
Retinoic acid and transforming growth factor-β (TGF-β) affect differentiation, proliferation and carcinogenesis of epithelial cells. The effect of both compounds on the proliferation of cells of the hormone sensitive human breast cancer cell line (ER+) MCF-7 was assessed in the presence of estradiol and tamoxifen. The assay was based on [3H]thymidine incorporation and the proliferative activity of PCNA- and Ki 67-positive cells. The apoptotic index and expression of the Bcl-2 and p53 antigens in MCF-7 cells were also determined. Exogenous TGF-β1 added to the cell culture showed antiproliferative activity within the concentration range of 0.003-30 ng/ml. Irrespective of TGF-β1 concentrations, a marked reduction in the stimulatory action of estradiol (10-9 and 10-8 M) was observed whereas in combination with tamoxifen (10-7 and 10-6 M) only 30 ng/ml TGF-β1 caused a statistically significant reduction to aproximately 30% of the proliferative cells. In further experiments we examined the effect of exposure of breast cancer cells to retinoids in combination with TGF-β1. The incorporation of [3H]thymidine into MCF-7 cells was inhibited to 52 ± 19% (control =100%) by 3 ng/ml TGF-β1, and this dose was used throughout. It was found that addition of TGF-β1 and isotretinoin to the culture did not decrease proliferation, while TGF-β1 and tretinoin at low concentrations (3 × 10-8 and 3 × 10-7 M) reduced the percentage of proliferating cells by aproximately 30% (67±8% and 67±5%, P <0.05 compared to values in the tretinoin group). Both retinoids also led to a statistically significant decrease in the stimulatory effect of 10-9 M estradiol, attenuated by TGF-β1. In addition, the retinoids in combination with TGF-β1 and tamoxifen (10-6 M) caused a further reduction in the percentage of proliferating cells. Immunocytochemical analysis showed that all the examined compounds gave a statistically significant reduction in the percentage of cells with a positive reaction to PCNA and Ki 67 antigen. TGF-β1, isotretinoin and tretinoin added to the culture resulted in the lowest percentage of PCNA positive cells. However, the lowest fraction of Ki 67 positive cells was observed after addition of isotretinoin. The obtained results also confirm the fact that the well-known regulatory proteins Bcl-2 and p53 play an important role in the regulation of apoptosis in the MCF-7 cell line, with lowered Bcl-2 expression accompanying easier apoptotic induction. The majority of the examined compounds act via the p53 pathway although some bypass this important proapoptotic factor.
3
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Bipolar affective disorder: A review of novel forms of therapy

75%
Dziwota E., Drapala B., Gaj M., Skoczen N., Olajossy M.
Current Issues in Pharmacy and Medical Sciences
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2015
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vol. 28
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issue 2
105-110
EN
Normothymic, antidepressant and antipsychotic pharmaceutics are, in accordance with international guidelines, employed both in the therapy and the prevention of bipolar disorder (BD). Long-term studies on the mechanisms of action of such medications, as well as on the pathogenetic background of BD, have led to the discovery of effective, albeit unconventional pharmacotherapeutic approaches. These methods have the potential to successfully treat mania and depression, as well as to counter affective episode relapse. Allopurinol - commonly used to treat gout, secondary hyperuricemia and Lesch-Nyhan syndrome, acts by inhibiting the synthesis of uric acid, levels of which are often increased in manic patients. Due to this, an evaluation of the potential effect of allopurinol on the reduction of mania symptoms seems to be reasonable. Additionally, the numerable research papers coming out of research regarding the role of purine neurotransmitters in mood alterations, indicate that adenosine agonists act analogously to dopamine antagonists. N-acetylcysteine (NAC), a supporting agent in the pharmacotherapy of depressive episodes in bipolar disorder, substantially accelerates mood stabilization in patients. In turn, memantine, known for its procognitive effect, not only has antimanic and normothymic properties, but also boosts the neuroprotective action of traditional lithium therapy. In view of the latest opinions, the subtle pro-inflammatory process is typical for the pathophysiology of bipolar disease. Acetylsalicylic acid (ASA) (a popular analgesic, antipyretic and antiphlogistic agent) may be useful in BD therapy. This is because that, via its effect upon cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), ASA modulates leukocyte recruitment in neuro-inflammation. Apart from the above-mentioned medications, this article introduces the results of recent investigations of ketamine, modafinil and tamoxifen, including their receptor mechanisms, as well as certain genetic aspects or elements of their pharmacodynamics, for use in BD therapy. We put forward that, possibly, more insightful cognition of these drugs will allow significant enrichment in the range of pharmacotherapy for BD in the near future.
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