人肺癌細胞帶紅色熒光A549+RFP種屬人別稱A549+RFP組織來源肺疾病肺腺癌傳代比例/細胞消化1：2-1:3傳代，消化3-5分鐘培養基配置Ham's F-12K培養基；10%胎牛血清；1%雙抗簡介該細胞系由D.J.Griad通過肺癌組織移植培養建系，患者為58歲白人男性
人肺癌細胞帶紅色熒光 A549+RFP
| 種屬 | 人 |
| 別稱 | A549+RFP |
| 組織來源 | 肺 |
| 疾病 | 肺腺癌 |
| 傳代比例/細胞消化 | 1：2-1:3傳代 ，消化3-5分鐘 |
| 培養基配置 | Ham's F-12K培養基；10%胎牛血清；1%雙抗 |
| 簡介 | 該細胞系由D.J.Griad通過肺癌組織移植培養建系 ，患者為58歲白人男性。A549能通過胞苷二磷酸途徑合成含有 高含量不飽和脂肪酸的。 |
| 形態 | 上皮細胞樣 |
| 生長特征 | 貼壁生長 |
| 倍增時間 | ~22h |
| STR | Amelogenin：X ，Y；CSF1PO：10 ，12；D13S317：11；D16S539：11 ，12；D18S51：14 ，17；
D19S433：13；D21S11：29；D2S1338：24；D3S1358：16；D5S818：11；D7S820：8 ，11；D8S1179： 13 ，14；FGA：23；TH01：8 ，9.3；TPOX：8 ，11；vWA：14； |
| 培養條件 | 氣相 ：空氣 ，95% ；二氧化碳 ，5%。 溫度 ：37攝氏度 ，培養箱濕度為70%-80%。 |
| 凍存條件 | 凍存液 ：90%FBS ，DMSO 10%,
或使用非程序凍存液 ：貨號JY-H040 |
| 備注 | 該細胞是通過慢病毒轉染熒光素酶的穩轉株 ，收到細胞傳代8代左右后 ，若要求需要維持熒光強度 ，建議可以加入嘌呤 霉素進行再次篩選。 |
| 產品使用 | 于科學研究 ，不可作為動物或人類疾病的治療產品使用。 |
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infiltration was reduced , cells were more neatly ar- ranged and fibrous hyperplasia improved; compared with the NC group , the HC group showed significantly higher Ishak score , Ishak stage , liver index , Epithelial ovarian cancer (EOC) can be highly lethal, with limited therapeutic options for patients with non-homologous recombination deficient (HRD) disease. Folate receptor alpha (FOLR1/FRα)-targeting agents have shown promise both alone and in combination with available therapies, but the relationship of FRα to other treatment-driving biomarkers is unknown. The Cancer Genome Atlas (TCGA) was queried to assess protein and mRNA expression and mutational burden in patients with differential FRα protein-expressing ovarian tumors, and the results referenced against the standard 324 mutations currently tested through FoundationOne Companion Diagnostics to identify targets of interest. Of 585 samples within TCGA, 121 patients with serous ovarian tumors for whom FRα protein expression was quantified were identified. FRα protein expression significantly correlated with FOLR1 mRNA expression (p=7.19×10 - 14 ). Progression free survival (PFS) for the FRα-high group (Q1) was 20.7 months, compared to 16.6 months for the FRα-low group (Q4, Logrank, p=0.886). Overall survival (OS) was 54.1 months versus 36.3 months, respectively; however, this result was not significant (Q1 vs. Q4, Logrank, p=0.200). Mutations more commonly encountered in patients with high FRα-expressing tumors included PIK3CA and FGF family proteins. Combinations of FRα-targeting agents with PI3K, mTOR, FGF(R) and VEGF inhibitors warrant investigation to evaluate their therapeutic potential.
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