Supplementary Figure S4 from Triple-Negative PAM50 Non-Basal Breast Cancer Subtype Predicts Benefit from Extended Adjuvant Capecitabine
Karama AslehAña LluchAngela GoytainCarlos H. BarriosXue Q. WangLaura TorrecillasDongxia GaoManuel Ruíz-BorregoSamuel LeungJosé BinesÁngel Guerrero-ZotanoJosé Á. García-SáenzJuan Miguel CejalvoJesús HerránzRoberto TorresJuan de la Haba-RodríguezFrancisco Ayala de la PeñaHenry GómezFederico RojoTorsten O. NielsenMiguel Martín
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Abstract:
<p>Supplementary Figure S4 shows a forest plot of the exploratory categorical analysis of selected (meta)gene expression and their association with disease free survival on the capecitabine arm vs. observation.</p>Keywords:
Triple-negative breast cancer
Basal (medicine)
Categorical variable
Exploratory analysis
Capecitabine is a 5-fluorouracil basedchemotherapeutic drug widely used in the treatmentof solid tumors, especially colorectal and breast. Someof the most common side effects of capecitabine arecutaneous in nature, including hand-foot syndrome(palmar-plantar erythrodysesthesia). Several reports inthe literature link capecitabine use with photosensitivelichenoid eruptions. Herein, we present a case ofcapecitabine-induced lichenoid eruption in an elderlyfemale with metastatic breast cancer and discuss ourfindings in relationship to previously reported cases ofthis and other capecitabine-induced skin pathologies.
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PURPOSE: To report our clinical experience with 25 patients receiving concurrent capecitabine and irradiation in the treatment of locally advanced or resected pancreatic cancer. METHODS AND MATERIALS: We reviewed the medical records of patients with pancreatic cancer who received treatment with capecitabine and irradiation for pancreatic cancer and received capecitabine 1200 to 1600 mg/m(2) orally twice daily Monday through Friday with concurrent radiation (5040-5400 cGy, 180 cGy, 5 days/week), followed by a 4-week rest, then 6 to 8 cycles of capecitabine alone 2000 to 2500 mg/m(2) twice daily for 14 days every 3 weeks (surgically resected), and capecitabine 2000 to 2500 mg/m(2) BID for 14 days every 3 weeks until progressive disease (unresected). RESULTS: The population consisted of 14 females and 11 males, with a median age of 64 years (range 37-80 years). Histology was adenocarcinoma in 23 patients and neuroendocrine tumor in 2 patients. One patient had resected tumor, 3 patients were resected with positive margins, 1 patient was resectable with poor performance status prohibiting resection, and 20 patients had unresected locally advanced disease. Median dose of capecitabine concurrent with radiation was 1500 mg/m(2)/day (600-1600 mg/m(2)/day) given orally in two divided doses, 5 days per week on days of treatment with radiation therapy. Patients received a median total radiation dose of 5040 cGy (4500-5040 cGy) over 6 weeks. Eleven patients were continued on capecitabine cycles after treatment with concurrent capecitabine and irradiation. The median number of cycles completed was 3, with one patient completing 8 cycles. Median survival was 14 months, with 18 patients surviving through the end of the study period. Median overall primary tumor response over the study period was -2% (-100%-100%). Five patients were taken to laparotomy after treatment based on radiographic response and two patients were successfully resected. By the end of the study period, there were 4 complete remissions, 2 partial remissions, 6 stable disease, and 13 progressive disease. Grade 3 or 4 toxicity was observed mainly with gastrointestinal symptoms including nausea, vomiting, diarrhea, and anorexia. Three patients had G3 hand-foot syndrome, 1 patient had G3 peripheral neuropathy, 1 patient had G4 gastrointestinal bleed, and 1 patient had G3 radiation enteritis. There was one death directly related to treatment secondary to uncontrolled GI bleeding. CONCLUSION: In patients with locally advanced pancreatic cancer, concurrent capecitabine and radiation had good survival response in patients and good tumor response. Toxicity of oral capecitabine was well tolerated.
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瞄准：为了估计基于 capecitabine 的治疗和联系复杂并发症的使用，在一个真实世界的治疗背景与胃的食道的癌症(GEC ) 在病人评价。方法：有在 2004 和 2005 之间的主张的病人从 Thomson 路透社 MarketScan (R) 数据库被识别。Capecitabine 政体与 5 氟尿嘧啶(5-FU ) 和另外的化疗政体相比，并且被治疗设定成层。结果：我们与 GEC 识别了 1013 个病人：近似，一半把治疗与 5-FU 政体开始了，而 11% 把治疗与 capecitabine 政体开始了。吝啬的 capecitabine 剂量外套是 2382 +/- 1118 mg/d，和 capecitabine 更经常被用作单音的治疗比在里面联合。总的来说， 5-FU 政体是在 neoadjuvant 和辅助背景的最普通的治疗选择，当另外的 non-capecitabine 政体在首要、第二线的背景更广泛地被使用时。为 capecitabine 政体的全面 unadjusted 复杂并发症率与 5-FU 政体就那的一半被看见。在里面多，变量分析，有的 capecitabine 接受者一 51%(95% CI：26%-81%) 比 5-FU 接受者开发任何复杂并发症的更低的风险做了。开发骨头髓的风险，宪政的、胃肠的道，传染，或皮肤复杂并发症比与 5-FU 与 capecitabine 治疗是更低的。结论：Capecitabine 看起来与 5-FU 相比有有利副作用侧面，它显示它可以是为 GEC 的一种治疗选择。
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Thymidine phosphorylase
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Capecitabine is an orally administered prodrug of 5-fluorouracil (5-FU) and was designed to specifically affect tumor cells more than normal tissues. Capecitabine is as effective and well tolerated as infusional 5-FU in the treatment of advanced gastric cancer (AGC). Following the REAL-2 and ML17032 studies, capecitabine has replaced infusional 5-FU for treating GC. Capecitabine plus platinum is one of the most widely used regimens for the first-line treatment of AGC, regardless of HER2 status. The adjuvant capecitabine/oxaliplatin regimen is one therapeutic option for resectable gastric cancer, especially after D2 resection. Compared with S-1, capecitabine has been shown to have a similar efficacy, but is associated with fewer ethnic differences than S-1, which accounts for the more widespread usage of capecitabine worldwide.
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手術不能または再発乳癌に対するpaclitaxel（PTX）毎週投与（2 週間投与1 週間休薬）とcapecitabine（2 週間投与1週間休薬）併用療法を行い，用量制限毒性（DLT），有害事象の発現割合・程度と推奨用量（RD）を検討した。初回投与量（level 1）をPTX 80 mg/m2，capecitabine 1,255 mg/m2と設定し，capecitabine を2 週間連日経口投与1 週間休薬，PTXをday 1，8 に投与した。3 週間を1 コースとして，level 1 から開始し，各投与levelで3 例に投与し，DLT 規準に抵触した例数により最大耐量（MTD）を求めた。2 コース終了後に安全性の判定を行った。2 コースのプロトコール中の有害事象としては，血液毒性は軽度であった。非血液毒性としては全例に脱毛がみられた。また，末梢神経障害，悪心・嘔吐，食欲不振，倦怠感や便秘がみられた。grade3 以上の有害事象はなく，手足症候群もなかった。次コース投与基準を満たさず，投与延期となった症例はなかった。また，PTX 投与基準を満たさず，PTXがskip となった症例もなかった。level 1 およびlevel 2（PTX 80 mg/m2，capecitabine 1,657 mg/m2）ともDLT はなく，level 2 にてMTDに達しなかったため，PTX 80 mg/ m2，capecitabine 1,657 mg/m2をRD とした。
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Capecitabine is a 5-fluorouracil basedchemotherapeutic drug widely used in the treatmentof solid tumors, especially colorectal and breast. Someof the most common side effects of capecitabine arecutaneous in nature, including hand-foot syndrome(palmar-plantar erythrodysesthesia). Several reports inthe literature link capecitabine use with photosensitivelichenoid eruptions. Herein, we present a case ofcapecitabine-induced lichenoid eruption in an elderlyfemale with metastatic breast cancer and discuss ourfindings in relationship to previously reported cases ofthis and other capecitabine-induced skin pathologies.
Drug eruption
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S-1 and capecitabine are orally administered fluoropyridines reported to be effective in the treatment of advanced gastric cancer(AGC). In fact, both S-1/CDDP and capecitabine/CDDP are considered to be the standard first-line treatments for AGC.However, no information concerning on the activity of capecitabine in S-1-pretreated patients with AGC has been reported. Here, we present a case of recurrent gastric cancer that showed a partial response resulting in 6 months of progres-sion-free survival, thanks to capecitabine/CDDP after the failure of multiple anticancer drugs such as S-1/CDDP. S -1 and capecitabine may exhibit cross-resistance because they both have the same final active metabolite: 5-fluorouracil(5-FU). Dihydropyrimidine dehydrogenase(DPD)is the rate-limiting enzyme in the degradation of 5-FU, and S-1 contains the inhibitor of DPD. Thus, S-1, but not capecitabine, is active against tumors with high DPD expression. On the other hand, capecitabine is activated to 5-FU by thymidine phosphorylase(TP)within the tumor tissue and is more effective against tumors with high TP expression. The present case suggests that S-1 and capecitabine do not always exhibit cross-resistance, and that capecitabine may be effective in S-1-pretreated patients with AGC.
Dihydropyrimidine dehydrogenase
Thymidine phosphorylase
Temozolomide
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