消化道癌原代培养体外药敏试验的研究

目的 研究肠癌、胃癌、肝癌细胞在8种不同抗癌药物作用下的细胞抑制率,以筛选出敏感的化疗药物.方法 采用四甲基偶氮唑蓝着色法（MTT）,对97例消化道癌（43例肠癌、33例胃癌、21例肝癌）新鲜瘤组织进行原代细胞培养,同时进行顺铂（DDP）、丝裂霉素（MMC）、卡铂（CBP）、5-氟尿嘧啶（5-FU）、表阿霉素（EADM）、长春新碱（VCR）、羟基喜树碱（OPT）和环磷酰胺（CTX）8种常用化疗药物敏感检测,并对其结果作比较.结果 在肠癌中高度敏感率大于50%药物依次为MMC、5-FU、DDP、CBP.总敏感率大于50%的药物依次为DDP、MMC、5-FU、CBP.在胃癌中高度敏感率大于50%的药物依次为DDP、CBP.总敏感率大于50%的药物依次为DDP、CBP、MMC、5-FU、CTX、VCR.其中胃癌对CTX、VCR的敏感率明显高于肠癌细胞（P＜0.05）.肝癌细胞中高度敏感率＞50%的药物为零,而总敏感率＞50%的药物依次排序为MMC、EADM、CBP.结论 消化道肿瘤细胞对化疗药物的选择虽有一定共性,但同种肿瘤的不同个体对同种化疗药物的敏感性差异却存有显著性.体外检测消化道肿瘤对化疗药物的敏感性可为临床化疗提供指导.     

88例卵巢上皮性癌行ATP-TCA体外药敏试验结果分析

该研究是探讨三磷酸腺苷生物荧光肿瘤抗癌药物药敏性分析实验（ATP-TCA）在卵巢癌患者化疗中的应用。研究选取88例卵巢上皮性癌新鲜组织行ATP-TCA体外药敏试验,分析结果、计算各种化疗药物敏感性,并与48例对照组患者进行临床近期有效率的比较。结果显示,在体外药敏试验敏感性最强的单药为紫杉醇（51.9%）,敏感性强弱依次为：紫杉醇〉卡铂〉顺铂〉吉西他滨〉拓泊替康〉多西他赛〉依托泊苷〉环磷酰胺〉博来霉素,联合用药方案敏感性较单药增加。药敏组患者临床近期有效率（85.23%）高于对照（68.75%）。ATP-TCA是一种有效的抗癌药物敏感性分析实验,可为卵巢癌患者临床化疗提供个体化的指导方案。     

甘草次酸-顺铂复合物的制备及其对人肝癌Bel-7402细胞的抗癌活性研究北大核心CSCD

以天然活性成分18β-甘草次酸和抗癌药顺铂为原料,经缩合制备甘草次酸-顺铂（GA-Pt）复合物;利用人肝癌细胞株Bel-7402做体外模型,用MTT法观察GA-Pt对癌细胞增殖的抑制活性。发现目标化合物对肝癌Bel-7402细胞的增殖显明显的抑制活性,浓度在5∽400μg/mL范围内,对肿瘤细胞增殖的抑制率可达29.31%∽92.25%。此结果显示,肝癌Bel-7402细胞对甘草次酸顺铂类复合物具有较好的敏感性;甘草次酸与顺铂的偶合可提高顺铂的抗癌活性,这可能是产生抗癌协同及化疗增敏作用的结果。此结果对新型肝靶向抗癌候选药物的筛选奠定了一定的基础。     

甘草次酸-顺铂复合物的制备及其对人肝癌Bel-7402细胞的抗癌活性研究

以天然活性成分18β-甘草次酸和抗癌药顺铂为原料,经缩合制备甘草次酸-顺铂(GA-Pt)复合物;利用人肝癌细胞株Bel-7402做体外模型,用MTT法观察GA-Pt对癌细胞增殖的抑制活性。发现目标化合物对肝癌Bel-7402细胞的增殖显明显的抑制活性,浓度在5~400μg/mL范围内,对肿瘤细胞增殖的抑制率可达29.31%~92.25%。此结果显示,肝癌Bel-7402细胞对甘草次酸顺铂类复合物具有较好的敏感性;甘草次酸与顺铂的偶合可提高顺铂的抗癌活性,这可能是产生抗癌协同及化疗增敏作用的结果。此结果对新型肝靶向抗癌候选药物的筛选奠定了一定的基础。     

β-tubulinIII在食管癌中的表达及在个体化化疗方案中的作用

目的：探讨β—tubulinIII在食管癌组织中的表达,分析其与食管癌生物学行为的关系,及根据其表达结果制定个体化化疗方案的疗效。方法：应用免疫组化（SP）法检测β-tubulinIII在55例食管癌组织中的阳性表达,采用X^2检验方法分析其阳性表达与肿瘤临床病理学特征之间的关系。依据低表达（阴性）对紫杉类抗微管药物相对敏感,选用紫杉醇联合顺铂方案;高表达（阳性）相对不敏感的原则,选择吉西他滨联合顺铂方案。对照组选用紫杉醇联合顺铂化疗方案。比较两组客观缓解率（ORR）及疾病控制率（DCR）的差异,及无进展生存时间（PFS）和中位生存期（MST）的差异。结果：B—tubulinIII在55例食管癌组织中阳性表达为16例（29．09％）,在肿瘤组织中的表达与食管癌的浸润深度、淋巴结转移及肿瘤分期相关（P〈0．05）,而与年龄、性别、组织学分化程度无关（P〉0．05）。实验组ORR为54．55％（30／55）优于对照组32．50％（13／40）,x^2=-4．543,P=0．033;DCR为69．09％（38／55）优于对照组47．50％（19／40）,xZ=-4．498,P=0．034。差异有统计学意义。实验组与对照组的PFS分别为5．2月和4．5月（x^2=4．215,P=0．040）,MST分别为8．9月和7．4月（x^2=6．146,P=0．013）,差异有统计学意义。结论：食管癌细胞存在β-mbulin III的表达,且与肿瘤细胞的浸润深度、淋巴结转移及临床分期相关。检肿瘤标本中13-tubulinⅢ表达,有助于为实施个体化化疗提供一种选择药物的方法。     

γ—谷氨酸半胱氨酸合成酶（γ—GCS）与肿瘤耐药

谷胱甘肽（glutathione,GSH）及其相关酶类对化疗药物的解毒作用是恶性肿瘤化疗耐药形成的主要原因之一。γ-谷氨酰半胱氨酸合成酶（γ-GCS）是GSH体内生物合成的限速酶,大量的体外及临床实验已证实γ-GCS与多种肿瘤细胞的耐药有关,抑制γ-GCS活性可降低细胞内GSH水平,同时使肿瘤细胞耐药得到不同程度的逆转。本文综述了γ-GCS的生物学特性、基因表达的调控及在肿瘤耐药形成中的作用。     

bFGF反义寡核苷酸增强鼠黑色素瘤B16细胞化疗药物敏感性研究

目的:研究bFGF反义硫代寡核苷酸增强肿瘤细胞对化疗药物敏感性作用。方法:设计、合成bFGF寡核苷酸,用聚乙烯亚胺(polyemyleneimine,PEI)介导bFGF反义硫代寡核苷酸转染入黑色素瘤B16细胞,MTT法检测bFGF反义硫代寡核苷酸及其与化疗药物联合处理后的细胞增殖率;半定量RT-PCR测定bFGF反义硫代寡核苷酸转染后细胞中bFGF mRNA水平;流式细胞仪分析bFGF反义硫代寡核苷酸诱导的细胞凋亡。结果:bFGF反义硫代寡核苷酸对B16细胞增殖的抑制率为64.8%,且呈剂量依赖效应。B16细胞中bFGF mRNA被bFGF反义硫代寡核苷酸显著降低,为对照细胞的57.9%,且bFGF反义硫代寡核苷酸诱导B16细胞凋亡,凋亡率为41.8%。bFGF反义硫代寡核苷酸转染能显著增强B16细胞对阿霉素、5-氟脲嘧啶及顺铂的敏感性,非特异性硫代寡核苷酸不影响阿霉素、5-氟脲嘧啶及顺铂抑制B16细胞增殖。结论:bFGF反义硫代寡核苷酸显著增强B16细胞的化疗敏感性,表明其可协同化疗药物用于治疗肿瘤。     

ERCC1多态性与肺癌铂类化疗耐药的关系研究

目的：研究DNA切除修复交叉互补基因1（excision repair cross-complementing gene1,ERCC1）单核苷酸多态性与非小细胞肺癌铂类药物化疗敏感性的关系。方法：应用基因测序方法检测89例以铂类药物为主要化疗方案的非小细胞肺癌患者的ERCC1 Asn118Asn基因型,,比较不同基因型与化疗疗效的关系。结果：89例患者化疗总有效率为29.2%。携带ERCC1 CC基因型、含至少一个变异基因型（TC和TT基因型）患者的有效率分别为38.5%和61.5%（X2=2.151,p=0.142）,基因型在化疗有效组和无效组之间的分布无差异（p〉0.05）。结论：ERCC1Asn118Asn单核苷酸多态性可能与非小细胞肺癌对铂类药物化疗的敏感性无关。     

体外药物敏感实验为依据的恶性脑胶质瘤个体化化疗初步研究

目的:建立胶质瘤细胞体外原代培养模型,利用MTT法进行体外药物敏感实验,为临床化疗方案的设计提供理论指导,实施个体化化疗。方法:32例术后病理证实为胶质瘤(WHOⅢ级)的新鲜标本,制备肿瘤单细胞悬液进行体外原代培养,与7种抗肿瘤药物在临床血浆峰值浓度(PPC)条件下作用72小时,MTT法标记存活的肿瘤细胞,用酶标仪检测光密度值(OD),计算出抑制率(IR),检测不同肿瘤个体对化疗药物的敏感和耐药情况,从而指导临床个体化化疗方案的制定。另选取同期符合上述入选标准的20例间变型星形细胞瘤患者作为对照组,按照VM-26加DDP方案经验化疗,化疗4个疗程结束后,复查影像学,按照WHO肿瘤疗效评价标准评价治疗效果,分为稳定(SD),进展(PD),缓解(PR)。结果:32例临床标本的原代培养及药敏试验,其PPC下的抑制率(IR%)>50%者,DDP有20例;VCR有9例;VM-26有12例;VP-16有17例;Procarbazine有7例;BCNU有6例;Taxol有3例;其敏感性依次为:DDP>VP-16>VM-26>VCR>Procarbazine>BCNU>Taxol。根据体外药物敏感实验结果制定个体化化疗方案治疗29例,肿瘤缓解率为47.2%,对照组为29.4%,2组x2检验统计P<0.05。结论:7种常用的抗肿瘤药物均有耐药的情况,进行化疗药物的敏感测定可以避免耐药药物的使用。根据体外药物敏感实验结果制定个体化化疗方案化疗与对照组相比近期疗效较满意。     

体外胶质瘤细胞原代培养对不同化疗药物敏感性初步研究

目的:现察7种抗肿瘤药物对体外原代培养的胶质瘤细胞的作用,为临床化疗方案的设计提供参考.方法:32例术后病理证实为胶质瘤的新鲜标本取材,制备肿瘤单细胞悬液进行体外原代培养,与肿瘤药DDP,VM-26,VP-16,BCNU,VCR,PCB,Taxol的临床血浆峰值浓度(PPC)作用72小时,MTT法检测不同肿瘤个体对不同化疗药物的敏感和耐药情况.结果:成功进行了32例临床标本的原代培养及药敏试验,其PPC下的抑制率(IR%)＞50%者,DDP有14例;VCR有5例;VM-26有7例;VP-16有9例;PCB有3例;BCNU有2例;Taxoi有1例;其敏感性依次为:DDP＞VP-16＞VM-26＞VCR＞PBZ＞BCNU＞Taxol.结论:7种常用的抗肿瘤药物均有耐药的情况,进行化疗药物的敏感测定可以避免耐药药物的使用,为提高临床化疗效果提供指导.     

胃癌细胞对化疗药物的敏感性及其与Pgp、GST-π和Topo Ⅱ表达的关系

目的探讨胃癌在体外对化疗药物的敏感性和与P-糖蛋白(P-glycoprotein Pgp)、谷胱甘肽S转移酶π(glutathione-S-transferase GST-π)和拓扑异构酶Ⅱ(topoisomeraseⅡ TopoⅡ)表达的关系。方法收集81例手术切除胃癌标本,制备单细胞悬液,分别加入HCPT、CDDP、ADM、5-Fu和MMC培养48h,用MTT比色法检测胃癌细胞对化疗药物的敏感性;免疫组化技术检测Pgp、GST-π和TopoⅡ蛋白在胃癌组织中的表达。结果胃癌细胞对不同化疗药物敏感性不同:5-Fu(43.4±9.2)、CDDP(41.9±8.7)和HCPT(40.6±8.3)对胃癌细胞的抑制率与ADM(31.6±7.8)和MMC(28.7±7.3)比较有统计学意义(P0.05)。胃癌组织中Pgp、GST-π和TopoⅡ蛋白的阳性率分别为61.33%、65.33%和68.00%。Pgp阳性者显示对ADM、HCPT有明显的体外耐药性(P0.05),GST-π在5-Fu、CDDP和MMC耐药组阳性率显著高于敏感组(P0.05),而TopoⅡ在HCPT、ADM和MMC耐药组中的表达显著低于敏感组(P0.05)。结论 Pgp、GST-π和TopoⅡ可以作为胃癌对化疗药物原发性耐药的标志,结合MTT药敏检测,有助于筛选有效化疗药物。     

小干扰RNA干扰缺氧诱导因子-1α增强口腔鳞癌细胞株化疗敏感性

目的:探讨针对缺氧诱导因子-1α(HIF-1α)的小干扰RNA(siRNA)对口腔鳞癌细胞(OSCC)化疗敏感性的影响。方法:用Western印迹检测OSCC和针对HIF-1α基因的siRNA导入OSCC后的HIF-1α蛋白表达水平;用MTT法检测细胞对化疗敏感性的影响;用流式细胞术检测化疗诱导细胞凋亡的凋亡率。结果:HIF-1α在OSCC中高表达,HIF-1α-siRNA转染后HIF-1α表达水平明显下降,细胞对化疗敏感性明显提高,化疗诱导肿瘤细胞凋亡率明显增加。结论:针对HIF-1α基因的siRNA能明显降低HIF-1α的表达,增强化疗对OSCC的凋亡诱导作用,有效提高OSCC对化疗的敏感性。     

Effect of selenite combined with chemotherapeutic agents on the proliferation of human carcinoma cell lines

Selenite is frequently used in combination with cancer chemotherapeutic agents to reduce side effects. However, the cytoprotective activity of selenite may also reduce the efficacy of chemotherapeutic drugs on tumor cells. This study was designed to examine the effects of selenite combined with cytotoxic agents used in clinical protocols [e.g., doxorubicine, docetaxel, 5-fluorouracil (5-FU), methotrexate (MTX), mafosphamide, mitomycin C, gemcitabine, etoposide, cisplatin, irinotecan, and oxaliplatin] on the proliferation of various carcinoma cell types. The data demonstrated that selenite had no marked effects on the antiproliferative activity of docetaxel, doxorubicine, 5-FU, MTX, and mafosphamide in MDA-MB-231 breast cancer cells. Likewise, no consistent changes were observed in A549 lung cancer cell proliferation when selenite was combined with cisplatin, etoposide, gemcitabine, or mitomycin C. On the other hand, selenite potentiated the cytotoxicity of 5-FU, oxaliplatin, and irinotecan in HCT116 colon cancer cells by approx 1.1-fold, 2.7-fold, and 2.6-fold, respectively. In SW620 colon cancer cells, selenite induced a 1.5-fold and 4.3-fold increase of the antiproliferative activity of 5-FU and oxaliplatin, respectively. Whereas irinotecan showed no effects on SW620 cell growth, a combination with selenite resulted in 23% inhibition. Our results indicate that selenite did not reduce the antiproliferative activity of chemotherapeutic agents in vitro. In addition, selenite was able to increase the inhibitory activity of docetaxel in A549 lung cancer cells, and of 5-FU, oxaliplatin, and irinotecan in HCT116 and SW620 colon cancer cells implying selenite is potentially useful as an adjuvant chemotherapeutic agent.     

Methyl jasmonate: A plant stress hormone as an anti-cancer drug

Jasmonates act as signal transduction intermediates when plants are subjected to environmental stresses such as UV radiation, osmotic shock and heat. In the past few years several groups have reported that jasmonates exhibit anti-cancer activity in vitro and in vivo and induce growth inhibition in cancer cells, while leaving the non-transformed cells intact. Recently, jasmonates were also discovered to have cytotoxic effects towards metastatic melanoma both in vitro and in vivo.Three mechanisms of action have been proposed to explain this anti-cancer activity. The bio-energetic mechanism – jasmonates induce severe ATP depletion in cancer cells via mitochondrial perturbation. Furthermore, methyl jasmonate (MJ) has the ability to detach hexokinase from the mitochondria. Second, jasmonates induce re-differentiation in human myeloid leukemia cells via mitogen-activated protein kinase (MAPK) activity and were found to act similar to the cytokinin isopentenyladenine (IPA). Third, jasmonates induce apoptosis in lung carcinoma cells via the generation of hydrogen peroxide, and pro-apoptotic proteins of the Bcl-2 family.Combination of MJ with the glycolysis inhibitor 2-deoxy-d-glucose (2DG) and with four conventional chemotherapeutic drugs resulted in super-additive cytotoxic effects on several types of cancer cells. Finally, jasmonates have the ability to induce death in spite of drug-resistance conferred by either p53 mutation or P-glycoprotein (P-gp) over-expression.In summary, the jasmonates are anti-cancer agents that exhibit selective cytotoxicity towards cancer cells, and thus present hope for the development of cancer therapeutics.     

In vivo antitumor activity of hydrosoluble derivatives of 7-hydroxycholesterols

Sodium bis-hemisuccinates of 7 beta- and 7 alpha-hydroxycholesterols are moderately water-soluble. They have been tested intraperitoneally against the murine Krebs-II carcinoma, grown as an ascitic tumour, and their action has been compared with that of usual chemotherapeutic drugs, cyclophosphamide, 5-fluoro-uracil, and methotrexate. The hydroxycholesterol derivatives show a faster and stronger activity (life prolongation), and lead to the complete disappearance of the tumour in about 1/3 of the cases, even with one single injection. Similar results have been obtained (on fewer cases) with two other experimental ascitic tumours, the S-180 sarcoma and the ZHC hepatoma. The mechanism of action is not known; it appears to be very different from that of the usual anti-cancer chemotherapeutic agents.     

p53 inhibits adriamycin-induced down-regulation of cyclin D1 expression in human cancer cells.

The tumor suppressor p53 gene product is an essential component of the cytotoxic pathway triggered by DNA-damaging stimuli such as chemotherapeutic agents and ionizing radiation. We previously demonstrated that adenovirus-mediated wild-type p53 gene transfer could enhance the cytotoxic actions of chemotherapeutic drugs both in vitro and in vivo; however, the molecular mechanism of this chemosensitization is still unclear. Cyclin D1 is a major regulator of the progression of cells into the proliferative stage of the cell cycle. Here we show that infection with an adenovirus vector expressing the wild-type p53 gene (Ad-p53) caused an increase in cyclin D1 protein levels in human colorectal cancer cell lines DLD-1 and SW620; treatment with the anti-cancer drug adriamycin, however, down-regulated their cyclin D1 protein expression in a dose-dependent manner. The suppression of cyclin D1 expression following adriamycin treatment could be blocked by simultaneous Ad-p53 infection. Furthermore, DLD-1 and SW620 cells transfected with the cyclin D1 expression construct displayed increased sensitivity to adriamycin compared to that of the vector-transfected control. Our results suggest that ectopic wild-type p53 gene transfer results in increased cyclin D1 expression and, consequently, sensitizes human colorectal cancer cells to chemotherapeutic agents.     

De novo ceramide synthesis is responsible for the anti-tumor properties of camptothecin and doxorubicin in follicular thyroid carcinoma

Doxorubicin and camptothecin are two cytotoxic chemotherapeutic agents triggering apoptosis in various cancer cells, including thyroid carcinoma cells. Recent studies revealed a critical role of ceramide in chemotherapy and suggested that anti-cancer drugs may kill tumor cells through sphingomyelinase activation. However, in comparison to sphingomyelin hydrolysis, the relative involvement of de novo ceramide synthesis remained poorly explored and highly controversial. Here, we evidenced that both doxorubicin and camptothecin triggered ceramide accumulation in thyroid carcinoma cells. We demonstrated that ceramide increase occurred via the de novo pathway without neither acidic nor neutral sphingomyelinase contribution. Interestingly, de novo ceramide generation was responsible for the drug-induced malignant cell apoptosis through a caspase-3-dependent pathway and a decrease of thrombospondin amount. Furthermore, blocking ceramide metabolism by inhibiting glucosylceramide synthase strengthened the camptothecin and doxorubicin-dependent effects. Altogether, we evidenced that de novo ceramide synthesis mediates the anti-tumor properties of doxorubicin and camptothecin in thyroid carcinoma and suggested that glucosylation of ceramide may contribute to the drug-resistance phenotype in thyroid malignancies.     

252例胸膜恶性肿瘤的临床病理分析

目的：探讨胸膜恶性肿瘤的病理类型、肿瘤所占比例、临床病理特征及鉴别诊断。方法：结合病理形态学及免疫组化方法对252例胸膜恶性肿瘤进行诊断及鉴别诊断。结果：252例胸膜恶性肿瘤包括胸膜穿刺活检120例,胸腔镜活检25例,伴有胸膜转移的恶性胸水107例;男性143例,女性109例,年龄19—87岁,平均年龄59．9岁。临床主要症状是胸闷、气短、咳嗽、胸痛等。CT表现为胸膜增厚、胸水（90％）、多发或单发胸膜结节和原发器官占位性病变。活检病例中,转移性癌86例（34．1％）,包括肺腺癌64例（25．4％）,小细胞癌11例（4．4％）,鳞癌11例（4．4％）,恶性间皮瘤47例（18．7％）,滑膜肉瘤9例（3．6％）,非霍奇金淋巴瘤3例（1．2％）;恶性胸水病例病例中转移性癌95例（37．7％）,包括肺腺癌85例（33．7％）,小细胞癌6例（2．4％）,鳞癌2例（0．8％）,乳腺腺癌2例（0．8％）,恶性间皮瘤8例（3．2％）,非霍奇金淋巴瘤4例（1．6％）。结论：胸膜恶性肿瘤中以转移性腺癌多见,其次为恶性间皮瘤,结合形态学及免疫组织化学检测不同标志物的表达有助于诊断胸膜恶性肿瘤的种类。     

Non-antioxidant properties of α-tocopherol reduce the anticancer activity of several protein kinase inhibitors in vitro

The antioxidant properties of α-tocopherol have been proposed to play a beneficial chemopreventive role against cancer. However, emerging data also indicate that it may exert contrasting effects on the efficacy of chemotherapeutic treatments when given as dietary supplement, being in that case harmful for patients. This dual role of α-tocopherol and, in particular, its effects on the efficacy of anticancer drugs remains poorly documented. For this purpose, we studied here, using high throughput flow cytometry, the direct impact of α-tocopherol on apoptosis and cell cycle arrest induced by different cytotoxic agents on various models of cancer cell lines in vitro. Our results indicate that physiologically relevant concentrations of α-tocopherol strongly compromise the cytotoxic and cytostatic action of various protein kinase inhibitors (KI), while other classes of chemotherapeutic agents or apoptosis inducers are unaffected by this vitamin. Interestingly, these anti-chemotherapeutic effects of α-tocopherol appear to be unrelated to its antioxidant properties since a variety of other antioxidants were completely neutral toward KI-induced cell cycle arrest and cell death. In conclusion, our data suggest that dietary α-tocopherol could limit KI effects on tumour cells, and, by extent, that this could result in a reduction of the clinical efficacy of anti-cancer treatments based on KI molecules.     

Cancer chemopreventive pharmacology of phytochemicals derived from plants of dietary and non-dietary origin: implication for alternative and complementary approaches

The poor survival statistics of the fatal cancer diseases highlight the need for multiple alternative treatment options. An impressive embodiment of evidence shows that naturally occurring herbal products contain a wide variety of phytochemicals that are regarded as effective cancer protective agents, possessing the ability to retard, block or reverse carcinogenesis. These include dietary agents often termed as nutraceuticals and also the components of non-dietary plants. Many studies in different cell lines, animal models and human epidemiological trials suggest a protective role of a large number of medicinal molecules of herbal origin against different types of cancers. The standard chemotherapeutic regime against cancer faces an unequivocal challenge due to the severity of the side-effects and the post therapeutic management of the disease. Cancer control may therefore benefit from the anti-cancer potential of alternative therapies that may include herbal treatment which nonetheless has been an effective curative strategy reported for a number of diseases since ancient times. In congruence of the above idea, it has been observed that in recent years the demand to utilize alternative approaches to the treatment of cancer is escalating. Additionally, the emergence of resistance to cancer chemotherapy has forced researchers to turn to natural products of herbal and marine origin. Currently, in the armamentarium of anti-cancer pharmaceuticals there are effective plant-derived drugs such as paclitaxel (a complex taxane diterpene isolated from the bark of Taxus brevifolia) which acts as microtubule disruptor. Further there are plant-based dietary agents such as sulphoraphane (an isothiocyanate derived from cruciferous vegetables) and non-dietary agents such as pomiferin (an isoflavonoid from Maclura pomifera) which strongly mimic chemotherapeutic drugs such as vorinostat (suberoylanilidehydroxamic acid) possessing histone diacetylase inhibition activity. In this review we provide a comprehensive outline of the translational potential of plant-based herbal medicine for complementing the current treatment modalities as an adjuvant or alternative therapy for cancer patients.