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  • American Association for Cancer Research (AACR)  (28)
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  • 1
    Online Resource
    Online Resource
    Abstract 6697: Deep learning algorithm for cancer detection using multimodal characteristics of whole methylome sequencing of cf-DNA
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 7_Supplement ( 2023-04-04), p. 6697-6697
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 7_Supplement ( 2023-04-04), p. 6697-6697
    Abstract: Background Various cell-free DNA (cfDNA) features including methylation and genomic profiles have been investigated for their potential use in early cancer detection. We developed deep learning models based the data generated by the enzymatic conversion based whole methylome sequencing of cfDNA. Methods Cell-free whole genome Enzymatic Methyl sequencing(cfWEMseq) data were generated from 198 cancer patients (stage I: 11%, II: 17%, III: 22%, IV: 20%, unknown: 31%) and 69 healthy controls. The cancer types were consisted of breast (n=31), liver (n=24), esophageal (n=38), pancreatic (n=30), colon (n=34), ovarian (n=18), and lung (n=23). Sequence data was produced on average of 200 million reads using Novaseq 6000 (Illumina). For model training and evaluation, data partitioning was stratified by cancer type, and 5-fold cross validation was used. Coverage and methylation beta values ​​were calculated by binning at fixed size of 100K, 1M, and 5M base and variable size from Topologically Associated Domains (TAD). Genome Coverage (GC), Genome Methylation Beta values ​​(GMB), and Mutation Signature (MS) features were trained using a one-dimensional convolutional neural network (1D-CNN). The performance of the model was evaluated by measuring the average value of the results measured in each test set of 5 fold. Results We tested the cancer detection performance of various feature combinations using all data from cfWEMseq (n=267). Regardless of the bin size, the GMB single model achieved higher performance than the GC single model. The best-performing model is the ensemble model of GMB (100k bin) and MS. The cancer detection performance of this ensemble model reached an accuracy 96% (CI: 93.6% to 98.1%), AUC 0.99 (CI: 0.97 to 1.0) and sensitivity 98.0% (CI: 92.4% to 99.5%) with a specificity of 90%. Conclusions These results provide an opportunity for higher accuracies by integrating methylation information and genomic data using cfWEMseq. This research was supported through the National Research Foundation (NRF) funded by the Ministry of Science and ICT (2020M2D9A3094213). Citation Format: Juntae Park, Minjung Kim, Sook Ryun Park, Ki-Byung Song, Eunsung Jun, Dongryul Oh, Jeong-Won Lee, Young Sik Park, Ki-Won Song, Jeong-Sik Byeon, Bo Hyun Kim, Chang-Seok Ki, Eunhae Cho. Deep learning algorithm for cancer detection using multimodal characteristics of whole methylome sequencing of cf-DNA. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6697.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2023-6697
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 2
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    Abstract 6371: Deep learning algorithm for multi-cancer detection and classification using cf-WGS
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Research Vol. 82, No. 12_Supplement ( 2022-06-15), p. 6371-6371
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 12_Supplement ( 2022-06-15), p. 6371-6371
    Abstract: Purpose: Several cell-free DNA (cf-DNA) features, such as genome-wide coverage, fragment size, and fragment end motif frequency, have shown their potentials for cancer detection. In this study, we developed two independent models, GC (gross chromatin), and FEMS (fragment end motif frequency and size). Each model uses images generated from genome-wide normalized sequencing coverage and cf-DNA fragment end motif frequencies according to the different cf-DNA size profiles. Then we integrated them into a single ensemble model to improve cancer detection and multi-cancer type classification accuracy. Methods: Low depth cf-WGS data was generated from 1,396 patients (stage I: 14.9%, stage II: 35.6%, stage III: 24.9%, stage IV: 24.2%, unknown: 0.4%) with breast (n=702), liver (n=213), esophageal (n=155), ovarian (n=151), pancreatic (n=85), lung (n=53), head and neck (n=16), biliary tract (n=15), and colon cancer (n=6) and 417 healthy individuals. Samples were randomly split into training, validation, and test set stratifying cancer type and stages. Cancer types with a small number of samples ( & lt;20) were excluded for multi-cancer type classification. Each model was trained using a convolutional neural network, then integrated into a single ensemble model by averaging the predicted probabilities calculated from each model. Results: For cancer detection, the ensemble model achieved sensitivities of 85.2% [95% confidence interval (CI): 71.8% to 94.5%], 74.9% (CI: 68.0% to 88.0%), 73.2% (CI: 66.7% to 85.9%) at a specificity of 95%, 98% and 99% and the AUC value of 0.97(CI: 0.95-0.99) in the test dataset. By the cancer stages, sensitivity was 62.8% (CI: 48.8% to 83.7%) in stage I, 66.3% (CI: 57.7% to 82.7%) in stage II, 85.9% (CI: 77.5% to 94.4%) in stage III, and 76.1% (CI: 63.4% to 87.3%) in stage IV at 99% specificity. For multi-cancer classification, the overall accuracy of 85.1% (CI: 80.4% to 89.3%) was achieved including 6 cancer types. Conclusions: Highly sensitive and accurate deep learning model for cancer detection and multi-cancer classification was generated by combining different types of cf-DNA features. This result provides the opportunity for general population multi-cancer screening using various cf-DNA features. Citation Format: Tae-Rim Lee, Jin Mo Ahn, Joo Hyuk Sohn, Sook Ryun Park, Min Hwan Kim, Gun Min Kim, Ki-Byung Song, Eunsung Jun, Dongryul Oh, Jeong-Won Lee, Joseph J Noh, Young Sik Park, Sun-Young Kong, Sang Myung Woo, Bo Hyun Kim, Eui Kyu Chie, Hyun-Cheol Kang, Youn Jin Choi, Ki-Won Song, Jeong-Sik Byeon, Junnam Lee, Dasom Kim, Chang-Seok Ki, Eunhae Cho. Deep learning algorithm for multi-cancer detection and classification using cf-WGS [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 6371.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2022-6371
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
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  • 3
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    T-Lymphokine–Activated Killer Cell–Originated Protein Kinase Functions as a Positive Regulator of c-Jun-NH2-Kinase 1 Signaling and H-Ras–Induced Cell Transformation
    American Association for Cancer Research (AACR) ; 2007
    In:  Cancer Research Vol. 67, No. 11 ( 2007-06-01), p. 5186-5194
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 67, No. 11 ( 2007-06-01), p. 5186-5194
    Abstract: T-lymphokine–activated killer cell–originated protein kinase (TOPK) is overexpressed in highly proliferating tumors such as leukemias and myelomas, and seems to play a key role in tumorigenesis or metastasis. However, the precise role and regulatory mechanism explaining the effects of TOPK on tumor cells still remain elusive. Here, we reported that TOPK regulates UVB-induced c-Jun-NH2-kinase 1 (JNK1) activity, and is essential for H-Ras–induced activator protein-1 activity and cell transformation. We showed that TOPK associated with and phosphorylated JNK1 following UVB irradiation in vitro or in vivo. Moreover, UVB-induced JNK1 activity was greatly augmented in mouse epidermal JB6 Cl41 cells that stably expressed TOPK cDNA. On the other hand, JNK1 activity was markedly attenuated by stable expression of small interfering RNA against TOPK in malignant melanoma RPMI 7951 cells. Interestingly, TOPK interacted with JNK-interacting protein 1 and caused an elevation of JNK-interacting protein 1 scaffolding activity, thereby enhancing JNK1 activity. Furthermore, JNK1 was required for TOPK-mediated activator protein-1 transcriptional activity and transformed foci induced by UVB or H-Ras. Taken together, these findings showed that TOPK positively modulated UVB-induced JNK1 activity and played a pivotal role in JNK1-mediated cell transformation induced by H-Ras. These studies might also provide a novel molecular mechanism for the role of TOPK in UVB-mediated skin carcinogenesis. [Cancer Res 2007;67(11):5186–94]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-06-4506
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2007
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  • 4
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    Mitogen- and Stress-Activated Kinase 1–Mediated Histone H3 Phosphorylation Is Crucial for Cell Transformation
    American Association for Cancer Research (AACR) ; 2008
    In:  Cancer Research Vol. 68, No. 7 ( 2008-04-01), p. 2538-2547
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 68, No. 7 ( 2008-04-01), p. 2538-2547
    Abstract: Mitogen- and stress-activated kinase 1 (MSK1) belongs to a family of dual protein kinases that are activated by either extracellular signal-regulated kinase or p38 mitogen-activated protein kinases in response to stress or mitogenic extracellular stimuli. The physiologic role of MSK1 in malignant transformation and cancer development is not well understood. Here, we report that MSK1 is involved in 12-O-tetradecanoylphorbol-13-acetate (TPA)–induced or epidermal growth factor (EGF)–induced neoplastic transformation of JB6 Cl41 cells. H89, a potent inhibitor of MSK1, strongly suppressed TPA-induced or EGF-induced cell transformation. When cells overexpressing wild-type MSK1 were treated with TPA or EGF, colony formation increased substantially compared with untreated cells or cells that did not overexpress MSK1. In contrast, MSK1 COOH terminal or NH2 terminal dead dominant negative mutants dramatically suppressed cell transformation. Introduction of small interfering RNA-MSK1 into JB6 Cl41 cells resulted in suppressed TPA-induced or EGF-induced cell transformation. In addition, cell proliferation was inhibited in MSK1 knockdown cells compared with MSK1 wild-type cells. In wild-type MSK1-overexpressing cells, activator protein (AP-1) activation increased after TPA or EGF stimulation, whereas AP-1 activation decreased in both MSK1 dominant-negative mutants and in MSK1 knockdown cells. Moreover, TPA-induced or EGF-induced phosphorylation of histone H3 at Ser10 was increased in wild-type cells but the induced phosphorylation was abolished in MSK1 dominant-negative mutant or MSK1 knockdown cells. Thus, MSK1 is required for tumor promoter-induced cell transformation through its phosphorylation of histone H3 at Ser10 and AP-1 activation. [Cancer Res 2008;68(7):2538–47]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-07-6597
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2008
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  • 5
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    Arrest Defective 1 Autoacetylation Is a Critical Step in Its Ability to Stimulate Cancer Cell Proliferation
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 11 ( 2010-06-01), p. 4422-4432
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 11 ( 2010-06-01), p. 4422-4432
    Abstract: The N-acetyltransferase arrest defective 1 (ARD1) is an important regulator of cell growth and differentiation that has emerged recently as a critical molecule in cancer progression. However, the regulation of the enzymatic and biological activities of human ARD1 (hARD1) in cancer is presently poorly understood. Here, we report that hARD1 undergoes autoacetylation and that this modification is essential for its functional activation. Using liquid chromatography-tandem mass spectrometry and site-directed mutational analyses, we identified K136 residue as an autoacetylation target site. K136R mutation abolished the ability of hARD1 to promote cancer cell growth in vitro and tumor xenograft growth in vivo. Mechanistic investigations revealed that hARD1 autoacetylation stimulated cyclin D1 expression through activation of the transcription factors β-catenin and activator protein-1. Our results show that hARD1 autoacetylation is critical for its activation and its ability to stimulate cancer cell proliferation and tumorigenesis. Cancer Res; 70(11); 4422–32. ©2010 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-09-3258
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 6
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    Abstract P1-21-01: Multicenter study for brain metastasis from breast cancer in Korea: The significance of molecular subtype (KROG 1612)
    American Association for Cancer Research (AACR) ; 2022
    In:  Cancer Research Vol. 82, No. 4_Supplement ( 2022-02-15), p. P1-21-01-P1-21-01
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 4_Supplement ( 2022-02-15), p. P1-21-01-P1-21-01
    Abstract: Background: We analyzed the treatment outcome of breast cancer patients with brain metastases (BM) in Korea to identify the prognostic factors and the role of whole brain radiation therapy (WBRT). Methods: Seven hundred thirty patients of breast cancer with BM treated at 17 institutions in Korea from 2000 to 2014 were analyzed. The median follow-up duration was 12 months. The analysis consisted of three cohorts: in cohort A, a total of 730 patients were included; in cohort B, 538 patients with available follow-up imaging after initial brain-directed treatment; and in cohort C, 54 patients receiving salvage WBRT due to recurrent BM after initial Stereotactic radiosurgery or WBRT. Overall survival (OS) was calculated from BM diagnosis in cohort A or from the last day of salvage WBRT in cohort C. Results: Median OS of cohort A was 15 months. In multivariate analysis, histologic grade 3, extracranial metastasis, number of BM & gt;4, hormone receptor (HR) or HER2 negativity, and shorter time interval to diagnosis of BM were associated with inferior OS. Among 538 patients in cohort B, 201 showed subsequent development of new BM at a median of 11 months after stereotactic radiosurgery or WBRT for the management of initial BM (at 1 year, HR+/HER2- 51.9%, HER2+ 44.0%, and TNBC 69.6%, respectively; p=0.008). Upfront WBRT reduced subsequent development of new BM, which showed the significant difference among molecular subtypes (HR+/HER2-, 42% reduction at 1 year, p & lt;0.001; HER2+, 18.5%, p=0.004; TNBC, 16.9%, p=0.071). Multivariate analysis of cohort B showed that shorter time interval to BM, TNBC subtype, extracranial systemic disease, number of BM & gt;4, and involvement of both tentoria increased subsequent development of new BM. Anti-HER2 therapy for HER2+ patients and upfront WBRT significantly reduced risk of new BM. In cohort C, upfront WBRT prolonged the salvage WBRT-free duration (median 6.9 vs. 8.7 months, p=0.058). Median OS was 6.8 months after salvage WBRT. Longer interval to salvage WBRT, controlled primary tumor, high dose of salvage WBRT (BED10 & gt;37.5 Gy), and systemic treatment after salvage WBRT showed better OS. Uncontrolled extracranial systemic disease and salvage WBRT due to local progression without distant intracranial failure showed worse OS. Conclusions: The rates of new BM showed the significant differences among molecular subtypes. Upfront WBRT decreased subsequent development of new BM and this effect was dependent on the molecular subtype as well. Anti-HER2 therapy for HER2+ patients significantly decreased the subsequent development of new BM. On salvage WBRT setting, the patients having high dose of salvage WBRT, stable extracranial systemic disease and subsequent systemic therapy showed better OS. Citation Format: Jae Sik Kim, Kyubo Kim, Wonguen Jung, Kyung Hwan Shin, Seock-Ah Im, Hee-Jun Kim, Yong Bae Kim, Jee Suk Chang, Jee Hyun Kim, Doo Ho Choi, Yeon Hee Park, Dae Yong Kim, Tae Hyun Kim, Byung Ock Choi, Sea-Won Lee, Suzy Kim, Jeanny Kwon, Ki Mun Kang, Woong-Ki Chung, Kyung Su Kim, Won Sup Yoon, Jin Hee Kim, Jihye Cha, Yoon Kyeong Oh, In Ah Kim. Multicenter study for brain metastasis from breast cancer in Korea: The significance of molecular subtype (KROG 1612) [abstract] . In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P1-21-01.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.SABCS21-P1-21-01
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
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  • 7
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    Tumor Genomic Profiling Guides Patients with Metastatic Gastric Cancer to Targeted Treatment: The VIKTORY Umbrella Trial
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Discovery Vol. 9, No. 10 ( 2019-10-01), p. 1388-1405
    Details
    In: Cancer Discovery, American Association for Cancer Research (AACR), Vol. 9, No. 10 ( 2019-10-01), p. 1388-1405
    Abstract: The VIKTORY (targeted agent eValuation In gastric cancer basket KORea) trial was designed to classify patients with metastatic gastric cancer based on clinical sequencing and focused on eight different biomarker groups (RAS aberration, TP53 mutation, PIK3CA mutation/amplification, MET amplification, MET overexpression, all negative, TSC2 deficient, or RICTOR amplification) to assign patients to one of the 10 associated clinical trials in second-line (2L) treatment. Capivasertib (AKT inhibitor), savolitinib (MET inhibitor), selumetinib (MEK inhibitor), adavosertib (WEE1 inhibitor), and vistusertib (TORC inhibitor) were tested with or without chemotherapy. Seven hundred seventy-two patients with gastric cancer were enrolled, and sequencing was successfully achieved in 715 patients (92.6%). When molecular screening was linked to seamless immediate access to parallel matched trials, 14.7% of patients received biomarker-assigned drug treatment. The biomarker-assigned treatment cohort had encouraging response rates and survival when compared with conventional 2L chemotherapy. Circulating tumor (ctDNA) analysis demonstrated good correlation between high MET copy number by ctDNA and response to savolitinib. Significance: Prospective clinical sequencing revealed that baseline heterogeneity between tumor samples from different patients affected response to biomarker-selected therapies. VIKTORY is the first and largest platform study in gastric cancer and supports both the feasibility of tumor profiling and its clinical utility. This article is highlighted in the In This Issue feature, p. 1325
    Type of Medium: Online Resource
    ISSN: 2159-8274 , 2159-8290
    URL: Article
    DOI: 10.1158/2159-8290.CD-19-0442
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
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  • 8
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    Abstract 3542: Effects of single nucleotide polymorphisms on treatment outcomes and toxicity in patients treated with sunitinib for biliary tract and gastric cancers.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 3542-3542
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 3542-3542
    Abstract: BACKGROUND: We analyzed the efficacy and toxicity profile of sunitinib according to single nucleotide polymorphisms (SNPs) of VEGFA and KDR among the patients with gastric or biliary tract cancer. METHODS: We examined 8 known SNPs of VEGFA and 5 SNPs of KDR among patients with gastric or biliary tract cancer who were treated with sunitinib in our two previous phase II studies. We assessed progression free survival (PFS), overall survival (OS), and toxicity and their relationships to these SNPs. RESULTS: A total of 63 patients were evaluable. Among candidate SNPs, rs2010963, rs833068, and rs1870377 were associated with poor PFS (P = .009, .002, and .029, respectively), while rs1870377 and rs7692791 were associated with poor OS (P = .001 and 0.03, respectively). Multivariate analysis showed that only rs1870377 had significant effects on both PFS and OS. Toxicity evaluation indicated that rs1531289 was associated with grade 3-4 anemia. (P = .03). CONCLUSIONS: Certain SNPs of KDR may affect treatment outcome and toxicity of patients treated with sunitinib. Citation Format: Chi Hoon MAENG, Jun Ho Lee, Jeeyun Lee, Jung Yong Hong, Moon Ki Choi, Young Saing Kim, Hyun Ae Jung, Joon Oh Park, Se Hoon Park, Young Suk Park, Won Ki Kang, Ho Yeong Lim. Effects of single nucleotide polymorphisms on treatment outcomes and toxicity in patients treated with sunitinib for biliary tract and gastric cancers. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3542. doi:10.1158/1538-7445.AM2013-3542
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-3542
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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  • 9
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    Abstract P3-05-06: Prognostic impact of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis-related liver fibrosis on postoperative long-term outcomes of breast cancer
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 5_Supplement ( 2023-03-01), p. P3-05-06-P3-05-06
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 5_Supplement ( 2023-03-01), p. P3-05-06-P3-05-06
    Abstract: Background: Obesity, the modern ‘epidemic’, has shared correlation with fatty liver disease and breast cancer. However, previous studies on the relation between fatty liver and breast cancer have shown conflicting results on the impact of fatty liver on the survival and recurrence of breast cancer patients. And there was no attempt to find out the effect of liver fibrosis, which is the consequence of fatty liver disease, on female breast cancer patients. So we attempted to investigate the prognostic value of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis(NASH)-related liver fibrosis in patients with breast cancer undergoing surgery, using noninvasive tools like liver-to-spleen attenuation(L/S) ratio and Fibrosis-4(FIB-4) score, respectively. Methods: A total of 933 patients diagnosed with primary invasive breast cancer and receiving surgery at the university-affiliated referral center between April 2006 and December 2019 were included. After excluding patients who had significant alcohol consumption and hepatitis viral infection,838 patients were divided into two groups according to the L/S ratio of 1 measured by the preoperative low-dose computed tomography: 91 patients(10.9%) with a L/S ratio & lt; 1 vs 747 patients(89.1%) with a L/S ratio≥1. They were also divided into two groups based on the FIB-4 score of 2.67: 804 patients (95.9%) with a FIB-4 score & lt; 2.67 vs 34 patients (4.1%) with a FIB-4 score≥2.67. The Cox proportional hazards model was used to calculate the hazard ratio (HR) and the 95% confidence interval (CI). Results: Patients with NAFLD were older, had higher BMI, and had a higher proportion of mastectomy and hyper-transaminasemia. They showed worse overall, disease-free, and regional recurrence-free survivals compared to those without NAFLD (p=0.008, 0.043, and 0.017, respectively), but no significant differences in local recurrence-free, systemic recurrence-free, and contralateral breast cancer-free survivals. The survival outcome of breast cancer did not show any relationship with NASH-related liver fibrosis (overall survival; p=0.061, disease-free survival; p=0.557). NAFLD was a significant risk factor for mortality in multivariable analysis (HR, 2.077; 95% CI, 1.052–4.102; p=0.035). After stratifying for subtypes of breast cancer, the L/S ratio remained a significant predictor of overall, disease-free, local recurrence-free, and regional recurrence-free survivals in only the hormone receptor-positive/HER2−negative subtype (p=0.007, 0.005, 0.009, and & lt; 0.001, respectively). Conclusion: NAFLD is significantly associated with decreased overall survival, disease-free survival and increased regional recurrence in patients with breast cancer especially the hormone receptor-positive/HER2−negative subtype. NASH-related fibrosis was not associated with survival. Therefore, NAFLD should be assessed in the preoperative setting for predicting long-term prognoses of breast cancer patients Citation Format: Hyunsu Yeoh, Siwon Jang, Jong-Ho Cheun, Jin Ah Kwon, Myoung Seok Lee, Bumjo Oh, In Sil Choi, Sohee Oh, Jongjin Kim, Jeong Hwan Park, Won Kim, Ki-Tae Hwang. Prognostic impact of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis-related liver fibrosis on postoperative long-term outcomes of breast cancer [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P3-05-06.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.SABCS22-P3-05-06
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 10
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    Impact of Breast Cancer Subtypes on Prognosis of Women with Operable Invasive Breast Cancer: A Population-based Study Using SEER Database
    American Association for Cancer Research (AACR) ; 2019
    In:  Clinical Cancer Research Vol. 25, No. 6 ( 2019-03-15), p. 1970-1979
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 25, No. 6 ( 2019-03-15), p. 1970-1979
    Abstract: To determine the prognostic roles of breast cancer subtypes in females with operable invasive breast cancer. Experimental Design: Data of 321,958 patients from Surveillance, Epidemiology, and End Results (SEER) database were analyzed. Breast cancer subtypes were classified into four categories according to the status of hormone receptor (HRc) and HER2: HRc(+)/HER2(−), HRc(+)/HER2(+), HRc(−)/HER2(+), and HRc(−)/HER2(−). Results: Proportions of HRc(+)/HER2(−), HRc(+)/HER2(+), HRc(−)/HER2(+), HRc(−)/HER2(−), and unknown subtype were 70.3%, 9.4%, 3.9%, 10.4%, and 6.0%, respectively. HRc(+)/HER2(−) showed the highest 5-year breast cancer–specific survival (BCSS) rate (95.5%), followed by HRc(+)/HER2(+) (94.1%), HRc(−)/HER2(+) (89.3%), and HRc(−)/HER2(−) (83.1%). HRc(+)/HER2(−) and HRc(+)/HER2(+) showed higher 5-year overall survival (OS) rates (88.4% and 88.2%, respectively) than HRc(−)/HER2(+) and HRc(−)/HER2(−) (83.9% and 76.5%, respectively). HRc(−)/HER2(−) showed the worst BCSS irrespective of race, age, or stage. Although proportions of HRc(−)/HER2(−) in the subgroup with negative event regarding BCSS and OS were 10.4% and 10.2%, respectively, they were 34.2% and 22.7%, respectively, in the subgroup with positive event. Subtype was a significant factor in both univariable and multivariable analyses regarding both BCSS and OS (all P & lt; 0.001). Conclusions: Breast cancer subtype was a significant independent prognostic factor regarding both BCSS and OS in multivariable analyses. HRc(+) subtypes showed better prognosis compared with HRc(−) subtypes regarding both BCSS and OS. HRc(−)/HER2(+) showed better prognosis than HRc(−)/HER2(−) but worse prognosis than HRc(+) subtypes regarding both BCSS and OS. The triple-negative subtype showed the worst BCSS compared with the other subtypes irrespective of race, age, or stage.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-18-2782
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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