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Cancer
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Elyce Cardonick, Charlotte Maggen, Puja Patel
HDT is contraindicated during pregnancy due to significant risks of fetal toxicity. For relapsed HL in pregnancy, the gestational age, the status of the disease, and the first-line treatments previously given should all be taken into account. If the relapse occurs in early pregnancy, termination of the pregnancy might become unavoidable. During the second trimester, platinum and/or gemcitabine-based regimens may be considered. For recurrent disease presenting in the third trimester, administering a short course of ABVD awaiting delivery or late preterm delivery should be considered [65].
Chemotherapy in pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Gemcitabine is indicated in the treatment of cancers of the ovary, pancreas, bladder, lung, and in sarcomas. There are little data regarding the intrapartum use of gemcitabine in the literature. Studies in mice have demonstrated teratogenicity including decreased fetal weight, cleft palette, and increased mortality (73). Kim et al. reported on a woman with non-small cell lung cancer, treated with palliative docetaxel, gemcitabine, and cisplatin from weeks 9 to 22 of an unrecognized pregnancy. A healthy infant was delivered at 33 weeks with no recognizable anomalies (38). Hematologic toxicity is commonly dose limiting and the compound should be used with caution toward the end of the third trimester. In the absence of more case reports, or perhaps a series of patients, other compounds might be considered prior to choosing gemcitabine during pregnancy.
Stomach, Duodenum, Liver, and Central Hepatobiliary Tract
Published in Tiziana Rancati, Claudio Fiorino, Modelling Radiotherapy Side Effects, 2019
Giovanni Mauro Cattaneo, Livia Marrazzo
Huang et al. (2012) retrospectively analyzed data from 46 patients with LAPC treated with definitive concurrent full-dose gemcitabine (1000 mg/cm2 weekly) and radiotherapy (18 patients received daily erlotinib). The stomach and the duodenum were separately contoured and grade ≥ 3 gastrointestinal (GI) toxicities (CTAE v4.0) were considered. For the entire cohort, considering both acute (22%) and late (17%) toxicities, only the V25Gy of duodenum (percent duodenum volume receiving ≥ 25 Gy) and the concurrent use of erlotibin were independent risk factors on multivariate analysis (MVA) (p=0.006 and p = 0.02, respectively). The receiver operating characteristic (ROC) analysis and stepwise discriminant analysis (SDA) showed that duodenum V25Gy > 45% was the optimal threshold: The 1 year GI toxicity rate was 8% vs. 48% for V25Gy ≤ 45% and V25Gy > 45%, respectively. Excluding the group receiving erlotinib (that increases radiation sensitivity), V35Gy > 20% was the best threshold (1 year GI toxicity rate of 0% vs. 41% for V35Gy ≤ 20% and V35Gy > 20%, respectively). The high overall rate of grade ≥ 3 toxicity reported in this study is partially related to the use of full-dose gemcitabine.
In silico identification and biological evaluation of a selective MAP4K4 inhibitor against pancreatic cancer
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Chao-Di Chang, Min-Wu Chao, Hsueh-Yun Lee, Yi-Ting Liu, Huang-Ju Tu, Ssu-Ting Lien, Tony Eight Lin, Tzu-Ying Sung, Shih-Chung Yen, Sing-Han Huang, Kai-Cheng Hsu, Shiow-Lin Pan
In the preclinical animal experiments, most studies used intraperitoneal (IP) injection instead of intravenous (IV) injection of gemcitabine to improve the convenience of administration67. Injections, whether through IV in clinical patients or IP in preclinical animal studies, display a high rate of bioavailability. However, for convenience, safety, and patient compliance, many anti-cancer drugs are expected to be taken orally63. Many FDA-approved small-molecule kinase inhibitors are effective when taken orally63. Orally administrating F389-0746 in vivo and comparing it to gemcitabine, which is injected into the murine models, would give indications of its effectiveness as an oral therapeutic. According to our in vivo results, orally administered F389-0746 displays a similar tumour growth inhibitory effect to IP-injected gemcitabine (Figure 8). The above results suggest that F389-0746 has the potential to be further optimised as an oral drug.
Gemcitabine enhances pharmacokinetic exposure of the major components of Danggui Buxue Decoction in rat via the promotion of intestinal permeability and down-regulation of CYP3A for combination treatment of non-small cell lung cancer
Published in Pharmaceutical Biology, 2023
Xin Xu, Xi-yang Sun, Ming Chang, Zhao-liang Hu, Ting-ting Cheng, Tai-jun Hang, Min Song
This study compared the pharmacokinetics of the four major constituents in DBD, namely, calycosin-7-O-β-d-glucoside, ononin, ligustilide and ferulic acid, with and without gemcitabine administration. Our results demonstrated that gemcitabine significantly enhanced the pharmacokinetic exposure of these components. In terms of mechanism, our study revealed that gemcitabine reinforced intestinal permeability by down-regulating the expressions of ZO-1 and occludin and down-regulated hepatic microsomal CYP3A expression. Both effects led to enhanced exposure in vivo. These findings provide valuable information on the pharmacokinetic herb–drug interaction between DBD and gemcitabine. Overall, these results could be applied in clinical practice to support the use of DBD as an auxiliary treatment with gemcitabine.
Integrative Management of Pancreatic Cancer (PDAC): Emerging Complementary Agents and Modalities
Published in Nutrition and Cancer, 2022
Mustafa B. A. Djamgoz, Valerie Jentzsch
The most common first-line treatment for PDAC is gemcitabine chemotherapy (7, 8). Gemcitabine is an “antimetabolite” pro-drug which becomes active once phosphorylated into diphosphate or triphosphate inside cells at very specific phases of the mitotic cycle. Thus, it works most effectively on fast-dividing cells, hence cancer cells. The basic mechanism of cell death is DNA damage (9). Apart from its inherent limited effectiveness and the common undesirable side effects of the treatment, use of gemcitabine suffers from the eventual onset of resistance to the drug. In these respects, therefore, any adjustment to gemcitabine chemotherapy that will increase its sensitivity (and hence lower its dosage of use) and lengthen its period of effectiveness (e.g., overcoming resistance) would be welcome. Our hypothesis is that these are possible by combining the gemcitabine chemotherapy with evidence-based complementary agents. Indeed, use of complementary agents in cancer treatment generally is increasingly, being favored by patients as well as by oncologists (10–14).