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  • Online Resource  (42)
  • American Association for Cancer Research (AACR)  (42)
  • Park, Sue K.  (42)
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  • Online Resource  (42)
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  • American Association for Cancer Research (AACR)  (42)
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  • 1
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 28, No. 24 ( 2022-12-15), p. 5383-5395
    Abstract: Advanced-stage mucinous ovarian carcinoma (MOC) has poor chemotherapy response and prognosis and lacks biomarkers to aid stage I adjuvant treatment. Differentiating primary MOC from gastrointestinal (GI) metastases to the ovary is also challenging due to phenotypic similarities. Clinicopathologic and gene-expression data were analyzed to identify prognostic and diagnostic features. Experimental Design: Discovery analyses selected 19 genes with prognostic/diagnostic potential. Validation was performed through the Ovarian Tumor Tissue Analysis consortium and GI cancer biobanks comprising 604 patients with MOC (n = 333), mucinous borderline ovarian tumors (MBOT, n = 151), and upper GI (n = 65) and lower GI tumors (n = 55). Results: Infiltrative pattern of invasion was associated with decreased overall survival (OS) within 2 years from diagnosis, compared with expansile pattern in stage I MOC [hazard ratio (HR), 2.77; 95% confidence interval (CI), 1.04–7.41, P = 0.042]. Increased expression of THBS2 and TAGLN was associated with shorter OS in MOC patients (HR, 1.25; 95% CI, 1.04–1.51, P = 0.016) and (HR, 1.21; 95% CI, 1.01–1.45, P = 0.043), respectively. ERBB2 (HER2) amplification or high mRNA expression was evident in 64 of 243 (26%) of MOCs, but only 8 of 243 (3%) were also infiltrative (4/39, 10%) or stage III/IV (4/31, 13%). Conclusions: An infiltrative growth pattern infers poor prognosis within 2 years from diagnosis and may help select stage I patients for adjuvant therapy. High expression of THBS2 and TAGLN in MOC confers an adverse prognosis and is upregulated in the infiltrative subtype, which warrants further investigation. Anti-HER2 therapy should be investigated in a subset of patients. MOC samples clustered with upper GI, yet markers to differentiate these entities remain elusive, suggesting similar underlying biology and shared treatment strategies.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
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  • 2
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 18 ( 2018-09-15), p. 5419-5430
    Abstract: Large-scale genome-wide association studies (GWAS) have identified approximately 35 loci associated with epithelial ovarian cancer (EOC) risk. The majority of GWAS-identified disease susceptibility variants are located in noncoding regions, and causal genes underlying these associations remain largely unknown. Here, we performed a transcriptome-wide association study to search for novel genetic loci and plausible causal genes at known GWAS loci. We used RNA sequencing data (68 normal ovarian tissue samples from 68 individuals and 6,124 cross-tissue samples from 369 individuals) and high-density genotyping data from European descendants of the Genotype-Tissue Expression (GTEx V6) project to build ovarian and cross-tissue models of genetically regulated expression using elastic net methods. We evaluated 17,121 genes for their cis-predicted gene expression in relation to EOC risk using summary statistics data from GWAS of 97,898 women, including 29,396 EOC cases. With a Bonferroni-corrected significance level of P & lt; 2.2 × 10−6, we identified 35 genes, including FZD4 at 11q14.2 (Z = 5.08, P = 3.83 × 10−7, the cross-tissue model; 1 Mb away from any GWAS-identified EOC risk variant), a potential novel locus for EOC risk. All other 34 significantly associated genes were located within 1 Mb of known GWAS-identified loci, including 23 genes at 6 loci not previously linked to EOC risk. Upon conditioning on nearby known EOC GWAS-identified variants, the associations for 31 genes disappeared and three genes remained (P & lt; 1.47 × 10−3). These data identify one novel locus (FZD4) and 34 genes at 13 known EOC risk loci associated with EOC risk, providing new insights into EOC carcinogenesis. Significance: Transcriptomic analysis of a large cohort confirms earlier GWAS loci and reveals FZD4 as a novel locus associated with EOC risk. Cancer Res; 78(18); 5419–30. ©2018 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 3
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 2163-2163
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 2163-2163
    Abstract: BACKGROUND: Incidence of thyroid cancer has been rapidly increased, in not only small sizes with improved detection devices but also large size of tumors whose underlying mechanisms remain unclear. Body size and weight change in adulthood were examined as the potential risk factors for thyroid cancer development. METHODS: A large scale case-control study was conducted with constructed questionnaire for their height, weight (current, 2 years ago, at the age of 20 and 35 years old) and confounders. Medical charts were reviewed for cancer histology, tumor aggressiveness and BRAF mutation status. A total of 2,003 cases (1,611 females and 392 males) and individually matched 17,700 controls (13,983 females and 3,717 males) by age, sex, 12-year education and birth year were included. Logistic regression model were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Having a tall height and heavy weight was associated with increased risk in both females [OR and 95%CI for height and weight: 1.46 (1.25-1.71) and 2.66 (2.24-3.15), respectably] and males [OR and 95%CI for height and weight: 1.71 (1.25-2.34) and 2.80 (2.00-3.92), respectably] compared to those in the lowest quartile for the body sizes. This study observed approximated tripled the risk of thyroid cancer [OR and 95%CI: 3.03 (2.10-4.37)] when female subjects gained 10kg or more within recent 2 years. Males who gained 10 kg or more after 35 years old were more likely to have a greater tumor size [ & lt;1cm vs. ≥1cm: 3.76 (2.62-5.38) vs. 6.87 (4.38-10.77)]. However, other factors were not significantly related to increased tumor aggressiveness (tumor size, lymph node metastasis, and mutlifocality) and BRAF mutation affected carriers. CONCLUSION: The results support plausible hormonal and metabolic factors related height, weight, and rapid weight gain in adulthood increase thyroid carcinogenesis. Citation Format: Yunji Hwang, Kyu-Eun Lee, Young Joo Park, Do Joon Park, Yeo-Kyu Youn, Yohwan Yeo, Seung-Hyun Ma, Daehee Kang, Keun-Young Yoo, Sue K. Park. Height, weight and weight changes during adulthood and thyroid cancer risk. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2163. doi:10.1158/1538-7445.AM2014-2163
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 3 ( 2020-02-01), p. 624-638
    Abstract: Pathogenic sequence variants (PSV) in BRCA1 or BRCA2 (BRCA1/2) are associated with increased risk and severity of prostate cancer. We evaluated whether PSVs in BRCA1/2 were associated with risk of overall prostate cancer or high grade (Gleason 8+) prostate cancer using an international sample of 65 BRCA1 and 171 BRCA2 male PSV carriers with prostate cancer, and 3,388 BRCA1 and 2,880 BRCA2 male PSV carriers without prostate cancer. PSVs in the 3′ region of BRCA2 (c.7914+) were significantly associated with elevated risk of prostate cancer compared with reference bin c.1001-c.7913 [HR = 1.78; 95% confidence interval (CI), 1.25–2.52; P = 0.001], as well as elevated risk of Gleason 8+ prostate cancer (HR = 3.11; 95% CI, 1.63–5.95; P = 0.001). c.756-c.1000 was also associated with elevated prostate cancer risk (HR = 2.83; 95% CI, 1.71–4.68; P = 0.00004) and elevated risk of Gleason 8+ prostate cancer (HR = 4.95; 95% CI, 2.12–11.54; P = 0.0002). No genotype–phenotype associations were detected for PSVs in BRCA1. These results demonstrate that specific BRCA2 PSVs may be associated with elevated risk of developing aggressive prostate cancer. Significance: Aggressive prostate cancer risk in BRCA2 mutation carriers may vary according to the specific BRCA2 mutation inherited by the at-risk individual.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 5
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 936-936
    Abstract: Objective: We investigated the role of single nucleotide polymorphisms (SNP) ODC-polyamine pathway related genes (ODC1, AMD1, OAZ2, NQO1, NOS2A) for gastric cancer risk. Additionally, we examined whether phytoestrogen levels modify the association of ODC-polyamine pathway SNPs and risk of gastric cancer. Materials and Methods: Twenty-five SNPs in five genes were genotyped in 59 incident gastric cancer cases and 175 matched controls recruited from the Korea Multi-Center Cancer Cohort. Candidate genes were selected based on genotype databases, and genotype assay was performed using Goldengate platform (Illumina). We calculated the unadjusted Wald p-value between each SNP and phytoestrogen level, as well as the false discovery rate (FDR) corrected p-values of the 25 SNPs according to each phytoestrogen biomarker. Unconditional logistic regression model was used to calculate the adjusted odds ratios (OR) and 95% CI for smoking history. Results: There was a significant association for NQO1 (rs1800566, rs1437135) and daidzein, AMD1 (rs1279599, rs7768897, rs811921) and equol, AMD1 (rs1279599, rs7768897, rs811921) and enterolactone (FDR p-value & lt;0.2). Conclusion: Certain phytoestrogens and ODC-polyamine related genes polymorphisms may interact to affect development of gastric cancer. Additional studies are needed to further elucidate the gene-environment interaction for gastric cancer risk. Citation Format: {Authors}. {Abstract title} [abstract] . In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 936.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 6
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 4720-4720
    Abstract: Background: DNA copy number variation (CNV) is a common phenomenon in human genome and some CNVs have been associated with susceptibility or resistance to disease. It has been suggested that gene copy number can be elevated in cancer cells. To evaluate potential role of CNV in breast cancer development, we conducted genome-wide association study of CNV in Seoul Breast Cancer Study. Methods: Cases were diagnosed with breast cancer and underwent curative surgery at two teaching hospitals located in Seoul, Korea, between 2001 and 2007 (n=2,386). Control subjects were selected from multi-center based cohort study in 2007 (n=2,386). The Affymetrix SNP assay 6.0 array, which includes 946,000 probes for the detection of copy number variation, was used. Nexus Copy Number version 4.1 was used for detecting CNVs (significance threshold=10−6; minimum number of probes per segment=4), and statistical analysis. After quality control step (i.e., robust variance sample QC), total 2,315 cases and 2,039 controls were compared for the difference of each CNV. In this study, we selected the CNVs that were different between cases and controls by at least 5% (P adjusted for multiple comparison & lt;0.01). Adjacent CNVs were grouped into CNV regions ranging 10 kb to 300 kb. Results: Between case and controls, thirteen CNV regions including chr115q11.2, chr3q26.1, chr6q16.3, chr17q31.1 were significantly different for copy number. We note that those regions include genes such as UGT2B17 (UDP glucuronosyltransferase 2 family, polypeptide B18), OR4C11 (olfactory receptor, family 4, subfamily C, member 11), LRRC37A2 (leucine rich repeat containing 37, member A2), ARL17P1 (ADP-ribosylation factor-like 17 pseudogene 1), LOC644974, and the others. We are planning validation study for the regions by quantitative PCR to verify the association with breast cancer risk found in this study. Conclusion: Our results suggest that common CNVs may be associated with breast cancer in Korean women. However, further variation study is essential to support our observation and underlying biological mechanisms for the associations needs to be elucidated. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4720.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 7
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 925-925
    Abstract: Objective: In order to investigate possible genetic contribution to childhood leukemia in the immune system, we evaluated the associations between 786 SNPs in 68 genes/gene regions related to immune response and childhood leukemia risk. Methods: Incident childhood leukemia cases (n=136) and non-cancer controls (n=254) were recruited from three teaching hospitals in Seoul between 2003 and 2006. Candidate genes/gene regions were selected based on SNP databases (CGAP and SNP500 database), and genotype assay was performed using GoldenGate (Illumina) oligonucleotide pool assay (OPA). First, we selected SNPs with dose response effect (Ptrend & lt;0.001). The 16 SNPs deemed unusable due to failure of genotyping or monomorphism (9 SNPs), low yield (2 SNPs), HWE p & lt;0.001 (5 SNPs) in each case and control were excluded from the analysis. A gene-level minP was computed using a permutation-based re-sampling procedure (10,000 permutations) taking all SNPs in each gene/gene region into account. We considered minP & lt;0.05 as noteworthy. Childhood leukemia risk was estimated as odds ratios (ORs) and 95% confidence intervals (CIs) adjusted for age, gender and birth weight. Results: Among the 786 SNPs, 134 SNPs in 7 genes/gene regions were significantly associated with childhood leukemia risk (Ptrend & lt;0.001). Five out of 7 genes/gene regions of immune response (MDM2 (murine double minute 2), CD81 (CD81 molecule), IL-2 (interleukin 2), TNF/LTA (tumor necrosis factor-a (TNF) and lymphotoxin-a), RELB (v-rel reticuloendotheliosis viral oncogene homolog B)) were significantly associated with childhood leukemia risk (minP & lt;0.01). Discussion: Our results suggest that genetic polymorphisms in immune regulatory may play a role in childhood leukemia development. Further large study is warranted confirm our findings. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 925.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 2845-2845
    Abstract: Objectives: Cytotoxin-associated antigen (CagA) produced by Helicobacter pylori (H. pylori) plays a role in gastric carcinogenesis, but the role of genes coding proteins in the CagA pathway remains unclear. This genetic association study aimed to evaluate which genes involved in CagA signal transduction pathway are associated with gastric cancer development. Methods: By literature reviews, we selected 34 candidate genes involved in CagA signal transduction pathway and screened a total of 580 SNPs within +/- 5kbp of target gene location. Within the Korean Multi-Center Cancer Cohort (KMCC), a 100 incident gastric cancer cases were matched to a cancer-free subject by age, sex, residential area and enrollment. Both raw and permutated p-values by 10,000 permutation tests were computed using the LRT with 1 degree of freedom in the trend model. Gastric cancer risk was estimated as odds ratios (ORs) and 95% confidence intervals (CIs) adjusted for age, smoking status, H. pylori infection, and CagA IgG antibody positivity in each genetic model. Results: Twenty five SNPs in 8 genes, Erk, Dock180, C3G, Rap1, Src, CrkL, Mek and Crk, were significantly associated with gastric cancer risk in the single SNP analysis (p & lt;0.05). Specifically, Erk rs5999749 and Dock180 rs9418677 remained significant after correction of multiple comparisons. Except for Dock180 rs9418677 and Rap1 rs17028287, most SNPs downstream CagA/Crk signaling (Dock180, C3G, Rap1 and Mek) were significantly associated with a reduced risk for gastric cancer. Conclusions: Our findings indicate that genes involved in the CagA signal transduction pathway can be major susceptible factors related to tyrosine kinase action, especially interaction with Crk. Further replication studies with wider genomic coverage and a greater number of subjects are still needed. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2845.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. LB-432-LB-432
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. LB-432-LB-432
    Abstract: Background: A model for predicting breast cancer risk has been developed in Korea. Associated risk factors included in the model were 1st degree relatives with breast cancer, age at menarche, menopausal status, number of children, age at first fullterm pregnancy, mammography, and exercise for patients less than 50 years of age and 1st degree relatives with breast cancer, age at menarche, age at menopause, number of children, BMI, mammography, and exercise for patients greater than 50 years of age. The area under the curve among over 50 year olds was 0.655 and 0.611 among under 50 year old. Objectives: The objective of the study was validation of an absolute risk prediction model for breast cancer in Korea by using a large, population cohort and patient registry. Method: The Korean Multi-center Cancer Cohort (KMCC) and registry data of breast cancer patients constructed by the Korean Breast Cancer Society were used to validate the model. 12221 women more than 30 years of age at baseline answered questions about demographic characteristics, reproductive factors, lifestyle, family history since 1993 and we identified 11 and 5 incident breast cancer patient more than 50 and less than 50 years of age, respectively. Age, resident area, and included year were matched to select controls; women aged less than 50 were matched 1:20 while women aged greater than 50 were matched 1:10. In the breast cancer registry, clinical, demographic characteristics and reproductive factors of breast cancer patients were collected since 1980. We selected 2727 patients under 50 years old and 2000 patients over 50 years old matched by age and diagnostic year and calculated their 10, 20, 30, and 40 year absolute risk. Result: In the KMCC data, 10 year absolute risk was 0.39 (95% CI 0.36-0.42) among cases and 0.36 (95% CI 0.35-0.37) among controls under 50 years old and 0.16 (95% CI 0.10-0.22) among cases and 0.08 (0.07-0.09) among controls over 50 years old and it was significantly different in the median test (P-value: 0.02 in both groups). Among breast cancer patient group over 50 years old, 10, 20, 30 and 40 year absolute risk were 0.22 (95% CI 0.21-0.23), 0.35 (95% CI 0.34-0.36), 0.43 (95% CI 0.42-0.45), 0.46 (95% CI 0.44-0.48) respectively and 0.56 (95% CI 0.55-0.57), 1.18 (95% CI 1.15-1.21), 1.53 (95% CI 1.50-1.57), 1.74 (95% CI 1.70-1.78). Conclusion: Due to the short follow up time and small number of cancer incidence in the KMCC cohort, although absolute risk was small, a significant difference was confirmed. Future validation study with a large number and enough follow up cohort time is needed. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-432.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 10
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 21, No. 8 ( 2012-08-01), p. 1371-1380
    Abstract: Background: Matrix metalloproteinase-2 (MMP-2) has been thought of as a predictor of recurrence or metastasis risk or prognostic markers in cancer. We evaluated whether preoperative serum levels of MMP-2 work as a prognostic biomarker in breast cancer prognosis. Methods: Preoperative serum levels of MMP-2 were measured with ELISA in 303 patients with histologically confirmed breast cancer. The median follow-up time for all patients was 4.24 years. The relationship of MMP-2 to survival was investigated using Cox proportional hazard regression model adjusted for the tumor–node–metastasis (TNM) stage and estrogen receptor (ER) status. Results: In the multivariate analysis, disease-free survival (DFS) was worse among patients with the third tertile of MMP-2 level than with the first tertile of MMP-2 level [hazard ratio, 1.80; 95% confidence interval (CI), 1.04–3.11; P = 0.04]. However, when the patients were stratified by age, ER status, histologic grade, and nuclear grade, inverse correlation was shown between serum MMP-2 levels and prognostic factors, and the associations between MMP-2 and DFS were only significant among patients with poor prognostic factors (HR, 2.75; 95% CI, 1.32–5.73 in ER-negative; HR, 2.90; 95% CI, 1.42–5.92 in histologic grade III; and HR, 2.61; 95% CI, 1.26–5.39 in nuclear grade III). Conclusions: Our results suggest that the preoperative serum levels of MMP-2 were associated with the survival in patients with breast cancer in ER-negative, higher histologic grade, or higher nuclear grade breast cancers. Impact: Our results indicate that serum levels of MMP-2 may play a role as prognostic biomarker in breast cancer survival. Cancer Epidemiol Biomarkers Prev; 21(8); 1371–80. ©2012 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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