Low-Dose Naltrexone
Sahar Swidan, Matthew Bennett in Advanced Therapeutics in Pain Medicine, 2020
The current body of literature on LDN and cancer explores the relationship between OGF and OGFr and their effect on cellular proliferation in ovarian, pancreatic, colorectal, and squamous cell carcinomas. Short-term LDN was observed to influence the OGF–OGFr axis, which is responsible for the regulation of cell proliferation.38 Many other studies have investigated the use of LDN alone or in combination with standard therapies in ovarian cancer and renal carcinomas with promising results. Donahue, McLaughlin, and Zagon39 observed that the combination of LDN and cisplatin in ovarian tumors enhanced the inhibition of tumorigenesis, depressed DNA synthesis, and reduced angiogenesis. Additionally, LDN seemed to reduce adverse events with cisplatin therapy. Another study confirmed that LDN upregulates OGF and OGFr, inhibiting tumorigenesis and cancer proliferation.40 An alternative theory is that LDN prevents the prolonged cellular state of arrest in response to DNA damage, which places the cells in a state of cytostasis. This state of cytostasis reduces the sensitivity of the cell to treatment, preventing the cell from entering the apoptosis pathway. The intermittent binding of LDN does not block cells from entering this apoptosis pathway.41Evidence seems to support LDN as an adjunct to current anticancer regimens, both by enhancing the drugs’ anti-tumorigenesis effects and by decreasing the severity of side effects related to chemotherapy regimens.
Macrophages As Effectors Of Cell-Mediated Immunity
Hans H. Gadebusch in Phagocytes and Cellular Immunity, 2020
Supernatants from activated macrophages can reproduce, at least in part, the nonspecific cytostatic effect of the cells.409,412 Unfortunately, macrophages readily excrete breakdown products — including thymidine — from phagocytosed cells and cell debris, and free thymidine is notoriously able to interfere with the incorporation of 3H-thymidine or 125I-iododeoxyuridine into DNA.413,417 This artifact can be eliminated by dialysis of active supernatants. It now seems possible, however, that arginase secreted by cultured macrophages can produce cytostasis by depletion of arginine from the medium.418 This may be an artifact in vitro or it may be a mechanism for local cytostasis in vivo. Quite obviously, the role of soluble factors in cytostasis and cytotoxicity requires further investigation.
Gallium and Other Main Group Metal Compounds as Antitumor Agents
Astrid Sigel, Helmut Sigel in Metal Ions in Biological Systems, 2004
In contrast, gallium nitrate proved to be a very effective agent for the treatment of cancer-related hypercalcemia due to its inhibitory effects onbone resorption by osteoclasts even at low doses and has gained approval for this indication. As the pathophysiological processes causing this hypercalcemia are also critical for the formation and progression of bone metastases from distant tumors and because gallium nitrate reduces biochemical parameters associated with accelerated bone turnover in patients with bone metastases from various solid tumors [23], the potential benefits for patients with bone involvement from breast cancer and multiple myeloma have been subject to further clinical investigations [24]. Life-prolonging effects of low-dose gallium nitrate have indeed been suggested by a retrospective analysis of in patients with advanced-stage multiple myeloma [25]. These effects are probably a result of its antiosteolytic and immunomodulatory properties rather than a direct cytostatic activity. However, the biochemical processes involved in the antiosteolytic and immunosuppressive activity of gallium nitrate are beyond the scope of this review. Knowledge about these mechanisms as well as investigations into the broader pharmacological potential of gallium nitrate have been summarized elsewhere [26,27].
Cytotoxicity, mutagenicity, and antimutagenicity of the gentisic acid on HTC cells
Published in Drug and Chemical Toxicology, 2018
Flavia Maria Lima Cavalcante, Igor Vivian Almeida, Elisângela Düsman, Mário Sérgio Mantovani, Veronica Elisa Pimenta Vicentini
The evaluation of CBPI in the mutagenicity test indicated no cytotoxic effects of gentisic acid on the HTC cells for this parameter and the percentages of cytostasis revealed an increment in the proliferating cells for the 0.8 and 8 μg/mL treatments when compared to the control. Similarly, Giri et al. (1996) observed an increment in the mitotic index in the bone marrow cells of mice that were treated with salicylic acid (50 mg/kg intraperitoneally or 350 mg/kg orally). For the antimutagenicity test, the cytostasis that was observed for the SIM treatment (48 h) decreased when compared to the 24 h-treatment, showing that after one more cycle, the cells possibly recovered from the induced damage. The cytostasis that was observed in the PRE and POST treatments showed that there was no stimulation of the cell proliferations.
Using blood calprotectin as a measure of blood neutrophils
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2021
Arne Åsberg, Lena Løfblad, Amela Felic, Marthe Wedø Aune, Gunhild Garmo Hov, Unn Merete Fagerli
Patients treated at St. Olavs hospital were asked to donate blood in two heparin vacuum tubes if they were treated with cytostatic drugs. The extra blood samples were taken simultaneously with blood samples for routine hematology testing, after written, informed consent was given. Permission was granted by the Regional Committees for Medical and Health Research Ethics (2019/580/REK sør-øst). Blood sampling was complete in 77 patients, 43 women aged 30–79 (median 59) years and 34 men aged 32–84 (median 66) years. They had various clinical diagnoses, 72 had some form of cancer, of which breast cancer was the most frequently diagnosed condition (16 (37%) of women). Consequently, most of the patients (83%) used a variety of cytostatic drugs. Routine blood samples for b-neutrophils and other hematology analyses were taken at relevant times for monitoring the cytotoxic effects and/or disease activity. We also used data from 120 healthy blood donors, part of which are previously published [5]. They were 55 women aged 20–69 (median 34) years, and 65 men aged 22–73 (median 40) years.
Interaction of tumor-associated macrophages and cancer chemotherapy
Published in OncoImmunology, 2019
Irina Larionova, Nadezhda Cherdyntseva, Tengfei Liu, Marina Patysheva, Militsa Rakina, Julia Kzhyshkowska
Enhancing the efficiency of antitumor therapy is the most relevant challenge in clinical oncology. The main goal of the established cytostatic therapeutic schemas is to achieve the maximal cytoreduction of the primary tumor and metastatic foci by inducing apoptosis or necrosis or blocking uncontrolled cancer cell proliferation.1 The outcome of cytostatic treatment depends on the biological (including genetic) characteristics of tumor cells and their sensitivity or resistance to therapeutic agents.2 On average, only 40–60% of the cancer patients benefit from antitumor chemotherapy (CT).3,4 Drug resistance in surviving cancer cells, in fact, leads to an inability to achieve complete pathological regression.5 However, even when complete pathological regression is achieved, tumors can relapse in 10–40% of the cases.3,6
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