Refine Search

New Search

Results: 7

(searched for: doi:10.3816/ccc.2011.n.011)
Save to Scifeed
Page of 1
Articles per Page
by
Show export options
  Select all
Published: 18 July 2020
Cancers, Volume 12; doi:10.3390/cancers12071955

Abstract:
Globally, the death rate of pancreatic ductal adenocarcinoma (PDAC) has doubled over 30 years and is likely to further increase, making PDAC a leading cause of cancer-related death in the coming years. PDAC is typically diagnosed at an advanced stage, and modified FOLFIRINOX or nab-paclitaxel and gemcitabine are the mainstay of systemic therapy. For elderly patients with good performance status, low-dose treatment can preserve quality of life without compromising cancer control or survival. Maintenance therapy should be considered in PDAC patients achieving disease control with systemic therapy. In particular, olaparib has demonstrated a progression-free survival benefit of 3.6 months in a subgroup of PDAC patients with germline BRCA1/2 mutations (ca. 10% of all PDAC). Pancreatic enzyme replacement therapy is often omitted in the treatment of patients with PDAC, with possibly deleterious consequences. Small intestinal bacterial overgrowth is highly prevalent in patients with PDAC and should be considered in the diagnostic algorithm of PDAC patients with bloating and diarrhea. Rivaroxaban has been associated with a reduced risk of thrombosis without an increase in major bleeding events, and its use should be considered in every patient with advanced PDAC undergoing systemic therapy.
Janet E. Murphy, Kimberly Shampain, Laura E. Riley, Jeffrey W. Clark, Kristen M. Basnet
New England Journal of Medicine, Volume 379, pp 1562-1570; doi:10.1056/nejmcpc1712230

The publisher has not yet granted permission to display this abstract.
Bee Ling Tan,
Anticancer plants: Properties and Application pp 91-127; doi:10.1007/978-981-10-8548-2_5

The publisher has not yet granted permission to display this abstract.
, A. Dili, A. Druez, B. Krug, C. Decoster, L. D’Hondt
Critical Reviews in Oncology/Hematology, Volume 115, pp 59-66; doi:10.1016/j.critrevonc.2017.03.029

Abstract:
The survival of colorectal cancer patients is frequently determined by the extent of metastatic invasion to the liver; in cases of major involvement, therapeutic strategies are limited because the liver is necessary for drug metabolism. We have reviewed articles about the pharmacokinetic profiles of each drug used in colorectal cancer patients with hepatic dysfunction to determine which of these treatments are most feasible. Some drugs appear to be feasible options for patients with hepatic insufficiency. Agents such as 5-fluorouracil and oxaliplatin, as well as monoclonal antibodies such as bevacizumab, cetuximab, and panitumumab, can potentially be used in these cases. On the other hand, irinotecan and regorafenib cannot be recommended because of the risk of increased toxicity. Treatment of patients with colorectal cancer and liver dysfunction represents a major challenge because the prognosis is usually very poor and alteration of liver function is normally an exclusion criterion in clinical trials. In this review, we present evidence regarding the use of each drug in patients with colorectal cancer and hepatic impairment.
Jun Gong, May Cho,
Journal of Gastrointestinal Oncology, Volume 8, pp 314-323; doi:10.21037/jgo.2016.09.17

Abstract:
Sorafenib and cisplatin plus gemcitabine currently represent first-line treatment standards in advanced hepatocellular carcinoma and biliary cancer, respectively. Conventional cytotoxic agents (monotherapy or combination therapy) have demonstrated activity in the second-line setting or in those in which first-line agents are contraindicated. A strategy for safe yet effective administration of such systemic therapies in patients with advanced hepatobiliary cancer and abnormal liver function needs to be strongly considered. Here, we highlight the safety and tolerability of systemic therapies routinely used for the treatment of advanced hepatobiliary cancer in patients with hepatic dysfunction. Based on data from available clinical studies, we review dosing strategies recommended for chemotherapy and targeted therapy in those with liver dysfunction. Dose modifications for many agents in this population remain empiric due to limited clinical evidence. Future dedicated phase I studies are needed to provide further dosing considerations for combination therapy in those with abnormal liver function in which data is lacking.
Xuejing Zou, Jiyun Liang, Jingyuan Sun, Xiaoyun Hu, Ling Lei, ,
Journal of Pharmacological Sciences, Volume 131, pp 233-240; doi:10.1016/j.jphs.2016.04.017

Abstract:
Drug resistance and hepatic dysfunction are the two major factors that limit the application of chemotherapy for hepatocellular carcinoma (HCC). It has been reported that allicin has the hepatic protective effect and antitumor activity. Hence allicin may be an ideal enhancer to chemotherapy regimen of HCC. In the present study, we demonstrated that allicin enhanced 5-fluorouracil (5-FU) inducing cytotoxicity in HCC cells. In vivo experiment, combined treatment group with allicin (5 mg/kg/d; every two days for 3 weeks) and 5-FU (20 mg/kg/d; 5 consecutive days) showed a dramatic inhibitory effect on the growth of HCC xenograft tumors in nude mice. The co-treatment group showed highly apoptotic level compared with 5-FU treated alone. Cells combined treatment with allicin and 5-FU increased intracellular reactive oxygen species (ROS) level, reduced mitochondrial membrane potential (ΔΨm), activated caspase-3 and PARP, and down-regulated Bcl-2 compared with DMSO, allicin and 5-FU treated alone. Moreover, the increase of activated caspase-3 and PARP was blocked by the ROS inhibitor antioxidant N-acetyl cysteine (NAC). In conclusion, this is the first study to demonstrate that allicin sensitized HCC cells to 5-FU induced apoptosis through ROS-mediated mitochondrial pathway. These results provided evidences for the combination used of allicin and 5-FU as a novel chemotherapy regimen in HCC.
Reactions Weekly, Volume 1552, pp 40-40; doi:10.1007/s40278-015-0836-y

Page of 1
Articles per Page
by
Show export options
  Select all
Back to Top Top