Mini Review: Relationship Between Platinum
Induced Toxicities and Nucleotide Excision Repair (NER) Pathway Polymorphisms
in Non-Small Cell Lung Cancer (NSCLC) Patients and Beyond
Shuai Guo, Qi Xu, Chen-Chen
Wang, Zhen-Shan Qi, Xiao-Lin Xiao
Shuai Guo, Northeastern University, Boston, MA, 02114, the United
States
Shuai Guo, Qi Xu, Xiao-Lin
Xiao, Central South University, 410083,
Hunan, China
Qi Xu, Test Centre, 361 Yinpen South Road,
410013, Hunan, China
Chen-Chen Wang, Department of Oncology, Third Hospital of Chengdu, Chengdu,
610015, Sichuan, China
Chen-Chen Wang, Medical University of Guangxi, 541000, Nanning, Guangxi,
China
Zhen-Shan Qi, Department of Oncology, People’s hospital of Fuzhou, Fuzhou,
350004, Fujian, China
Zhen-Shan Qi, College of Medicine, National Taiwan University, 10051,
Taipei, Taiwan
Xiao-Lin Xiao, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial
College, London, W12 0NN, the United Kingdom
Correspondence to: Xiaolin Xiao, PhD, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College
London, Du Cane Road, London, UK, zip code: W12 0NN.
Email: xiaolin.xiao@csc.mrc.ac.uk
Received: September 15, 2013 Revised: October 15, 2013
Accepted: October 20, 2013
Published online: December 18, 2013
ABSTRACT
Platinum-induced toxicities severely impede successful chemotherapy in
non-small cell lung cancer (NSCLC) patients. The nucleotide excision repair
(NER) pathway is considered as one of the major factors contributing to
platinum effects. Furthermore, genetic variances of the NER pathway influence
platinum toxicities. Several genetic loci have recently been reported to
contribute to the susceptibility of platinum-induced toxicities. In order to
further understand the genetic influence on the risk of platinum-induced
toxicities in NSCLC patients, we reviewed and collected articles from PUBMED
for genes that reported by recent clinical pharmacogenetic studies. At the
conclusion of our search, we summarized the publications about relative
clinical trials and summarized five candidate genes, which might relate with
platinum-induced toxicities in NSCLC patients. Despite the findings of this and
other similar, contemporary research projects, many of the special details and
underlying mechanisms in this field of study are still, to a great extent,
unknown. As a result, future studies are needed to gain a full appreciation
regarding the identification of high toxicity risk in human beings
© 2013 ACT. All rights reserved.
Key words: DNA repair; Nucleotide excision repair (NER)
pathway; Non-small cell lung cancer (NSCLC); Platinum; Toxicity; Copper
transport protein 1 (CTR1)
Guo S, Xu Q, Wang
CC, Qi ZS, Xiao XL. Mini Review: Relationship Between Platinum Induced
Toxicities and Nucleotide Excision Repair (NER) Pathway Polymorphisms in
Non-Small Cell Lung Cancer (NSCLC) Patients and Beyond. Journal of Tumor 2013;
1(7): 66-72 Available from: URL:
http://www.ghrnet.org/index.php/JT/article/view/544
INTRODUCTION
Lung cancer is the
leading cause of cancer-related death worldwide, with a total five-year
survival rate of about 15%[1]. There are two major histological
subtypes of lung cancer, small cell lung cancer (SCLC) and non-small cell lung
cancer (NSCLC). The most common types of NSCLC are squamous cell carcinoma,
large cell carcinoma and adenocarcinoma[2]. The incidence of NSCLC
is continues growing up rapidly recently years[3].
Platinum-based chemotherapy
is considered as the first-line treatment for lung cancer, but NSCLC is
relatively insensitive to chemotherapy compare to SCLC[4]. Thus,
more attention has been paid to improve the chemotherapy efficacy in NSCLC
patients[5]. Cisplatin, carboplatin and oxaliplatin are the first-,
second- and third-generation of platinum-containing anti-cancer chemotherapy
drugs, respectively[6]. However, both of the chemotherapy resistance
and platinum-induced toxicities are common and constitute the major obstacle
for successful chemotherapy in NSCLC patients[7]. Basically, the
most common severe platinum-induced toxicities include nephrotoxicity,
ototoxicity, neurotoxicity, myelosuppression, electrolyte disturbances, nausea
and anaphylactic reactions[7].
Chemotherapy induced
toxicities are multifactorial: they depend on several internal and external
factors, such as health status, disease stage, patient age and smoking status[5].
Furthermore, genetic factors, such as single-nucleotide polymorphism (SNP), are
important determinants of platinum induced side effects[6].
Personalized medicine, which tailors intervention to individual variation in
risk and treatment response, has been considered as one of the potential
medicine models that will greatly improve the clinical efficacy of
platinum-based chemotherapy, and the use of genetic information has been played
a major role in the design of personalized medicine[8]. Personalized
medicine have been widely researched in several complex diseases, such as
diabetes[9-11], seizures[12-14], and so on. As the rapid
development of SNP detection technologies[15] and integrative
network-based computational methods[16,17] more researches has
investigated the potential ability of using certain SNPs to predict the chemo
toxicities in cancer patients[18].
Nucleotide excision repair
(NER) pathway, as a major form of DNA repair pathway, has been suggested to be
the main cellular defense mechanism against platinum-induced intra-strand
cross-links in DNA repair pathway[19]. Genes involve in NER pathway,
including its up-stream genes, are considered as candidate genes for prediction
of different response to platinum-based chemotherapy in NSCLC patients[20].
Some SNPs have been described as important factors contributing to the activity
of NER pathways, thus it would influence platinum-based chemotherapeutic
toxicities in NSCLC patients[19].
The aim of the study is to
provide a comprehensive assessment on the association between genetic
polymorphism within NER pathway and platinum-based chemotherapy toxicity in
NSCLC, and further appraise the prediction ability of these potential
biomarkers.
METHODS
We
searched the relative literatures about NER pathway genetic polymorphisms and
platinum induced toxicities in NSCLC patients through PubMed, with key words
“gene name + NSCLC + toxicity/toxicities”. Gene names included a total of 23
genes associated with NER pathway, with the detailed gene information listed in
table 1. The time period for literature searching was from the first available
article to September 1st 2013. Publications meeting the following
criteria were including: (1) patients were diagnosed with NSCLC; (2) patients
had been received platinum-based chemotherapy; (3) the data of toxicity rate
stratified by polymorphisms could be obtained from the original article.
Candidate NER genes were selected as the genes had been reported by more than
one qualified literature to show its potential relationship with
platinum-induced toxicities, thus three genes were remained. Besides three
candidates NER genes, one up-stream gene of NER pathway and a copper transport
family gene were also selected, due to the emerging evidence of their
relationship with platinum response. Figure 1 illustrates the literatures and
candidate genes selection process. And the detailed summarized information
about these studies was presented in table 2-4.
Genetic polymorphism in NER pathway
Nucleotide excision
repair includes certain key steps and there are some core proteins that should
significantly influence the DNA repair ability[21]. After literature
selection, this study focused on three core genes in NER pathway[22].
ERCC1 (excision repair
cross-complementing rodent repair deficiency, complementation group 1)
ERCC1 is a component
of the 5’ endonuclease of the nucleotide excision repair complex, and it is
crucial for the repair of DNA damage caused by interstrand and intrastrand
cross-links that prevent both replication and transcription. Two major
polymorphisms have been widely tested in pervious pharmacogenetic studies.
These two SNPs include ERCC1 C118T (ERCC1 Asn119Asn, rs11615), as well as ERCC1
C8029A (rs3212986), with the detailed descriptions shown in table 2.
For ERRC1 C8029A, Suk R et
al[23] reported a significant relationship between ERCC1 C8029A
and grade 3~4 gastrointestinal toxicity (p=0.03) in white population.
But the other Chinese study[24] in 300 patients did not replicate
the results.
For ERCC1 C118T, a total of
eight studies failed to find a significant association between this
polymorphism and any platinum-induced toxicity. These eight clinical studies
were composed of the followings: two of them were Italian studies, with one
enrolled[25] 192 patients and the other[26] enrolled 65
patients; another two were Asian studies, with one[27] enrolled 95
Chinese and the other one[28] enrolled 526 Japanese; the remaining
four studies were a Greek study[19] enrolled 119 patients, a Spanish
study[29] enrolled 94 subjects, a white study[23]
enrolled 214 patients and a multi-ethnicities study (White, Black, Asian and
others) enrolled 137 subjects in Netherland.
Among these published
studies, only Suk R et al[23] reported a significant
relationship between C8029A and gastrointestinal toxicity in white population,
which has not be successfully replicated. As far as we know from our literature
research, there is no evidence to show the significant effect of ERCC1 C118T on
platinum induced toxicities.
XPD (Xeroderma Pigmentosum D)
XPD is also known as
ERCC2 (excision repair cross completing group 1 gene product). It helps unwind
DNA and generates a junction between the double-stranded and single-stranded
DNA around the transcription bubble. There are three major genetic
polymorphisms within XPD gene which has been widely studied. These three SNPs
include XPD Lys751Gln (XPD K751Q, rs1052559), XPD Asp312Asn (XPD D312N,
rs1799793), and XPD Arg156Arg (XPD R156R, rs238406). Their detailed study
information was shown in table 3.
In recent years, some relevant
studies reported some significant relationships between XPD genotypes and
platinum toxicities. Wu W et al[30] enrolled 209 Chinese
NSCLC patients and reported a significant relationship between XPD R156R and
grade 3~4 hematologic toxicity (p=0.009), especially severe leukopenia
toxicity (p=0.005). Moreover, they reported that the haplotype “CG”
(D312N and R156R) revealed a protective effect of on the risk of grade 3~4
hematologic toxicity (p=0.025). On the other hand, Petty WJ et al[31]
reported a study included 49 patients (whites and blacks), and found the XPD
genotype was associated with a significant higher risk of grade 4 neutropenia (p=0.02).
Another study reported by Booton R et al[32] found a
significant association between XPD D312N/K751Q haplotype and grade 4
neutropenia (p=0.05) in white NSCSL patients.
However, there were another
nine studies that did not find any significant relationship between XPD
genotypes and platinum-induced toxicities. These nine studies were composed of
the followings: three of them were Spanish studies, one enrolled 180 and
analyzed XPD K751Q and XPD D312N mutations[33], one enrolled 94
patients and carried out the analysis of XPD K751Q genotype[29], the
another one enrolled 203 patients and also tested XPD K751Q genotype[34];
three of them were Italian studies, one enrolled 208 patients and tested XPD
K751Q genotype[35], one enrolled 65 patients and carried out the
test of XPD K751Q and XPD D312R genotype[26], and another one
enrolled 192 patients and tested XPD K751Q genotype[25]; one of the
nine studies was a Chinese study included 115 patient and tested XPD K751Q
genotype[36]; one of the nine studies was a Greek study[19]
included 119 patients and carried out the test of XPD K751Q genotype; the last
one was published by Gandara DR et al[28] and enrolled 256
Japanese NSCLC patients.
Based on the aforementioned studies, only Wu W et al[30]
and Petty WJ et al[31] found a significant association
between XPD polymorphism and hematologic toxicity. Although some ethnicity
difference might exist, the relationship between XPD genotypes and platinum
induced toxicities needs to be further confirmed by larger and multi-ethnicity
based studies.
RRM1 (regulatory subunit of
ribonucleotide reductase 1)
RRM1 functions as
the regulatory subunit of ribonucleotide reductase and controls substrate
specificity and the on/off function of ribonucleotide reductase, whereas the catalytic
subunit (RRM2) converts nucleoside diphosphates to the corresponding
deoxynucleotides. As shown in table 4, two major polymorphisms of RRM1 gene,
RRM1 C37A (RRM1 rs1042858) and RRM1 C524T (RRM1 rs11030918), have been tested
in recent studies.
Zhang L et al[37]
investigated the relationship between RRM1 C37A and platinum-induced toxicities
in 388 Chinese stage IIIB-IV NSCLC patients. The patients received
cisplatin/carboplatin based chemo together with
vinorelbine/gemcitabine/gocetaxcel/paclitaxel. They found this C37A genotype
was significantly related with the total grades 3~4 adverse events (P=0.047),
including hematological toxicity and non-hematologic toxicity. On the other
hand, Zhang L et al[37] reported that this SNPs also related
with grade 3~4 vomiting (P=0.046), whereas a clinical study of Spain,
Vinolas N et al[29] did not replicate the results. In this
Spanish study, a total of 94 NSCLC patients in stage III-IV were enrolled and
they were treated with cisplatin and vinorelbine. The study[23] did
not find any significant relationship between RRM C37A and platinum-induced
toxicities. In addition, Ludovini V et al[25] published an
Italian study that enrolled 192 chemotherapy-native NSCLC patients in advance
stages. This study analyzed the relationship between RRM1 C524T and platinum
toxicities, but no significant relationship was found in this study.
Since only a limited numbers
of studies are available and the sample size they studied are relatively small,
the relationship between RRM1 genetic polymorphism and platinum induced
toxicities need to be further investigated in larger clinical pharmacokinetics
studies.
Genetic polymorphism in up-stream gene
of NER pathway
eIF3a is the largest
subunit of eukaryotic translation initiation factor 3 (eIF3), known to be
over-expressed in many malignancies, both in vivo and in vitro[38,39].
It has been suggested that eIF3a is an upstream gene of NER pathway. The eIF3a
knockdown cell line showed increased cellular resistance to cisplatin, increased
DNA repair ability and up-expression of DNA repaired proteins[40],
while the eIF3a over expressed cell line showed the opposite results. In
vivo, the gene expression levels of eIF3a significantly associated with
response of lung cancer patients to platinum-based chemotherapy[41].
Xu X et al[42]
explored the association between eIF3a polymorphism and platinum-based
chemotherapy response, and further investigated the overall survival in Chinese
lung cancer patients. They found that rs3740556 conferred a significant
increase in platinum-based chemotherapy response and a favorable survival for
NSCLC patients. More importantly, Xu X et al[43] further
investigated the role of eIF3a polymorphism in relation to severe platinum
toxicity in Chinese NSCLC patients, and found a novel missense SNP Arg803Lys
was associated with nephrotoxicity and ototoxicity. Although these results need
to be replicated by further larger studies, these results bring the light of
the essential role of eIF3a in identification of individuals at risk of severe
toxicity, which will lead to more attraction on up-stream genes of NEP pathway
and to contribute to the improvement of chemotherapeutic efficacy in NSCLC
patients.
Genetic polymorphism in copper
transport family
Beyond this NER
pathway, an interesting possibility has emerged that copper transporter family
performs as the major plasma-membrane transporter in platinum uptake as well as
exportation[44]. Both of the platinum cellular uptake and DNA repair
ability are suggested as the major cause of severe toxicities in platinum
treatment in vivo[45]. Copper transporter family is comprised
of CTR1 (copper transport protein 1), ATP7A (copper-transporting ATPase 1), and
ATP7B (ATPase, Cu2+ transporting, beta polypeptide)[46].
It has been confirmed that CTR1 plays an essential role in platinum influx
among these three components[46].
A
multi-institutions based study found that rs7851395 and rs1268377 genotypes of
the CTR1 gene affect the platinum-based chemotherapeutics response, as well as
the overall survival rate in Chinese NSCLC patients[47]. Moreover,
Xu X et al[48] investigated the role of CTR1 polymorphism in
susceptibility to severe platinum toxicities. They found that the rs10,981,694
mutation was associated with platinum induced severe ototoxicity and C allele
carrier patients seemed to have poorer toxicity tolerance in Chinese NSCLC
patients. On the basis of these findings, it may be possible to use CTR1 in the
further as a biomarker to predict the outcomes of personalized platinum
chemotherapy.
CONCLUSION
Based on the results
of published clinical trials, we have selected these candidate genes (i.e.,
ERCC1, XPD, RRM1, eIF3a, and CTR1) that are more likely to have effect on
platinum-induced toxicities in NSCLC patients. Confounding variables such as
environmental influence and unknown gene-gene interaction do undoubtedly exist[49,50].
Twin modeling based genetic research might also be used to inspire further
exploration of potential biomarkers[51]. Additionally, unidentified
associations corresponding to differences in ethnicity, age, study sample
sizes, and study-specific methods of analysis do further complicate the
situation[52,53]. Beyond these genetic factors, epigenetics,
especially DNA methylation[54,55], should be considered as another
potential biomarker which has been suggested contribute greatly to the variance
of individual drug response[56,57].
In conclusion, the complex
occurrence of chemo toxicities and our current lack of knowledge both prevent
us from fully explaining the precise mechanism. Consequently, future studies
encompassing larger sample sizes and novel perspectives are called for in
overcoming current problems. If allowed to transpire, these studies will
facilitate a better understanding of the regulatory pathways in chemo
toxicities in human beings.
ACKNOWLEDGMENTS
Shuai Guo, Qi Xu, These authors
contribute equally.
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Peer reviewer: Takashi Ogino, Medical Director, Medipolis Proton
Therapy and Research Center, 5188 Higashikata, Ibusuki, Kagoshima 891-0304,
Japan.
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