I should be starting chemo mid February on a combination of those two. I’m really nervous!
I don’t mind losing my hair, I’ve accepted that and already ordered cute head scarves and wigs
I’m more afraid that I’ll be so weak and tired that I won’t be able to live my life at all.
Does anyone have any experience or advice for this combo?
I had bep, ep, veip, radiation, surgery but cancer relapsed into liver anyway in multiple nodules largest being 5.5cm. Now i am receiving paclitaxel gemcitabine combo . Did anybody get this? I am starting to be sceptical that it will be cured at all and i might die from it.
If the steroids give you really bad side effects on weekly paclitaxel, ask your oncologist to reduce them and maybe even eliminate them. This published study ("Feasibility of Stopping Paclitaxel Premedication in Patients Not Experiencing A Pre-Infusion Hypersensitivity Reaction", 2012) had these results:
"After receiving the first two doses of paclitaxel-based chemotherapy without experiencing an infusion hypersensitivity reaction (any grade), 55 breast cancer patients had their premedications discontinued for all remaining paclitaxel doses."
Your doctor will have to weigh the risks and benefits in your case.
https://doi.org/10.1111/ejn.15397
https://pubmed.ncbi.nlm.nih.gov/34318540
Abstract
Chemotherapy-induced peripheral neuropathy (CIPN) is a common side effect during the course of cancer treatment, which is mainly manifested as a series of sensory abnormalities. At present, there are no recommended prevention or treatment strategies, and the underlying mechanisms are unclear. The ketogenic diet (KD), a special diet that is high in fat and low in carbohydrate intake, shows good therapeutic potential in children with epilepsy. In this study, it was found that KD significantly prevented paclitaxel-induced neuropathic nociception. Using the GSE113941 database, 281 differentially expressed genes (DEGs) were found in an animal model of CIPN and controls. The DEGs were mainly enriched in peroxisome proliferator activated receptor (PPAR) and oxidative phosphorylation signaling pathways. As a main regulatory pathway of lipid metabolism, the PPARγ signaling pathway was significantly upregulated in the KD model. In addition, KD also inhibited the expression of pro-inflammatory cytokines and the TLR4/NF-κB signaling pathway in the dorsal root ganglion (DRG) in paclitaxel-treated rats. In vitro, rat primary DRG neurons were used to investigate the role of PPARγ in paclitaxel-induced neurotoxicity. It was found that PPARγ agonist rosiglitazone significantly protected DRG neurons against cell apoptosis and reactive oxygen species generation induced by paclitaxel administration. Therefore, KD is a prospective treatment option when applied as a dietary intervention in the prevention and treatment of paclitaxel-induced neuropathic nociception, possibly through the activation of PPARγ and its neuroprotective functions.
------------------------------------------ Info ------------------------------------------
Open Access: False
Authors: Shanshan Zhong - Zhike Zhou - Xinyu Lin - Fangxi Liu - Chang Liu - Zhouyang Liu - Wenyun Deng - Xiuchun Zhang - Hongtao Chang - Chuansheng Zhao -
Additional links: None found
The innate hypoxic microenvironment of most solid tumors has a major influence on tumor growth, invasiveness and distant metastasis. Here, hypoxia‐activated self‐immolative paclitaxel prodrug (PTX 2 ‐Azo) was synthesized and combined with photodynamic therapy (PDT) to prepare light‐boosted PTX nanoparticle (Ce6/PTX 2 ‐Azo NP) by encapsulation PTX 2 ‐Azo into photosensitizer chlorine (Ce6) decorated peptide copolymer. In this nanoparticle, PTX 2 ‐Azo prevents unexpected premature drug leakage and realizes specific release in hypoxic tumor microenvironment and photosensitizer Ce6 not only efficiently generates singlet oxygen under light irradiation but also acts as a positive amplifier to promote the release of PTX. Moreover, chemotherapy compensates the deficiency of PDT as well. Such combination of PDT and chemotherapy displays excellent antitumor efficacy. This study represents hypoxia‐activatable chemotherapeutic prodrug system and its great potential for synergistic cancer therapy .
https://ift.tt/2QwnLjQ
