凝固因子C4（Clotting Factor C4）
| 型 號： | 美國Seracare |
| 報 價： |  |
美國Seracare凝固因子C4（Clotting Factor C4） 陽性質(zhì)控品對照品 需要了解更多Seracare產(chǎn)品可以咨詢我們，本產(chǎn)品由廣州健侖生物科技有限公司提供
- 產(chǎn)品描述
美國Seracare凝固因子C4（Clotting Factor C4）
廣州健侖生物科技有限公司
廣州健侖長期供應(yīng)各種生物原料，主要代理品牌：美國Seracare、西班牙Certest、美國Fuller等等。
主要產(chǎn)品包括各種標準品、陽性對照品、單克隆抗原抗體。
其中常見的有：弓形蟲病、西尼羅河病毒、類風(fēng)濕因子、瘧疾、麻疹、萊姆病、百日咳桿菌、大腸桿菌、鼠傷寒沙門氏菌、李斯特菌等陽性對照品。
美國Seracare凝固因子C4（Clotting Factor C4）
我司還提供其它進口或國產(chǎn)試劑盒：登革熱、瘧疾、流感、A鏈球菌、合胞病毒、腮病毒、乙腦、寨卡、黃熱病、基孔肯雅熱、克錐蟲病、違禁品濫用、肺炎球菌、軍團菌、化妝品檢測、食品安全檢測等試劑盒以及日本生研細菌分型診斷血清、德國SiFin診斷血清、丹麥SSI診斷血清等產(chǎn)品。
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【Seracare產(chǎn)品介紹】
編號 | 英文名稱 | 中文名稱 |
JL-FA-01 | Amebiasis (AME) | 阿米巴病 |
JL-FA-02 | Allergens, Rast scores | 過敏原，放射性過敏原吸收實驗。指對特定的人群引起免疫反應(yīng)或者過敏反應(yīng)的食品中的蛋白質(zhì) |
JL-FA-03 | Allergens, Rast scores negative | 過敏原，放射性過敏原吸收實驗陰性 |
JL-FA-04 | Anti-cyclic citrullinated peptide Antibody (CCP) Arthritis | 抗環(huán)瓜氨酸肽抗體 |
JL-FA-05 | ASCA Saccharomyces Cerevi | 人抗釀酒酵母抗體（ASCA） |
JL-FA-06 | Aspergillis | 麴菌病 |
JL-FA-07 | Beta 2 Glycoprotein | β2糖蛋白 |
JL-FA-08 | Beta 2 Glycoprotein IgM | β2糖蛋白 IGM |
JL-FA-09 | Bordela Pertussis | 百日咳桿菌 |
JL-FA-10 | Bordela Pertussis IgM | 百日咳桿菌 IGM |
JL-FA-11 | C-ANCA | C-抗中性粒細胞胞漿抗體（ANCA) |
JL-FA-12 | Cardiolipin | 心肌磷脂 |
JL-FA-13 | Cardiolipin IgA | 心肌磷脂 IGA |
JL-FA-14 | Cardiolipin IgG | 心肌磷脂 IGG |
JL-FA-15 | Cardiolipin IgM | 心肌磷脂 IGM |
JL-FA-16 | Cerebral Spinal Fluid | 腦脊髓液 |
JL-FA-17 | Chagas | 恰加斯病/南美錐蟲 |
JL-FA-18 | Chlamydia | 衣原體 |
JL-FA-19 | Chlamydia IgA | 衣原體IGA |
JL-FA-20 | Chlamydia IgG | 衣原體IGG |
JL-FA-21 | Chlamydia IgM | 衣原體IGM |
JL-FA-22 | Chlamydia Neg | 衣原體陰性 |
JL-FA-23 | Clotting Factor C3 | 凝固因子C3 |
JL-FA-24 | Clotting Factor C4 | 凝固因子C4 |
JL-FA-25 | Coccidiodes | 球孢菌 |
JL-FA-26 | Cytomegalovirus (CMV) Neg | 巨細胞病毒抗體陰性 |
JL-FA-27 | CMV IgG | 巨細胞病毒 IGG陽性 |
JL-FA-28 | CMV IgM VCA | 巨細胞病毒 IGM 陽性 |
JL-FA-29 | C-Reactive Protein (CRP) | C-反應(yīng)蛋白質(zhì) |
JL-FA-30 | Dengue Fever | 登革熱 |
JL-FA-31 | Dengue Fever IgM | 登革熱 IGM |
JL-FA-32 | DS (Double Stranded) DNA | 雙鏈脫氧核糖核酸 |
JL-FA-33 | EBNA (Epstein-Barr nuclear antigen) IgG | EB病毒核抗原 IGG |
JL-FA-34 | EBNA (Epstein-Barr nuclear antigen) IgM | EB病毒核抗原 IGM |
JL-FA-35 | Epstein Barr Virus (EBV) Negative Plasma | EB病毒陰性血漿 |
JL-FA-36 | Epstein Barr Virus (EBV) EA IgM | EB病毒早期抗原 IGM |
JL-FA-37 | Epstein Barr Virus (EBV) VCA IgM | EB病毒殼蛋白 IGM |
JL-FA-38 | Epstein Barr Virus (EBV) EA IgG | EB病毒早期抗原 IGG |
JL-FA-39 | EMA (Endomysial Antibodies) | 肌內(nèi)膜 |
JL-FA-40 | Gliadin | 麩蛋白,麥醇溶蛋白,麥膠蛋白 |
JL-FA-41 | Gliadin IgG | 麥醇溶蛋白 IGG |
JL-FA-42 | Gliadin IgA | 麥醇溶蛋白 IGA |
JL-FA-43 | Glomerular Basement Membrane (GBMA) | 腎小球基底膜病 |
JL-FA-44 | Helicobacter pylori IgA | 幽門螺旋桿菌IGA |
JL-FA-45 | Helicobacter pylori IgG | 幽門螺旋桿菌IGG |
JL-FA-46 | Helicobacter pylori IgM | 幽門螺旋桿菌IGM |
JL-FA-47 | Helicobacter pylori Negative | 幽門螺旋桿菌陰性 |
JL-FA-48 | Helicobacter pylori Positive Plasma | 幽門螺旋桿菌陰性血漿 |
JL-FA-49 | Hepatitis A Virus (HAV) Pos. Plasma | 甲型肝炎病毒陽性血漿 |
JL-FA-50 | Hepatitis A Virus (HAV) IgM | 甲型肝炎病毒IGM |
JL-FA-51 | Hepatitis B Core (HBc) IgG | 乙型肝炎病毒核心 IGG |
JL-FA-52 | Hepatitis B Core (HBc) IgM | 乙型肝炎病毒核心 IGM |
JL-FA-53 | Anti Hbe (Antibody to HBV antigen) | 乙肝抗體 |
JL-FA-54 | Hepatitis Delta Virus | 丁型肝炎病毒 |
JL-FA-55 | HBeAg (HBV e antigen) | 乙肝 E抗原 |
JL-FA-56 | anti-HBs (HBV surface antibody) | 乙肝表面抗體 |
JL-FA-57 | Hepatitis B (HBsAg) "Chronic" | 乙型肝炎（乙肝表面抗原）“慢性病 |
JL-FA-58 | HBsAg (HBV surface antigen) Serum | 乙肝表面抗原血清 |
JL-FA-59 | HBsAg (AD) | 乙肝表面抗原（AD） |
JL-FA-60 | HBsAg (AY) | 乙肝表面抗原（AY） |
JL-FA-61 | HBV Positive Plasma | 乙肝陽性血漿 |
JL-FA-62 | HBV DNA Plasma | 乙肝DNA血漿 |
JL-FA-63 | HBV DNA Serum | 乙肝DNA血清 |
JL-FA-64 | HBV DNA type A | A型 乙肝DNA |
JL-FA-65 | HBV DNA type B | B型 乙肝DNA |
JL-FA-66 | HBV DNA type C | C型 乙肝DNA |
JL-FA-67 | HBV DNA type D | D型 乙肝DNA |
JL-FA-68 | HBV DNA type E | E型 乙肝DNA |
JL-FA-69 | HBV DNA type F | F型 乙肝DNA |
JL-FA-70 | HBV Antibody HCV Antibody Plasma CO-INFECTED | 乙肝和丙肝聯(lián)合感染血漿 |
JL-FA-71 | HCV (Hepatitis C Virus) Antibody | 丙型肝炎抗體 |
JL-FA-72 | HCV Core Antigen Positive | 丙肝核心抗原 陽性 |
JL-FA-73 | HCV RNA PLASMA Genotype 1 | 基因1型丙肝RNA 血漿 |
JL-FA-74 | HCV RNA PLASMA Genotype 2 | 基因2型丙肝RNA 血漿 |
JL-FA-75 | HCV RNA PLASMA Genotype 3 | 基因3型丙肝RNA 血漿 |
JL-FA-76 | HCV RNA PLASMA Genotype 4 | 基因4型丙肝RNA 血漿 |
JL-FA-77 | HCV RNA PLASMA Genotype 5 | 基因5型丙肝RNA 血漿 |
JL-FA-78 | HCV RNA PLASMA Genotype 6 | 基因6型丙肝RNA 血漿 |
JL-FA-79 | HCV Riba single band | 丙肝免疫印跡單波段 |
JL-FA-80 | HCV RIBA Pos. (multiple bands) | 丙肝免疫印跡陽性多波段 |
JL-FA-81 | HCV Negative | 丙肝陰性 |
JL-FA-82 | HCV RNA Pos (quantitative) | 丙肝RNA陽性（定量） |
JL-FA-83 | Hepatitis E | 戊型肝炎 |
JL-FA-84 | Herpes Simplex Virus (HSV)1/2 Positive Plasma | 單純性皰疹病毒1/2陽性血漿 |
JL-FA-85 | Herpes Simplex Virus (HSV) 1 Negative Plasma | 單純性皰疹病毒1 陰性血漿 |
JL-FA-86 | Herpes Simplex Virus (HSV) 1 IgG | 單純性皰疹病毒1 IGG |
JL-FA-87 | Herpes Simplex Virus (HSV 1) IgM | 單純性皰疹病毒1 IGM |
JL-FA-88 | Herpes Simplex Virus (HSV) 2 IgG | 單純性皰疹病毒2 IGG |
JL-FA-89 | Herpes Simplex Virus (HSV) 2 IgM | 單純性皰疹病毒2 IGG |
JL-FA-90 | Histone | 組蛋白 |
JL-FA-91 | Human Anti Mouse Ab (HAMA) | 人抗鼠抗體 |
JL-FA-92 | Human immunodeficiency virus (HIV) 1 Neg | HIV I 陰性 |
JL-FA-93 | anti Human immunodeficiency virus (HIV) 1 Plasma | 抗HIV I 血漿 |
JL-FA-94 | anti Human immunodeficiency virus (HIV) 1 Serum | 抗HIV I 血清 |
JL-FA-95 | anti Human immunodeficiency virus (HIV) 2 Western Blot Tested | 抗HIV 2 免疫印跡 |
JL-FA-96 | anti Human immunodeficiency virus (HIV) 1/2 2 HIV (+) | 抗HIV 1/2 2 HIV陽性 |
JL-FA-97 | Human immunodeficiency virus (HIV) Ag | HIV抗原 |
JL-FA-98 | HIV RNA (quantitative) Plasma | HIV RNA 定量血漿 |
JL-FA-99 | HIV RNA (quantitative) Serum | HIV RNA 定量血清 |
JL-FA-100 | HIV1 Subtype A | HIV1 亞型A |
JL-FA-101 | HIV1 Subtype B | HIV1 亞型B |
JL-FA-102 | HIV1 Subtype C | HIV1 亞型C |
JL-FA-103 | HIV1 Subtype D | HIV1 亞型D |
JL-FA-104 | HIV1 Subtype E | HIV1 亞型E |
JL-FA-105 | HIV1 Subtype F | HIV1 亞型F |
JL-FA-106 | HIV1 Subtype G | HIV1 亞型G |
JL-FA-107 | HIV1 Subtype H | HIV1 亞型H |
JL-FA-108 | HIV1 Subtype J | HIV1 亞型J |
JL-FA-109 | HIV1 Subtype K | HIV1 亞型K |
JL-FA-110 | HIV1 Group O | HIV1 亞型O |
JL-FA-111 | Human immunodeficiency virus (HIV) 2 Antibody Plasma | HIV 2 抗體血漿 |
JL-FA-112 | Human immunodeficiency virus (HIV) 2 Antibody Serum | HIV 2 抗體血清 |
JL-FA-113 | HPV (Human Papiloma Virus) Negative | 人乳狀瘤病毒HPV陰性 |
JL-FA-114 | HPV (Human Papiloma Virus) Positive | 人乳狀瘤病毒HPV陽性 |
JL-FA-115 | Human immunodeficiency virus (HIV) Antibody HCV Antibody Plasma COINFECTED | HIV 抗體 HCV |
JL-FA-116 | Human T-cell Lymphotropic Virus (HTLV) I/II | 人嗜T淋巴細胞病毒(HTLV) I/II |
JL-FA-117 | Human T-cell Lymphotropic Virus (HTLV) I | 人嗜T淋巴細胞病毒(HTLV) I |
JL-FA-118 | Human T-cell Lymphotropic Virus (HTLV) II | 人嗜T淋巴細胞病毒(HTLV) II |
JL-FA-119 | Jo-1 | 多發(fā)性肌炎抗原JO-1 |
JL-FA-120 | IgE < 5,000 Ku/L | IgE < 5,000 Ku/L |
JL-FA-121 | Legionella | 軍團桿菌屬 |
JL-FA-122 | Leptospira | 軍團桿菌屬 |
JL-FA-123 | Lyme Disease | 萊姆(氏)病:蜱傳播的全身性疾病,常在夏季發(fā)生 |
JL-FA-124 | Lyme IgG | 萊姆(氏)病 IGG |
JL-FA-125 | Lyme IgM | 萊姆(氏)病 IGM |
JL-FA-126 | Lyme Disease Neg | 萊姆(氏)病 陰性 |
JL-FA-127 | Malaria | 瘧疾 |
JL-FA-128 | Mononucleosis (infectious) | 單核細胞增多癥（有傳染性的） |
JL-FA-129 | Mononucleosis Negative | 單核細胞增多癥陰性 |
JL-FA-130 | Measles Negative | 麻疹 陰性 |
JL-FA-131 | Measles IgG | 麻疹 IGG |
JL-FA-132 | Measles IgM | 麻疹 IGM |
JL-FA-133 | Microsomal Anti-thyroid peroxidase antibody (TPO) Positive Plasma Standard Titer (typically 1,000-3,000 IU/mL) | 微粒體抗甲狀腺過氧化物酶抗體 |
JL-FA-134 | Microsomal Anti-thyroid peroxidase antibody (TPO) Negative Plasma | 微粒體抗甲狀腺過氧化物酶抗體 |
JL-FA-135 | Anti-mitochondrial antibody (AMA) | 抗線粒體抗體 |
JL-FA-136 | Multiple Sclerosis | 多發(fā)性硬化癥 |
JL-FA-137 | Mumps IgG | 流行性腮腺炎 IGG |
JL-FA-138 | Mumps Ab IgM | 流行性腮腺炎抗體 IGM |
JL-FA-139 | Mumps Antibody Negative Plasma | 流行性腮腺炎抗體陰性血漿 |
JL-FA-140 | Mumps Antibody Negative Serum | 流行性腮腺炎抗體陰性血清 |
JL-FA-141 | Myeloma Plasma | 骨髓瘤血漿 |
JL-FA-142 | Myeloma IgA | 骨髓瘤IGA |
JL-FA-143 | Myeloma IgE | 骨髓瘤IGE |
JL-FA-144 | Myeloma IgG | 骨髓瘤IGG |
JL-FA-145 | Myeloma IgM | 骨髓瘤IGM |
JL-FA-146 | Mycoplasma | 支原體 |
JL-FA-147 | Mycoplasma Negative | 支原體陰性 |
JL-FA-148 | Mycoplasma IgG | 支原體IGG |
JL-FA-149 | Mycoplasma IgM | 支原體IGM |
JL-FA-150 | Mycoplasma PCR | 支原體PCR |
JL-FA-151 | Normal Human Plasma | 正常人血漿 |
JL-FA-152 | Normal Human Serum | 正常人血清 |
JL-FA-153 | Nuclear Antibody Centromere | 核抗體著絲粒 |
JL-FA-154 | Nuclear Antibody, Speckled ANA | 核抗體，斑點抗核抗體 |
JL-FA-155 | Nuclear Antibody, Nucleolar ANA | 核抗體,核仁抗核抗體 |
JL-FA-156 | Nuclear Antibody, Homogeneous ANA | 核抗體，同質(zhì)抗核抗體 |
JL-FA-157 | Nuclear Antiobody, Speckled. (ANA) Negative | 核抗體，斑點。抗核抗體陰性 |
JL-FA-158 | P-ANCA (associated neutrophil cytoplasmic antibodies) | 相關(guān)的嗜中性粒細胞胞漿抗體 |
JL-FA-159 | Parietal Cell Antibody (PCA) | 胃)壁細胞抗體 |
JL-FA-160 | Parvo positive plasma | 細小病毒陽性血漿 |
JL-FA-161 | Parvo IgM | 細小病毒 IGM |
JL-FA-162 | Parvo IgG | 細小病毒 IGG |
JL-FA-163 | Parvo Negative Plasma | 細小病毒陰性血漿 |
JL-FA-164 | Parvo DNA positive | 細小病毒 DNA 陽性 |
JL-FA-165 | Phospholipid Positive Plasma | 磷脂陽性血漿 |
JL-FA-166 | Prothrombin | 凝血酶原,凝血因子 |
JL-FA-167 | Rheumatoid Factor (RF) <1000 IU/mL | 類風(fēng)濕因子<1000 IU/mL |
JL-FA-168 | Rheumatoid Factor (RF) 1001-2000 IU/mL | 類風(fēng)濕因子1001-2000 IU/mL |
JL-FA-169 | Rheumatoid Factor (RF) 2001-4000 IU/mL | 類風(fēng)濕因子 2001-4000 IU/mL |
JL-FA-170 | Rheumatoid Factor (RF) 4001-5000 IU/mL | 類風(fēng)濕因子 4001-5000 IU/mL |
JL-FA-171 | Rheumatoid Factor (RF) >5000 IU/mL | 類風(fēng)濕因子>5000 IU/mL |
JL-FA-172 | Ribonucleoprotein (RNP) Positive | 核糖核蛋白陽性 |
JL-FA-173 | Rubella Chimeric | 風(fēng)疹 |
JL-FA-174 | Rubella Negative | 風(fēng)疹陰性 |
JL-FA-175 | Rubella IgG | 風(fēng)疹I(lǐng)GG |
JL-FA-176 | Rubella IgM | 風(fēng)疹I(lǐng)GM |
JL-FA-177 | Rubeola Negative Plasma | 風(fēng)疹陰性血漿 |
JL-FA-178 | Rubeola IgG | 風(fēng)疹I(lǐng)GG |
JL-FA-179 | Scleroderma (Scl-70) Pos | 膠原沉著病,硬皮病,硬皮癥 陽性 |
JL-FA-180 | Scleroderma (Scl-70) Negative | 硬皮病陰性 |
JL-FA-181 | Sickle Cell Fresh Whole Blood | 鐮刀形紅細胞新鮮全血 |
JL-FA-182 | Smith (SM) | 抗Smith抗體陽性血清（SLE的特征性抗體） |
JL-FA-183 | SMITH RNP | 抗RNP抗體陽性血清（SLE的特征性抗體） |
JL-FA-184 | Smooth Muscle (ASMA) | 抗平滑肌抗體陽性血清 |
JL-FA-185 | Sjogren syndrome antigen A (SSA) Positive | 舍格倫綜合征或干燥綜合征抗原A 陽性 |
JL-FA-186 | Sjogren syndrome antigen B (SSB) Positive | 舍格倫綜合征抗原B 陽性 |
JL-FA-187 | Sjogren syndrome antigen B (SSB) Negative | 舍格倫綜合征抗原B陰性 |
JL-FA-188 | Streptolysin O Ab (ASO) | 鏈球菌溶血素O抗體 |
JL-FA-189 | Syphilis (RPR - Rapid Plasma Reagin) Positive Plasma | 梅毒（梅毒-快速血漿反應(yīng)）陽性血漿 |
JL-FA-190 | Syphilis (RPR - Rapid Plasma Reagin) Negative Plasma | 梅毒（梅毒-快速血漿反應(yīng)）陰性血漿 |
JL-FA-191 | Syphilis/ATA/T. pallidum IgG | 梅毒ATA/T，蒼白球IGG |
JL-FA-192 | Syphilis/ATA/T. pallidum IgM | 梅毒ATA/T，蒼白球IGM |
JL-FA-193 | Systemic Lupus Erythematosus (SLE) Positive | 全身性紅斑狼瘡陽性 |
JL-FA-194 | Systemic Lupus Erythematosus (SLE) Negative | 全身性紅斑狼瘡陰性 |
JL-FA-195 | TG/TPO Positive (Standard Titer 1,000 - 3000 IU/mL) | 甲狀腺球蛋白/甲狀腺過氧化物酶陽性 |
JL-FA-196 | TG/TPO Negative | 甲狀腺球蛋白/甲狀腺過氧化物酶陰性 |
JL-FA-197 | TTG (Tissue Transglutaminase) | 組織轉(zhuǎn)谷氨酰胺酶 |
JL-FA-198 | TTG (Tissue Transglutaminase) IgA | 組織轉(zhuǎn)谷氨酰胺酶 IGA |
JL-FA-199 | ToRCH (Toxo, Rubella, CMV, HSV) Positive | 優(yōu)生優(yōu)育（弓形蟲，風(fēng)疹，巨細胞，單胞）陽性 |
JL-FA-200 | ToRCH (Toxo, Rubella, CMV, HSV) Negative | 優(yōu)生優(yōu)育（弓形蟲，風(fēng)疹，巨細胞，單胞）陰性 |
JL-FA-201 | Toxoplasmosis (Toxo) | 弓形蟲病 |
JL-FA-202 | Toxoplasmosis (Toxo) IgG | 弓形蟲病IGG |
JL-FA-203 | Toxoplasmosis (Toxo) IgM | 弓形蟲病IGM |
JL-FA-204 | Thyroglobulin (TG) Positive Plasma | 甲狀腺球蛋白陽性血漿 |
JL-FA-205 | Thyroglobulin (TG) Negative | 甲狀腺球蛋白陰性 |
JL-FA-206 | Varicella-Zoster Virus (VZV) Negative | 水痘-帶狀皰疹病毒陰性 |
JL-FA-207 | Varicella-Zoster Virus (VZV) IgG | 水痘-帶狀皰疹病毒IGG |
JL-FA-208 | Varicella-Zoster Virus (VZV) IgM | 水痘-帶狀皰疹病毒IGM |
JL-FA-209 | West Nile Virus (WNV) | 西尼羅河腦炎病毒 |
JL-FA-210 | West Nile Virus (WNV) IgM | 西尼羅河腦炎病毒IGM |
美國Seracare
此次研究中，研究人員通過導(dǎo)入這個基因的拷貝，實現(xiàn)了該受體的過量表達。而實際生活中，并不能將這一做法應(yīng)用到人身上，因而，研究人員將進一步開發(fā)靶向這一基因的藥物。
一項來自美國俄亥俄州立大學(xué)綜合癌癥中心的證據(jù)顯示，經(jīng)基因修飾的免疫細胞或?qū)Χ喟l(fā)性骨髓瘤的治療有效果，且這些細胞可在實驗室中培養(yǎng)增殖。該研究成果5月28日刊載在Clinical Cancer Research雜志。
研究人員對人類免疫細胞(來自患者的細胞系和骨髓瘤細胞)——T淋巴細胞進行修飾，靶向存在于大多數(shù)(占比95%以上)的骨髓瘤細胞中的CS1分子，以期殺死細胞。研究人員在實驗室中培養(yǎng)增殖這些修飾細胞，然后將其注入動物模型中，殺死人骨髓瘤細胞。
與對照組t細胞相比，修飾T細胞可以更好地識別過表達CS1的多發(fā)性骨髓瘤細胞，并激活。注射修飾T細胞的所有小鼠在接受治療后存活了44天，而在另外兩個對照組中，這一數(shù)據(jù)只有29%和17%。
這種療法的一個重要的優(yōu)勢是，這些治療T細胞在體內(nèi)有復(fù)制潛能，所以或許可以抑制腫瘤生長，長時間內(nèi)避免復(fù)發(fā)。
墨爾本的研究人員證明，A型白血病能成功地‘逆轉(zhuǎn)’通過誘騙癌癥細胞回到正常發(fā)育狀態(tài)。這一發(fā)現(xiàn)使用B-前體急性淋巴細胞白血病(B-ALL)模型，是一種zui常見的影響兒童的癌癥。研究人員揭示關(guān)閉一個稱為Pax5的基因在B-ALL模型中能夠誘發(fā)癌癥，而恢復(fù)它的功能能夠‘治愈’這種疾病。研究發(fā)表在《Genes & Development》期刊上。
研究者之一的劉女士說團隊利用一種發(fā)展的‘基因開關(guān)’技術(shù)去抑制然后再活化Pax5在白血病模型中。
“隨著其它基因變化一起，失活的Pax5驅(qū)動正常血細胞變成白血病細胞，之前已經(jīng)報道過，”劉女士說。“然而我們*揭示重新復(fù)活Pax5能夠使細胞重新開始其正常發(fā)育并丟失那些類似癌癥的特性，有效地治療白血病。吸引我們的是只是回復(fù)Pax5就足夠使這些癌細胞恢復(fù)常態(tài)化，盡管其它基因是改變的。”
白血病中，未成熟白血細胞復(fù)制異常并在骨髓中累積，干擾正常血細胞的產(chǎn)生。
劉女士說在兒童B-ALL中Pax5常常是一個‘消失’的基因。“Pax5對于一種白血細胞——b細胞正常發(fā)育*的，”她說。“當Pax5功能缺乏抵抗力時，發(fā)育中的B細胞陷入一種不成熟狀態(tài)并且變成癌性的。我們證明恢復(fù)Pax5功能，即使是在已經(jīng)發(fā)生癌病的細胞中，移除這個‘阻塞’，使得細胞發(fā)育成正常白血細胞。”
Dickins博士說這項研究揭示了Pax5的功能，是約100種已知‘抑制’人類腫瘤的基因之一。“當這些腫瘤抑制基因通過改變DNA而被失活時，腫瘤開始發(fā)育，”Dickins博士說。
美國Seracare
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【公司名稱】 廣州健侖生物科技有限公司
【】 楊永漢
【】
【騰訊 】 2042552662
【公司地址】 廣州清華科技園創(chuàng)新基地番禺石樓鎮(zhèn)創(chuàng)啟路63號二期2幢101-3室
【企業(yè)文化】
In this study, researchers introduced an overexpression of this gene by introducing a copy of this gene. And in real life, this practice can not be applied to people, so the researchers will further develop drugs that target this gene.
Evidence from the Ohio State University Comprehensive Cancer Center shows that genetically modified immune cells or treatments for multiple myeloma can be effective and that these cells can be cultured and proliferated in the laboratory. The research was published May 28 in Clinical Cancer Research.
Researchers have modified human immune cells (cell lines from patients and myeloma cells), T-lymphocytes, to target CS1 molecules present in the majority (over 95%) of myeloma cells in order to kill cell. The researchers cultured and cultured these modified cells in a laboratory and injected them into animal models to kill human myeloma cells.
Modification of T cells allows better identification and activation of CS1-overexpressing multiple myeloma cells as compared to control t-cells. All mice injected with modified T cells survived for 44 days after treatment, compared with only 29% and 17% of the other two controls.
An important advantage of this therapies is that these therapeutic T cells have the potential to replicate in the body and so may be able to inhibit tumor growth and avoid relapse for long periods of time.
Researchers in Melbourne have demonstrated that type A leukemia can successfully 'reverse' by inducing cancer cells to return to their normal developmental state. This finding, using the B-ALL acute lymphoblastic leukemia (B-ALL) model, is one of the most common cancers in children. Researchers have revealed that the closure of a gene called Pax5 is capable of inducing cancer in the B-ALL model, and restoring its function to 'cure' the disease. Research published in "Genes & Development" journal.
Ms. Liu, one of the researchers, said the team took advantage of a newly developed 'gene switch' technique to repress and then reactivate Pax5 in leukemia models.
"As other genetic changes, inactivated Pax5 drives normal blood cells to become leukemic cells, as previously reported," Ms. Liu said. "However, for the first time, we have shown that resuscitation of Pax5 allows cells to restart their normal development and lose those cancers-like properties that effectively treat leukemias, and it is enough to appeal to Pax5 that these cells are restored to normalization, although other genes are changed."
In leukemia, immature white blood cells replicate abnormally and accumulate in the bone marrow, interfering with the production of normal blood cells.
Ms. Liu said Pax5 is often a 'vanishing' gene in children with B-ALL. "Pax5 is essential for the normal development of a white blood cell-b cell," she said. "When Pax5 function lacks resistance, developing B cells plunge into an immature state and become cancerous.We show that restoring Pax5 function, even in cells where cancer has already occurred, removes this 'obstruction' , Making the cells develop into normal white blood cells. "
Dr. Dickins said the study revealed the function of Pax5 and is one of about 100 genes known to 'suppress' human tumors. "Tumors begin to develop when these tumor suppressor genes are inactivated by changing DNA," says Dr. Dickins.
