Expression of copper-transporting P-type adenosine triphosphatase (ATP7B) as a prognostic factor in human endometrial carcinoma

Aida, Taku Michael; Takebayashi, Yuji; Shimizu, Takao; Okamura, Chikako; Higasimoto, Masashi; Kanzaki, Atsuko; Nakayama, Kentaro; Terada, Kunihiko; Sugiyama, Toshihiro; Miyazaki, Kohji; Itō, Kiyoshi; Takenoshita, Seiichi; Yaegashi, Nobuo

doi:10.1016/j.ygyno.2004.12.042

Cited by 49 publications

(33 citation statements)

References 17 publications

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“…These proteins are upregulated in cisplatin-resistant cancer cell lines , and their transfection-enforced overexpression has been shown to drive the acquisition of the cisplatin-resistant phenotype . Importantly, clinical studies indicate that ATP7B expression levels might predict the sensitivity of ovarian and endometrial cancers to cisplatin chemotherapy (Nakayama et al, 2002(Nakayama et al, , 2004Aida et al, 2005). Still, in line with the multifactorial nature of cisplatin efflux (and resistance; see below), small molecules that inhibit specific ABC transporters (for example, the P-glycoprotein-specific inhibitor 5-bromotetrandrine) appear to be unable per se to restore cisplatin accumulation and sensitivity (Jin et al, 2005).…”

Section: Mechanisms Of Pre-target Resistancementioning

confidence: 99%

Molecular mechanisms of cisplatin resistance

et al. 2011

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Platinum-based drugs, and in particular cis-diamminedichloroplatinum(II) (best known as cisplatin), are employed for the treatment of a wide array of solid malignancies, including testicular, ovarian, head and neck, colorectal, bladder and lung cancers. Cisplatin exerts anticancer effects via multiple mechanisms, yet its most prominent (and best understood) mode of action involves the generation of DNA lesions followed by the activation of the DNA damage response and the induction of mitochondrial apoptosis. Despite a consistent rate of initial responses, cisplatin treatment often results in the development of chemoresistance, leading to therapeutic failure. An intense research has been conducted during the past 30 years and several mechanisms that account for the cisplatin-resistant phenotype of tumor cells have been described. Here, we provide a systematic discussion of these mechanism by classifying them in alterations (1) that involve steps preceding the binding of cisplatin to DNA (pre-target resistance), (2) that directly relate to DNAcisplatin adducts (on-target resistance), (3) concerning the lethal signaling pathway(s) elicited by cisplatin-mediated DNA damage (post-target resistance) and (4) affecting molecular circuitries that do not present obvious links with cisplatin-elicited signals (off-target resistance). As in some clinical settings cisplatin constitutes the major therapeutic option, the development of chemosensitization strategies constitute a goal with important clinical implications.

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Section: Mechanisms Of Pre-target Resistancementioning

confidence: 99%

Molecular mechanisms of cisplatin resistance

et al. 2011

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“…Expression of copper-transporting P-type ATPase has been proposed as a prognostic factor for human endometrial carcinoma [432]. The P2X7 receptor has been claimed to be a novel biomarker for uterine epithelial cancers [433].…”

Section: Ovarian Cancermentioning

confidence: 99%

Purinergic signalling and cancer

Burnstock

Virgilio

2013

Purinergic Signalling

267

265

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Receptors for extracellular nucleotides are widely expressed by mammalian cells. They mediate a large array of responses ranging from growth stimulation to apoptosis, from chemotaxis to cell differentiation and from nociception to cytokine release, as well as neurotransmission. Pharma industry is involved in the development and clinical testing of drugs selectively targeting the different P1 nucleoside and P2 nucleotide receptor subtypes. As described in detail in the present review, P2 receptors are expressed by all tumours, in some cases to a very high level. Activation or inhibition of selected P2 receptor subtypes brings about cancer cell death or growth inhibition. The field has been largely neglected by current research in oncology, yet the evidence presented in this review, most of which is based on in vitro studies, although with a limited amount from in vivo experiments and human studies, warrants further efforts to explore the therapeutic potential of purinoceptor targeting in cancer.

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“…Clinical investigations demonstrated elevated mRNA levels of ATP7B in ovarian [133] , gastric [134] and breast cancer [135] tissue samples. Recent investigations suggest that the level of ATP7B expression is a prognostic marker in human endometrial [136] and ovarian [133] carcinoma.…”

Section: B1mentioning

confidence: 99%

Resistance to Chemotherapy in Cancer: A Complex and Integrated Cellular Response

Mellor¹,

Callaghan²

2008

Pharmacology

150

100

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Inherent and acquired resistance pathways account for the high rate of failure in cancer chemotherapy. The mechanisms or pathways mediating resistance may be classified as pharmacokinetic (i.e. alter intratumour drug exposue) or pharmacodynamic (i.e. failure to elicit cytotoxicity). More often than not, the resistant phenotype is characterised by alterations in multiple pathways. Consequently, the pathways may act synergistically or generate a broad spectrum of resistance to anticancer drugs. There has been a great deal of systematic characterisation of drug resistance in vitro. However, translating this greater understanding into clinical efficacy has rarely been achieved. This review explores the phenomenon of drug resistance in cancer and highlights the gap between in vitro and in vivo observations. This gap presents a major obstacle in overcoming drug resistance and restoring sensitivity to chemotherapy.

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Expression of copper-transporting P-type adenosine triphosphatase (ATP7B) as a prognostic factor in human endometrial carcinoma

Cited by 49 publications

References 17 publications

Molecular mechanisms of cisplatin resistance

Molecular mechanisms of cisplatin resistance

Purinergic signalling and cancer

Resistance to Chemotherapy in Cancer: A Complex and Integrated Cellular Response

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