Faculty Profiles - Tanioka Maki

Papers - Tanioka Maki

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Survival outcomes in patients with human epidermal growth factor receptor 2 positive metastatic breast cancer administered a therapy following trastuzumab emtansine treatment. International journal

Rurina Watanuki, Akihiko Shimomura, Shu Yazaki, Shoko Noda-Narita, Hitomi Sumiyoshi-Okuma, Tadaaki Nishikawa, Maki Tanioka, Kazuki Sudo, Tatsunori Shimoi, Emi Noguchi, Kan Yonemori, Kenji Tamura

Medicine 99 ( 38 ) e22331 2020.9

Language：English Publishing type：Research paper (scientific journal)

Since 2013, trastuzumab emtansine (T-DM1) has been widely used in Japan to treat patients with human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer (MBC) who were previously administered trastuzumab and a taxane. However, there is no information about the treatment outcomes after exposure to T-DM1 in Japanese patients with HER2-positive MBC. In this study, we aimed to describe the survival outcomes of patients with HER2-positive MBC who received a treatment following T-DM1 and clarify the predictive factors of their prognosis.We retrospectively identified patients with HER2-positive MBC who received T-DM1 between April 1, 2014, and December 31, 2018, at the National Cancer Center Hospital, and focused on the population that received another line of therapy following T-DM1 discontinuation.Thirty patients were available for the outcome analysis. Median progression-free survival (PFS) of the first subsequent therapy was 6.0 months [95% confidence interval (95% CI) 4.1-6.4], whereas the median overall survival (OS) from the first subsequent therapy was 20.6 months (95% CI 13.5 months to not reached). We divided the patients into 2 groups according to their PFS with T-DM1 treatment and compared their PFS with the subsequent therapy. The results revealed a significant difference in the median PFS with the first subsequent treatment between patients with the PFS of less than and more than 3 months [5.1 (95% CI 1.7-6.2) vs 6.2 (95% CI 4.0-11.3) months, P = .03].This is the first study to evaluate the survival outcomes of post-T-DM1 therapy in Japanese patients with HER2-positive MBC. A short PFS with T-DM1 might affect the PFS with a treatment after T-DM1.

DOI： 10.1097/MD.0000000000022331

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Simple vs. comprehensive prediction models of homologous recombination deficiency based on mutational and clinical features in three independent breast cancer datasets Reviewed

Tanioka Maki, Watanabe Tomoko, Honda Takayuki, Totsuka Hirohiko, Arai Eri, Kanai Yae, Shiraishi Kouya, Tamura Kenji, Kohno Takashi

CANCER RESEARCH 80 ( 16 ) 2020.8

Simple prediction model for homologous recombination deficiency in breast cancers in adolescents and young adults. International journal

Tomoko Watanabe, Takayuki Honda, Hirohiko Totsuka, Masayuki Yoshida, Maki Tanioka, Kouya Shiraishi, Yoko Shimada, Eri Arai, Mineko Ushiama, Kenji Tamura, Teruhiko Yoshida, Yae Kanai, Takashi Kohno

Breast cancer research and treatment 182 ( 2 ) 491 - 502 2020.7

Language：English Publishing type：Research paper (scientific journal)

PURPOSE: Homologous recombination deficiency (HRD), which influences the efficacy of PARP inhibitor- and platinum agent-based therapies, is a prevalent phenotype of breast cancer in adolescents and young adults (AYAs; 15-39 years old). However, HRD score, indicating HRD status, is not routinely assessed in the breast oncology clinic, particularly in patients without germline BRCA1/2 mutations. Hence, we sought to develop a model for determining HRD status based on genetic and clinicopathological factors. METHODS: Subjects were our own cohort of 46 Japanese AYA breast cancer patients and two existing breast cancer cohorts of US and European patients. Models for prediction of the HRD-high phenotype, defined as HRD score ≥ 42, were constructed by logistic regression analysis, using as explanatory variables genetic and clinicopathological factors assessable in the clinical setting. RESULTS: In all three cohorts, the HRD-high phenotype was associated with germline BRCA1/2 mutation, somatic TP53 mutation, triple-negative subtype, and higher tumor grade. A model based on these four factors, developed using the US cohort, was validated in the Japanese and European AYA cases: area under the receiver operating characteristic curve [AUC] was 0.90 and 0.96, respectively. A model based on three factors excluding germline BRCA1/2 mutation also yielded high-predictive power in cases from these two cohorts without germline BRCA1/2 mutations: AUC was 0.92 and 0.90, respectively. CONCLUSIONS: The HRD-high phenotype of AYA breast cancer patients can be deduced from genomic and pathological factors that are routinely examined in the oncology clinic, irrespective of germline BRCA1/2 mutations.

DOI： 10.1007/s10549-020-05716-0

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Unlocking the transcriptomic potential of formalin-fixed paraffin embedded clinical tissues: comparison of gene expression profiling approaches. International journal

Arran K Turnbull, Cigdem Selli, Carlos Martinez-Perez, Anu Fernando, Lorna Renshaw, Jane Keys, Jonine D Figueroa, Xiaping He, Maki Tanioka, Alison F Munro, Lee Murphy, Angie Fawkes, Richard Clark, Audrey Coutts, Charles M Perou, Lisa A Carey, J Michael Dixon, Andrew H Sims

BMC bioinformatics 21 ( 1 ) 30 - 30 2020.1

Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: High-throughput transcriptomics has matured into a very well established and widely utilised research tool over the last two decades. Clinical datasets generated on a range of different platforms continue to be deposited in public repositories provide an ever-growing, valuable resource for reanalysis. Cost and tissue availability normally preclude processing samples across multiple technologies, making it challenging to directly evaluate performance and whether data from different platforms can be reliably compared or integrated. METHODS: This study describes our experiences of nine new and established mRNA profiling techniques including Lexogen QuantSeq, Qiagen QiaSeq, BioSpyder TempO-Seq, Ion AmpliSeq, Nanostring, Affymetrix Clariom S or U133A, Illumina BeadChip and RNA-seq of formalin-fixed paraffin embedded (FFPE) and fresh frozen (FF) sequential patient-matched breast tumour samples. RESULTS: The number of genes represented and reliability varied between the platforms, but overall all methods provided data which were largely comparable. Crucially we found that it is possible to integrate data for combined analyses across FFPE/FF and platforms using established batch correction methods as required to increase cohort sizes. However, some platforms appear to be better suited to FFPE samples, particularly archival material. CONCLUSIONS: Overall, we illustrate that technology selection is a balance between required resolution, sample quality, availability and cost.

DOI： 10.1186/s12859-020-3365-5

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Response to Dabrafenib and Trametinib of a Patient with Metaplastic Breast Carcinoma Harboring a BRAF V600E Mutation. International journal

Takuji Seo, Emi Noguchi, Masayuki Yoshida, Taisuke Mori, Maki Tanioka, Kazuki Sudo, Akihiko Shimomura, Kan Yonemori, Yasuhiro Fujiwara, Kenji Tamura

Case reports in oncological medicine 2020 2518383 - 2518383 2020

Language：English

Background: Metaplastic breast carcinomas are rare and carry poor prognoses. They are also more aggressive than other breast cancers and are known for their resistance to chemotherapy. Prolonged treatment with dabrafenib and trametinib is a therapy for malignant melanoma that improves the progression-free survival and overall survival. Such molecular-targeted therapies are also being developed for cancers with BRAF mutation, a driver of malignant melanoma. Case Presentation. A 57-year-old woman with metaplastic breast cancer and chemotherapy-refractory massive pleural effusion. After contained anthracycline regimen failure, her breast cancer progressed to an advanced stage. We ordered next-generation sequencing- (NGS-) based tumor molecular profiling from core needle biopsy of the breast. The NGS report indicated the presence of a BRAF V600E mutation. After initiation of dabrafenib and trametinib, her symptom and the pleural effusion were decreased. The first assessment of CT scans showed a decreased pleural effusion and shrunken subcutaneous lesions. Approximately 2 weeks later, a new lesion appeared. She died from 12 weeks after initiation of dabrafenib and trametinib treatment. Conclusion: To the best of our knowledge, this is the first report of BRAF mutation breast cancer treated with dabrafenib and trametinib and it heralds the possibility of targeted therapy for rare breast cancers.

DOI： 10.1155/2020/2518383

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[Ifosfamide and Paclitaxel for Recurrent or Metastatic Uterine Carcinosarcoma].

Yohei Ohtake, Kazuki Sudo, Yuki Kojima, Takuji Seo, Hitomi Okuma, Tadaaki Nishikawa, Masaya Uno, Takashi Uehara, Mitsuya Ishikawa, Maki Tanioka, Emi Noguchi, Akihiko Shimomura, Kan Yonemori, Tomoyasu Kato, Yasuhiro Fujiwara, Kenji Tamura

Gan to kagaku ryoho. Cancer & chemotherapy 46 ( 10 ) 1525 - 1529 2019.10

Language：Japanese Publishing type：Research paper (scientific journal)

AIM: This study aimed to retrospectively evaluate the efficacy and safety of ifosfamide plus paclitaxel(IT)in Japanese patients with recurrent or metastatic uterine carcinosarcoma. METHODS: This study included 15 patients who received IT(ifosfamide [1.6 g/m / 2 on days 1-3]and paclitaxel[135mg/m2 on day 1]every 3 weeks)for recurrent or metastatic uterine carcinosarcoma. RESULTS: The overall response rate was 38.4%, and the disease control rate was 92.3%. The median progression- free survival was 7.0 months, and the median overall survival was 9.0 months after initiation of IT therapy. The most common hematological adverse event was Grade 1-2 neutropenia. Peripheral neuropathy of Grade 1 or 2 was observed in 33.3% of cases. There was no treatment-related death. CONCLUSION: IT therapy showed good efficacy and tolerability in Japanese patients with recurrent or metastatic uterine carcinosarcoma.

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I-Boost: an integrative boosting approach for predicting survival time with multiple genomics platforms. International journal

Kin Yau Wong, Cheng Fan, Maki Tanioka, Joel S Parker, Andrew B Nobel, Donglin Zeng, Dan-Yu Lin, Charles M Perou

Genome biology 20 ( 1 ) 52 - 52 2019.3

Language：English Publishing type：Research paper (scientific journal)

We propose a statistical boosting method, termed I-Boost, to integrate multiple types of high-dimensional genomics data with clinical data for predicting survival time. I-Boost provides substantially higher prediction accuracy than existing methods. By applying I-Boost to The Cancer Genome Atlas, we show that the integration of multiple genomics platforms with clinical variables improves the prediction of survival time over the use of clinical variables alone; gene expression values are typically more prognostic of survival time than other genomics data types; and gene modules/signatures are at least as prognostic as the collection of individual gene expression data.

DOI： 10.1186/s13059-019-1640-4

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Identification of Jun loss promotes resistance to histone deacetylase inhibitor entinostat through Myc signaling in luminal breast cancer. International journal

Maki Tanioka, Kevin R Mott, Daniel P Hollern, Cheng Fan, David B Darr, Charles M Perou

Genome medicine 10 ( 1 ) 86 - 86 2018.11

Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: Based on promising phase II data, the histone deacetylase inhibitor entinostat is in phase III trials for patients with metastatic estrogen receptor-positive breast cancer. Predictors of sensitivity and resistance, however, remain unknown. METHODS: A total of eight cell lines and nine mouse models of breast cancer were treated with entinostat. Luminal cell lines were treated with or without entinostat at their IC50 doses, and MMTV/Neu luminal mouse tumors were untreated or treated with entinostat until progression. We investigated these models using their gene expression profiling by microarray and copy number by arrayCGH. We also utilized the network-based DawnRank algorithm that integrates DNA and RNA data to identify driver genes of resistance. The impact of candidate drivers was investigated in The Cancer Genome Atlas and METABRIC breast cancer datasets. RESULTS: Luminal models displayed enhanced sensitivity to entinostat as compared to basal-like or claudin-low models. Both in vitro and in vivo luminal models showed significant downregulation of Myc gene signatures following entinostat treatment. Myc gene signatures became upregulated on tumor progression in vivo and overexpression of Myc conferred resistance to entinostat in vitro. Further examination of resistance mechanisms in MMTV/Neu tumors identified a portion of mouse chromosome 4 that had DNA copy number loss and low gene expression. Within this region, Jun was computationally identified to be a driver gene of resistance. Jun knockdown in cell lines resulted in upregulation of Myc signatures and made these lines more resistant to entinostat. Jun-deleted samples, found in 17-23% of luminal patients, had significantly higher Myc signature scores that predicted worse survival. CONCLUSIONS: Entinostat inhibited luminal breast cancer through Myc signaling, which was upregulated by Jun DNA loss to promote resistance to entinostat in our models. Jun DNA copy number loss, and/or high MYC signatures, might represent biomarkers for entinostat responsiveness in luminal breast cancer.

DOI： 10.1186/s13073-018-0597-3

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Integrated Analysis of RNA and DNA from the Phase III Trial CALGB 40601 Identifies Predictors of Response to Trastuzumab-Based Neoadjuvant Chemotherapy in HER2-Positive Breast Cancer. International journal

Tanioka M, Fan C, Parker JS, Hoadley KA, Hu Z, Li Y, Hyslop TM, Pitcher BN, Soloway MG, Spears PA, Henry LN, Tolaney S, Dang CT, Krop IE, Harris LN, Perou CM

Clinical cancer research : an official journal of the American Association for Cancer Research 24 ( 21 ) 5292 - 5304 2018.7

Language：English Publishing type：Research paper (scientific journal)

Purpose: Response to a complex trastuzumab-based regimen is affected by multiple features of the tumor and its microenvironment. Developing a predictive algorithm is key to optimizing HER2-targeting therapy.Experimental Design: We analyzed 137 pretreatment tumors with mRNA-seq and DNA exome sequencing from CALGB 40601, a neoadjuvant phase III trial of paclitaxel plus trastuzumab with or without lapatinib in stage II to III HER2-positive breast cancer. We adopted an Elastic Net regularized regression approach that controls for covarying features within high-dimensional data. First, we applied 517 known gene expression signatures to develop an Elastic Net model to predict pCR, which we validated on 143 samples from four independent trials. Next, we performed integrative analyses incorporating clinicopathologic information with somatic mutation status, DNA copy number alterations (CNA), and gene signatures.Results: The Elastic Net model using only gene signatures predicted pCR in the validation sets (AUC = 0.76). Integrative analyses showed that models containing gene signatures, clinical features, and DNA information were better pCR predictors than models containing a single data type. Frequently selected variables from the multiplatform models included amplifications of chromosome 6p, TP53 mutation, HER2-enriched subtype, and immune signatures. Variables predicting resistance included Luminal/ER+ features.Conclusions: Models using RNA only, as well as integrated RNA and DNA models, can predict pCR with improved accuracy over clinical variables. Somatic DNA alterations (mutation, CNAs), tumor molecular subtype (HER2E, Luminal), and the microenvironment (immune cells) were independent predictors of response to trastuzumab and paclitaxel-based regimens. This highlights the complexity of predicting response in HER2-positive breast cancer. Clin Cancer Res; 24(21); 5292-304. ©2018 AACR.

DOI： 10.1158/1078-0432.ccr-17-3431

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Increased risk of SSEs in bone-only metastatic breast cancer patients treated with zoledronic acid Reviewed International journal

Masashi Yanaea, Shinichiro Fujimoto, Kaori Tane, Maki Tanioka, Kimiko Fujiwara, Masanobu Tsubaki, Yuzuru Yamazoe, Yoshiyuki Morishima, Yasutaka Chiba, Shintaro Takao, Yoshifumi Komoike, Junji Tsurutani, Kazuhiko Nakagawa, Shozo Nishida

JOURNAL OF BONE ONCOLOGY 8 18 - 22 2017.9

Cisplatin with dose-dense paclitaxel before and after radical hysterectomy for locally advanced cervical cancer: a prospective multicenter phase II trial with a dose-finding study International journal

Maki Tanioka, Satoshi Yamaguchi, Muneaki Shimada, Shoji Nagao, Kazuhiro Takehara, Masato Nishimura, Satoshi Morita, Shunichi Negoro, Kiyoshi Fujiwara, Junzo Kigawa

Medical Oncology 34 ( 8 ) 134 - 134 2017.8

Language：English Publishing type：Research paper (scientific journal) Publisher：Springer Nature

The aim of this study is to evaluate the outcome and safety of the multidisciplinary strategy using cisplatin plus dose-dense paclitaxel (dose-dense TP) before and after radical hysterectomy (RH) for stage IB2, IIA2, or IIB patients with cervical cancer. In the dose-finding phase, 12 patients received 3 cycles of cisplatin (75 mg/m2, day 1) with paclitaxel (70 or 80 mg/m2, days 1, 8, and 15) every 21 days as neoadjuvant chemotherapy (NAC). In the phase II study, 51 patients received 3 cycles of dose-dense TP at the recommended dose as NAC, and another 2 cycles of the same regimen after RH. The primary endpoint was 2-year progression-free survival (PFS). The secondary endpoints were 2-year overall survival (OS), adverse events (AEs), response rate (RR), and pathological complete response (pCR) rates. The recommended dose of paclitaxel at dose-finding phase was 80 mg/m2. In the phase II study, 34 patients (66.7%) had FIGO stage IIB disease. The RR and pCR rates were 94 and 28%. With a median follow-up duration of 58 months, each of the 2- and 5-year PFS rates was 88.2%, the 2- and 5-year OS rates were 94.1 and 88.2%, respectively. The incidence of grade 3/4 AEs was neutropenia (34%), nausea (12%), appetite loss (10%), fatigue (6%), and anemia (6%). Febrile neutropenia was uncommon (2%). Dose-dense TP before and after RH achieved a good long-term survival and was feasible for patients with locally advanced cervical cancer.

DOI： 10.1007/s12032-017-0992-4

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Corrigendum: Proteogenomic integration reveals therapeutic targets in breast cancer xenografts. International journal

Kuan-Lin Huang, Shunqiang Li, Philipp Mertins, Song Cao, Harsha P Gunawardena, Kelly V Ruggles, D R Mani, Karl R Clauser, Maki Tanioka, Jerry Usary, Shyam M Kavuri, Ling Xie, Christopher Yoon, Jana W Qiao, John Wrobel, Matthew A Wyczalkowski, Petra Erdmann-Gilmore, Jacqueline E Snider, Jeremy Hoog, Purba Singh, Beifang Niu, Zhanfang Guo, Sam Qiancheng Sun, Souzan Sanati, Emily Kawaler, Xuya Wang, Adam Scott, Kai Ye, Michael D McLellan, Michael C Wendl, Anna Malovannaya, Jason M Held, Michael A Gillette, David Fenyö, Christopher R Kinsinger, Mehdi Mesri, Henry Rodriguez, Sherri R Davies, Charles M Perou, Cynthia Ma, R Reid Townsend, Xian Chen, Steven A Carr, Matthew J Ellis, Li Ding

Nature communications 8 15479 - 15479 2017.4

Proteogenomic integration reveals therapeutic targets in breast cancer xenografts. International journal

Huang KL, Li S, Mertins P, Cao S, Gunawardena HP, Ruggles KV, Mani DR, Clauser KR, Tanioka M, Usary J, Kavuri SM, Xie L, Yoon C, Qiao JW, Wrobel J, Ding L

Nature communications 8 14864 - 14864 2017.3

Language：English Publishing type：Research paper (scientific journal)

Recent advances in mass spectrometry (MS) have enabled extensive analysis of cancer proteomes. Here, we employed quantitative proteomics to profile protein expression across 24 breast cancer patient-derived xenograft (PDX) models. Integrated proteogenomic analysis shows positive correlation between expression measurements from transcriptomic and proteomic analyses; further, gene expression-based intrinsic subtypes are largely re-capitulated using non-stromal protein markers. Proteogenomic analysis also validates a number of predicted genomic targets in multiple receptor tyrosine kinases. However, several protein/phosphoprotein events such as overexpression of AKT proteins and ARAF, BRAF, HSP90AB1 phosphosites are not readily explainable by genomic analysis, suggesting that druggable translational and/or post-translational regulatory events may be uniquely diagnosed by MS. Drug treatment experiments targeting HER2 and components of the PI3K pathway supported proteogenomic response predictions in seven xenograft models. Our study demonstrates that MS-based proteomics can identify therapeutic targets and highlights the potential of PDX drug response evaluation to annotate MS-based pathway activities.

DOI： 10.1038/ncomms14864

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乳癌骨転移患者におけるゾレドロン酸治療に関する後ろ向きコホート研究

田根香織, 柳江正嗣, 鶴谷純司, 谷岡真樹, 藤本伸一郎, 藤原季美子, 山添譲, 千葉康敬, 中川和彦, 菰池佳史, 高尾信太郎

日本乳癌学会総会プログラム抄録集 23回 358 - 358 2015.7

4-step 4-h carboplatin desensitization protocol for patients with gynecological malignancies showing platinum hypersensitivity: a retrospective study.

Takase N, Matsumoto K, Onoe T, Kitao A, Tanioka M, Kikukawa Y, Yamaguchi S, Fujiwara K, Negoro S

International journal of clinical oncology 20 ( 3 ) 566 - 73 2015.6

Language：English Publishing type：Research paper (scientific journal)

BACKGROUND: Platinum agents are essential for treating gynecological malignancies, particularly ovarian cancer. However, multiple carboplatin doses may cause hypersensitivity reactions (HSRs). Carboplatin desensitization prevents life-threatening HSRs and promotes the successful completion of planned chemotherapy. METHODS: Since January 2010, carboplatin desensitization was performed at our institution. Solutions with 1/1000, 1/100, and 1/10 dilutions of carboplatin and an undiluted solution were prepared in 250 mL of 5% glucose. Each solution was administered as a 1-h intravenous infusion (4-step 4-h protocol). This retrospective analysis was approved by the institutional review board. RESULTS: From January 2010 to December 2013, 20 patients with gynecological malignancies (median age 62 years, range 43-74 years) received desensitization treatment. The International Federation of Gynecology and Obstetrics stages at presentation were I, II, III, and IV in 1, 1, 15, 13 patients, respectively. During first-line and second-line treatments, 3 and 17 patients, respectively, experienced carboplatin-induced HSRs. The median carboplatin cycle number was 11 (range 2-16). In the first desensitization cycle, 17 (85%) patients completed treatment without adverse events, 2 experienced Grade 1 HSRs but completed treatment, and 1 experienced Grade 3 HSR and discontinued treatment. The first desensitization cycle completion rate was 95%. Of 83 desensitization cycles administered, 79 (95.2%) were completed. No treatment-related deaths occurred. CONCLUSIONS: Most patients completed the planned chemotherapy. Our protocol could be conducted safely with shorter duration and simpler procedures than previous protocols. Carboplatin desensitization seems beneficial for patients with a history of carboplatin-induced HSRs; however, the risk of HSR recurrence still remains. Desensitization should therefore be performed only by well-trained staff.

DOI： 10.1007/s10147-014-0731-1

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Dose-dense paclitaxel with cisplatin as perioperative chemotherapy for locally advanced cervical cancer: Early efficacy results of a multicenter phase II study.

Takuma Onoe, Maki Tanioka, Satoshi Yamaguchi, Shinya Sato, Muneaki Shimada, Masato Nishimura, Shinichi Okame, Atsumi Kojima, Junzo Kigawa, Kiyoshi Fujiwara

JOURNAL OF CLINICAL ONCOLOGY 33 ( 15 ) 2015.5

Transcriptional CCND1 expression as a predictor of poor response to neoadjuvant chemotherapy with trastuzumab in HER2-positive/ER-positive breast cancer.

Tanioka M, Sakai K, Sudo T, Sakuma T, Kajimoto K, Hirokaga K, Takao S, Negoro S, Minami H, Nakagawa K, Nishio K

2014.10

Pathologic complete response after neoadjuvant chemotherapy in HER2-overexpressing breast cancer according to hormonal receptor status. International journal

Tanioka M, Sasaki M, Shimomura A, Fujishima M, Doi M, Matsuura K, Sakuma T, Yoshimura K, Saeki T, Ohara M, Tsurutani J, Watatani M, Takano T, Kawabata H, Mukai H, Naito Y, Hirokaga K, Takao S, Minami H

BREAST 23 ( 4 ) 466 - 472 2014.8

HER2陽性乳癌に対するweekly Paclitaxel+TrastuzumabとFEC術前逐次併用療法の追加検討

高尾信太郎, 広利浩一, 前川陽子, 田根香織, 松本光史, 谷岡真樹, 宮下勝, 奥野敏隆, 小西宗治, 重岡靖, 三好康雄

日本癌治療学会誌 49 ( 3 ) 1377 - 1377 2014.6

Applicability of the concept of "platinum sensitivity" to recurrent endometrial cancer: the SGSG-012/GOTIC-004/Intergroup study. International journal

Nagao S, Nishio S, Michimae H, Tanabe H, Okada S, Otsuki T, Tanioka M, Fujiwara K, Suzuki M, Kigawa J

Gynecologic oncology 131 ( 3 ) 567 - 73 2013.12

Language：English Publishing type：Research paper (scientific journal)

OBJECTIVE: The concept of "platinum sensitivity" has been widely applied in the management of recurrent ovarian cancer. This study aimed to evaluate the applicability of this concept to recurrent endometrial cancer. PATIENTS AND METHODS: In this multicenter retrospective cohort study, the clinical data of patients with recurrent endometrial cancer, who had a history of receiving first-line platinum-based chemotherapy and who received second-line platinum-based chemotherapy at the time of recurrence between January 2005 and December 2009 were reviewed. RESULTS: A total of 262 patients from 30 centers with initial FIGO stage classifications of I (29), II (23), III (122), and IV (88) were enrolled. In total, 153 endometrioid adenocarcinomas, 34 serous adenocarcinomas, 17 clear cell adenocarcinomas, 36 carcinosarcomas, and 22 "other" tumors were documented. The response rates for patients with platinum-free intervals of <6 months, 6-11 months, 12-23 months, and ≥24 months were 25%, 38%, 61%, and 65%, respectively. The median progression-free survival after second-line platinum-based chemotherapy for patients with platinum-free intervals of <12 months and ≥12 months was 4.4 (95% confidence interval (CI)=3.7-5.8) months and 10.3 (95% CI=8.2-12.6) months, respectively (log-rank P<0.0001), and the median overall survival was 13.8 (95% CI=10.6-18.1) months and 40.9 (95% CI=25.3-54.2) months, respectively (log-rank P<0.0001). CONCLUSION: Platinum-free interval is a predictor of response and survival after second-line platinum-based chemotherapy in patients with recurrent endometrial cancer. The concept of "platinum sensitivity" could be applicable to recurrent endometrial cancer.

DOI： 10.1016/j.ygyno.2013.09.021

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