Dose Individualization for High-dose anti-cancer Chemotherapy

2006 ◽  
pp. 239-253 ◽  
Author(s):  
Gary L. Rosner ◽  
Peter Müller ◽  
Feng Tang ◽  
Timothy Madden ◽  
Borje S. Andersson
Keyword(s):  
Cancer Chemotherapy ◽  
High Dose ◽  
Dose Individualization ◽  
Anti Cancer

scholarly journals Neurological complications of medical anti-cancer therapies

2011 ◽  
Vol 2 (2) ◽  
pp. 80
Author(s):  
Jerzy Hildebrand
Keyword(s):  
Cancer Patients ◽  
Cancer Chemotherapy ◽  
Epileptic Seizures ◽  
Neurological Complications ◽  
High Dose Chemotherapy ◽  
Intrathecal Administration ◽  
High Dose ◽  
Cancer Therapies ◽  
Spinal Root ◽  
Anti Cancer

This review describes the features of central and peripheral neurological disorders caused by anti-cancer chemotherapy and supportive medications, such as antiepileptic drugs, glucocorticosteroids and opioids, frequently used in cancer patients. Diffuse encephalopathy with or without epileptic seizures, cerebellar disorders and aseptic meningitis may occur after systemic administration of conventional drug doses, but their incidence is much higher when either high-dose chemotherapy, or intrathecal or intracarotid administration is used. Spinal cord and/or spinal root lesions have been reported after intrathecal administration of methotrexate or cytosinearabinoside. Anti-cancer chemotherapy is the leading cause of peripheral neuropathy in cancer patients. The main culprits are vinca alkaloids, platinum derivatives and taxanes. Anti-cancer chemotherapy has no significant toxic effect on muscle tissue, but heavy administration of glucocorticosteroids is a common cause of disabling, predominantly pelvic, muscle atrophy.

scholarly journals Neurological complications of medical anti-cancer therapies

2011 ◽  
pp. 80-85
Author(s):  
Jerzy Hildebrand
Keyword(s):  
Cancer Patients ◽  
Cancer Chemotherapy ◽  
Epileptic Seizures ◽  
Neurological Complications ◽  
High Dose Chemotherapy ◽  
Intrathecal Administration ◽  
High Dose ◽  
Cancer Therapies ◽  
Spinal Root ◽  
Anti Cancer

This review describes the features of central and peripheral neurological disorders caused by anti-cancer chemotherapy and supportive medications, such as antiepileptic drugs, glucocorticosteroids and opioids, frequently used in cancer patients. Diffuse encephalopathy with or without epileptic seizures, cerebellar disorders and aseptic meningitis may occur after systemic administration of conventional drug doses, but their incidence is much higher when either high-dose chemotherapy, or intrathecal or intracarotid administration is used. Spinal cord and/or spinal root lesions have been reported after intrathecal administration of methotrexate or cytosinearabinoside. Anti-cancer chemotherapy is the leading cause of peripheral neuropathy in cancer patients. The main culprits are vinca alkaloids, platinum derivatives and taxanes. Anti-cancer chemotherapy has no significant toxic effect on muscle tissue, but heavy administration of glucocorticosteroids is a common cause of disabling, predominantly pelvic, muscle atrophy.

Abstract 453: Angiogenesis Inhibition-Induced Hypertension and Nephrotoxicity: Not All Antihypertensives are the Same

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Stephanie Lankhorst ◽  
Mariëtte H Kappers ◽  
Joep H Van Esch ◽  
Frank M Smedts ◽  
Stefan Sleijfer ◽  
...  
Keyword(s):  
Ace Inhibitor ◽  
Ace Inhibition ◽  
Cell Swelling ◽  
Histological Evaluation ◽  
High Dose ◽  
Angiogenesis Inhibition ◽  
Vegf Inhibitor ◽  
Renal Histology ◽  
Anti Cancer ◽  
Induced Hypertension

Angiogenesis inhibition with the VEGF inhibitor sunitinib is an established anti-cancer therapy inducing hypertension and nephrotoxicity. Here we compared the effects of the endothelin antagonist (ET-R) macitentan (30 mg/kg/day, p.o; n=8), the calcium channel blocker (CCB) amlodipine (3 mg/kg/day, p.o; n=9), or the ACE-inhibitor captopril (3 or 12 mg/kg/day, s.c.; n=9) vs. no treatment (n=14) in sunitinib (26.7 mg/kg/day, p.o)-exposed hypertensive WKY rats. Treatment lasted 8 days; mean arterial pressure (MAP) was monitored telemetrically. At the end of the treatment period, 24-hour urine samples for protein and endothelin-1 (ET-1) measurements, and blood samples and kidneys for histological evaluation were collected. With sunitinib, MAP increased from 94.7±0.9 mmHg to 125.8±1.5 mmHg (Δ31.1±0.9 mmHg, p<0.001). Co-administration of macitentan (Δ12.3±1.5 mmHg, p<0.001) or amlodipine (Δ11.4±1.7 mmHg, p<0.001) attenuated the sunitinib-induced MAP rise, whereas low and high captopril doses did not (Δ28.1±2.0 and Δ27.2±1.1 mmHg). With sunitinib, serum creatinine increased from 8.0±2.7 to 29.9±4.6 μmol/l (p<0.01) and proteinuria from 7.5±1.3 to 33.3±4.8 mg/day, p<0.05. Although no agent could prevent the sunitinib-induced rise in creatinine, the induced proteinuria was attenuated by 62% (p<0.01) with macitentan and by 88% with low and 114% (p<0.001) with high dose of captopril, while proteinuria increased by 56% (p=NS) with amlodipine. With sunitinib, urinary ET-1 increased from 3.3±0.5 to 4.8±1.0 pg/day (p<0.05). Macitentan and captopril abolished this increase. Renal histology revealed extensive glomerular ischemia and endothelial cell swelling. Concomitant with the decrease in proteinuria, glomerular intra-epithelial protein deposition decreased with macitentan and captopril. In conclusion, ET-R antagonism and CCB effectively reduced the sunitinib-induced hypertension, whereas ACE-inhibition did not. Both ET-R antagonism and ACE inhibition diminished the sunitinib-induced proteinuria. Since ET-R antagonists are not yet available as anti-hypertensive agents, CCBs are preferred in angiogenesis inhibition-induced hypertension, while adding an ACE-inhibitor might be considered when proteinuria is also present.

Cyclodextrin polymers decorated with RGD peptide as delivery systems for targeted anti-cancer chemotherapy

2018 ◽  
Vol 37 (4) ◽  
pp. 771-778 ◽  
Author(s):  
Maurizio Viale ◽  
Rita Tosto ◽  
Valentina Giglio ◽  
Giuseppe Pappalardo ◽  
Valentina Oliveri ◽  
...  
Keyword(s):  
Cancer Chemotherapy ◽  
Delivery Systems ◽  
Rgd Peptide ◽  
Anti Cancer ◽  
Cyclodextrin Polymers

Doxorubicin, Cisplatin, High-dose Methotrexate, and Ifosfamide for Osteosarcoma

2007 ◽  
Vol 42 (9) ◽  
pp. 801-811 ◽  
Author(s):  
John E. Mbue ◽  
Dominic A. Solimando ◽  
J. Aubrey Waddell
Keyword(s):  
Cancer Chemotherapy ◽  
High Dose ◽  
High Dose Methotrexate ◽  
Malignant Diseases ◽  
Dose Methotrexate ◽  
Toxic Agents

The increasing complexity of cancer chemotherapy now requires that pharmacists be familiar with these highly toxic agents. This column will review various issues related to preparation, dispensing, and administration of cancer chemotherapy, and review various agents, both commercially available and investigational, used to treat malignant diseases.

Unresectable Non-Small Cell Lung Cancer Chemotherapy with High-Dose Cisplatin and Etoposide

Oncology ◽  
1985 ◽  
Vol 42 (4) ◽  
pp. 224-228 ◽  
Author(s):  
Giorgio V. Scagliotti ◽  
Donatella Lodico ◽  
Felice Gozzelino ◽  
Franco Bardessono ◽  
Carlo Albera ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Chemotherapy ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
High Dose ◽  
Small Cell Lung

Bone Marrow Necrosis

1995 ◽  
Vol 10 (4) ◽  
pp. 171-178 ◽  
Author(s):  
Marcel E. Conrad
Keyword(s):  
Bone Marrow ◽  
Cancer Chemotherapy ◽  
Case Reports ◽  
Blood Stasis ◽  
Pathological Finding ◽  
Vascular Occlusion ◽  
High Dose ◽  
Bone Marrow Necrosis ◽  
Clinical Illness ◽  
Lost To Follow Up

Bone marrow necrosis is regarded as an uncommon entity that is associated with a poor prognosis. However, organized studies using either bone marrow biopsy specimens or autopsy material showed that bone marrow necrosis can be demonstrated in approximately one third of specimens. It is found in a large number of both malignant and nonmalignant disorders, in addition to occurring following large exposures to radiation or high dose cancer chemotherapy. In the absence of radiation or cancer chemotherapy, it probably eventuates from either vascular occlusion or blood stasis in small blood vessels. When bone marrow necrosis is prolonged, it may be associated with the development of bone marrow fibrosis, and it may serve as a predisposing etiology for idiopathic myelofibrosis. Most patients discovered with bone marrow necrosis have few symptoms, and they are eventually lost to follow-up without evident progression or development of a clinical illness. In acute disorders and in those who undergo effective therapy, recovery appears to occur without complications. This frequently overlooked finding is the subject of many case reports in the medical literature, but it has only been rarely systematically investigated. The latter is probably warranted because of the potential role of bone marrow necrosis in the pathophysiology of a number of disorders and the paucity of information for treatment of this pathological finding.

scholarly journals Cholecalciferol Inhibits Cell Growth and Induces Apoptosis in the CaSki Cell Line

2020 ◽  
Vol 8 (1) ◽  
pp. 12 ◽  
Author(s):  
Sachin Bhoora ◽  
Yuvelia Pather ◽  
Sumari Marais ◽  
Rivak Punchoo
Keyword(s):  
Cell Cycle ◽  
Vitamin D ◽  
Cell Death ◽  
Cell Count ◽  
Cell Line ◽  
Cervical Cancer Cell Line ◽  
High Dose ◽  
Caski Cell ◽  
Anti Cancer ◽  
Caski Cell Line

Vitamin D has displayed anti-cancer actions in numerous in vitro studies. Here, we investigated the anti-cancer actions of cholecalciferol, a vitamin D precursor, on a metastatic cervical cancer cell line, namely, CaSki. Experimental cultures were incubated for 72 h and treated with cholecalciferol (10–1000 ng/mL). In the present study, cell count, viability, proliferation and cell cycle were analyzed by a crystal violet assay, trypan blue assay, Ki67 proliferation, and a cell cycle assay, respectively. Biomarkers of apoptosis, necrosis, and autophagic cell death were measured by the Caspase 3/7 and Annexin V/7-AAD Muse™ assays, a LC3-II assay, and a lactate dehydrogenase release assay, respectively. The ultrastructural features of cell death were assessed by transmission electron microscopy. A statistical analysis was performed using a one-way ANOVA and Bonferroni’s post-hoc analysis test, and p < 0.05 is considered statistically significant here. The results identify statistical decreases in cell count and viability at high-dose treatments (100 and 1000 ng/mL). In addition, significant increases in apoptotic biochemical markers and apoptotic ultrastructure are shown to be present at high-dose treatments. In conclusion, high-dose cholecalciferol treatments inhibit cell count and viability, which are both mediated by apoptotic induction in the CaSki cell line.

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