ZEZ-2型智能癌肿治疗仪原理与设计

ＺＥＺ－２型智能癌肿治疗仪治疗癌肿，是基于电化学治疗肿瘤的机理。与其它电化学癌肿治疗仪相比，该仪器具有治疗路数多，阳极可控稳流，阴极自动均流，整个治疗过程自动管理等特点，是一种能满足临床应用需要的新型治疗仪器。

ZEZ-4型便携式智能癌肿治疗仪原理与设计

介绍一种便携式电化学癌肿治疗仪，该仪器采用单片机控制，具有６ 路阳极独立可控稳流输出，１６ 路阴极自动均流，整个治疗过程自动管理。与其它电化学癌肿治疗仪相比，该仪器具有精度高，操作携带方便等特点，是一种满足临床需要的新型治疗仪器。

泛素-蛋白酶体途径与疾病

泛素一蛋白酶体途径（ubiquitin—proteasome pathway,UPP）是一种高效的蛋白分解途径，其生物学作用非常广泛，该途径的异常与诸多疾病如遗传性疾病、炎症、自身免疫性疾病及肿瘤等有密切关系。泛素-蛋白酶体自被发现以来，受到了极大的关注和重视。在2004年，以色列科学家阿龙．切哈诺沃、阿夫拉姆．赫尔什科和美国科学家欧文．罗斯因发现了泛素对蛋白质降解的调节，获得了诺贝尔化学奖。近期已注意到UPP在癌肿治疗中的作用，并已开展了以泛素-蛋白酶体为靶的治疗试验。目前对UPP的研究已经取得了很大的进展。本文就UPP与疾病和治疗的关系进行综述。

Expression of HMGB1 Protein in Human Cervical Squamous Epithelium Carcinoma

OBJECTIVE To investigate the expression of the high mobility group boxl（HMGB1） in human cervical squamous epithelial carcinoma （CSEC） and to explore the relationship of HMGB1 expression to the differentiation degree, size, invasion and metastasis of CSEC. METHODS Immunohistochemical staining of tissue microarrays and Western blot analysis were conducted to detect the expression of HMGB1 in the following tissue samples： 30 carcinoma in situ, 90 invasive CSEC without metastasis, 30 invasive CSEC with metastasis, 30 cases of normal cervical squamous epithelia. RESULTS The positive-expression rate of HMGB1 was 58.7% （88/150） in CSEC, showing a significant difference compared to normal cervical squamous epithelia. The expression of HMGB1 was correlated with tumor size, invasion and metastasis of CSEC （respectively, P〈0.01）, but had no relationship with the degree of differentiation （P〉0.05）. CONCLUSION The over-expression of HMGB1 in CSEC might be a useful parameter as an indication of tumor invasion, metastasis, prognosis and overall biological behavior of human CSEC, as well as a noval target site for gene therapy.

Prognostic Impact of Histopathologic Response after Neoadjuvant Chemotherapy in Stage Ⅲ_A Non-small Cell Lung Cancer

Objective： To investigate prognostic impact of histopathologic response induced by neoadjuvant chemotherapy in patients with stage ⅢA non-small cell lung cancer （NSCLC）. Methods： Forty patients with stage ⅢA NSCLC underwent two cycles of neoadjuvant chemotherapy with mitomycin, vindosine, and cisplatin followed by surgery. Histopathologic response in resection of the tumor was examined after surgery. Tumor regression was classified as grade Ⅳ, grade Ⅲ, grade Ⅱ, and grade Ⅰ according to the extent of tumor necrosis and the extent of the vital tumor tissues. The tumor regression grading was correlated with the survival time of the patients. Results： After two cycles of chemotherapy, 19 （47.5%） of 40 patients had objective response （2 complete and 17 partial response）. In 40 resected tumor specimens, 2 （5%） were classified as regression grade Ⅳ, 16 （40%） as regression grade Ⅲ, 18 （45%） as regression gradeⅡ, and 4 （10%） as regression grade Ⅰ. The rate of complete surgical resection was significantly higher in patients with tumor regression grade Ⅲ-Ⅳ （〈10% vital tumor tissue）（P〈0.05）. The median survival time in patients classified as having tumor regression grade Ⅲ-Ⅳ was significantly longer than that in patients who had regression grade Ⅰ-Ⅱ （P〈0.05）. The 3-year survival rate in patients with regression grade Ⅲ-Ⅳ was markedly higher than that in patients who had regression grade Ⅰ-Ⅱ （P〈0.05）. Conclusion： The extent of tumor regression induced by neoadjuvant chemotherapy is a critical issue for successful therapeutic approach in patients with stage ⅢA NSCLC. In resected specimens of tumors after chemotherapy, the presence of marked tumor regression （regression grade Ⅲ-Ⅳ） is predictive for superior survival time.

Significance of the Expression of CyclinD1 and Ki67 Antigen in Nasopharyngeal Carcinoma

Objective: To detect the expression of cyclinD1 and Ki67 in nasopharyngeal carcinoma (NPC) and their correlation with the biological behaviors and prognosis. Methods: 56 cases of biopsy specimens of NPC which had been embedded with para?n in 1996 in our hospital were collected and immunostained with cyclinD1 and Ki67 monoclonal antibodies by means of the streptavidin peroxides method. The patients were followed up periodically, and then their biological behaviors and prognosis were statistically analyzed. Results: The percentage of cyclinD1 and Ki67 positive cells in the NPC specimens ranged from 0–54% and 0–31% respectively. The staining was nuclear. Of the 56 cases, 30 cases (56.6%) highly expressed cyclinD1 or Ki67 HPI and 26 cases (46.4%) lowly expressed cyclinD1, while only 16 cases (28.6%) showed Ki67 HPI (high proliferated index) and 40 cases (71.4%) showed Ki67 LPI (low proliferated index). Patients who lowly expressed cyclinD1 or highly expressed Ki67 had a higher radiosensitivity and a better prognosis. Conclusion: CyclinD1 and Ki67 immunohistochemical staining is considered to be useful, not only as an independent factor of radiosensitivity and prognosis respectively, but also as a means of determining the optimum treatment for each individual patient with NPC.

Histopathological study of hepatocellular carcinoma after transcatheter hepatic arterial embolization

AIMS To study the histopathological changes in hepatocellular carcinoma (HCC) after transcatheter arterial embolization (TAE). METHODS Histopathological analysis was made in 39 cases of liver neoplasms after TAE and 11 cases of liver neoplasms after digital selective angiography (DSA), including pathological type, histological grade, necrotic degree, capsule, times of treatment, injured vessel and lymphocyte infiltration. RESULTS Six cases with 100% necrosis, 14 cases with 30% 95% necrosis, 19 cases with 0% 5% necrosis after TAE and 11 cases without necrosis after DSA were found histologically. The necrosis was related to the pathological type, capsule, injured vessels, but not to the histological grade, time of treatment and lymphocyte infiltration of the liver neoplasms. CONCLUSIONS TAE is an effective therapy for the late stage HCC. The encapsulated HCC is a preferable indicator for TAE.

Effect of Bcl-2 Antisense Oligodeoxynucleotides on Human Lung Carcinoma Transplanted Subcutaneously in Nude Mice

Objective： To investigate the inhibitory effects of the Bcl-2 antisense oligodeoxynucleotides （ASODN） on tumor formation and growth of human lung carcinoma transplanted subcutaneously in nude mice. Methods： Human NCI-H460 cells treated with Bcl-2 ASODN or nonesense oligodeoxynucleotide （NSODN） and untreated NCI-H460 cells were respectively implanted subcutaneously into nude mice. When the diameters of tumor were above 0.5 cm after untreated NCI-H460 cells injection, the mice bearing tumor were randomly divided into three groups： saline control group, Bcl-2 ASODN group, NSODN group. ODN was directly injected into the tumor body for 3 weeks. The weight and volume of subcutaneous tumors were measured, and the morphology of tumor cells was observed. Results： The tumorigenic ability of the treated NCI-H460 cells by Bcl-2 ASODN was reduced. The mean time at which tumor can be detected was prolonged up to 12.6 days （P〈0.01）. The maximum tumor growth inhibitory rate was 87.5%. In therapeutic efficacy, growth of tumor was significantly inhibited in Bcl-2 ASODN group as compared with that in NSODN group, saline-treated group （P〈0.01）. The NSODN control was ineffective. In comparison with NSODN-treated, saline-treated mice, those treated with Bcl-2 ASODN showed a significant decrease in median weight of subcutaneous tumors （P〈0.01）. The growth inhibitory rate was 71.0% in ASODN group. Conclusion： Bcl-2 ASODN could inhibit tumor formation and tumor growth in nude mice.

直肠癌Miles术后会阴复发的防治（附34例报告）

本文报道３４例直肠癌Ｍｉｌｅｓ术后会阴复发，主要表现为会阴部不适和疼痛，局部出现结节或肿块。根据不同情况分别采用局部切除病灶、局部切除加放疗或单纯放疗。作者认为加强术后随防，定期进行ＣＥＡ、ＣＡ－５０和ＣＴ检查，有助于早期发现会阴复发；防止术后复发的主要措施在于首次手术应尽可能达到根治性切除，术前术后应积极配合化疗和放疗。

Adjuvant and neoadjuvant treatment in pancreatic cancer

Pancreatic adenocarcinoma is one of the most aggressive human malignancies,ranking 4th among causes for cancer-related death in the Western world including the United States.Surgical resection offers the only chance of cure,but only 15 to 20 percent of cases are potentially resectable at presentation.Different studies demonstrate and confirm that advanced pancreatic cancer is among the most complex cancers to treat and that these tumors are relatively resistant to chemotherapy and radiotherapy.Currently there is no consensus around the world on what constitutes"standard"adjuvant therapy for pancreatic cancer.This controversy derives from several studies,each fraught with its own limitations.Standards of care also vary somewhat with regard to geography and economy,for instance chemo-radiotherapy followed by chemotherapy or vice versa is considered the optimal therapy in North America while chemotherapy alone is the current standard in Europe.Regardless of the efforts in adjuvant and neoadjuvant improved therapy,the major goal to combat pancreatic cancer is to find diagnostic markers,identifying the disease in a pre-metastatic stage and making a curative treatment accessible to more patients.In this review,authors examined the different therapy options for advanced pancreatic patients in recent years and the future directions in adjuvant and neoadjuvant treatments for these patients.

Over-expressed and truncated midkines promote proliferation of BGC823 cells in vitro and tumor growth in vivo

AIM： To determine whether midkine （M/O and its truncated form （tMK） contribute to gastric tumorigenesis using in vitro and in vivo models. METHODS： Human MK and tMt（ plasmids were constructed and expressed in BGC823 （a gastric adenocarcinoma cell line） to investigate the effect of over-expressed MK or tMK on cell growth and turmorigenesis in nude mice. RESULTS： The growth of MK-transfected or tMK- transfected cells was significantly increased compared with that of the control cells, and tMK-transfected cells grew more rapidly than MK-transfected cells. The number of colony formation of the cells transfected with MK or tMK gene was larger than the control cells. In nude mice injected with MK-transfected or tMK-transfected cells, visible tumor was observed earlier and the tumor tissues were larger in size and weight than in control animals that were injected with cells without the transfection of either genes. CONCLUSION： Over-expressed MK or tMtC can promote human gastric cancer cell growth in vitro and in vivo, and bMK has greater effect than MK. tMK may be a more promising gene therapeutic target compared with MK for treatment of malignant tumors.

Resveratrol engages selective apoptotic signals in gastric adenocarcinoma cells

AIM： To investigate the intracellular apoptotic signals engaged by resveratrol in three gastric adenocarcinoma cancer cell lines, two of which （AGS and SNU-1） express p53 and one （KATO-M） with deleted p53. METHODS： Nuclear fragmentation was used to quantitate apoptotic cells; caspase activity was determined by photometric detection of cleaved substrates; formation of oxidized cytochrome C was used to measure cytochrome C activity, and Western blot analysis was used to determine protein expression, RESULTS： Gastric cancer cells, irrespective of their p53 status, responded to resveratrol with fragmentation of DNA and cleavage of nuclear lamins A and B and PARP. Resveratrol, however, has no effect on mitochondria-associated apoptotic proteins Bcl-2, Bcl- xl, Bax, Bid or Smac/Diablo, and did not promote sub-cellular redistribution of cytochrome C, indicating that resveratrol-induced apoptosis of gastric carcinoma cells does not require breakdown of mitochondrial membrane integrity. Resveratrol up-regulated p53 protein in SNU-1 and AGS cells but there was a difference in response of intracellular apoptotic signals between these cell lines. SNU-1 cells responded to resveratrol treatment with down-regulation of survivin, whereas in AGS and KATO- 111 cells resveratrol stimulated caspase 3 and cytochrome C oxidase activities. CONCLUSION： These findings indicate that even within a specific cancer the intracellular apoptotic signals engaged by resveratrol are cell type dependent and suggest that such differences may be related to differentiation or lack of differentiation of these cells.

Importance of gastrin in the pathogenesis and treatment of gastric tumors

In addition to regulating acid secretion, the gastric antral hormone gastrin regulates several important cellular processes in the gastric epithelium including proliferation, apoptosis, migration, invasion, tissue remodelling and angiogenesis. Elevated serum concentrations of this hormone are caused by many conditions, particularly hypochlorhydria (as a result of autoimmune or Helicobacter pylori (H pylori)-induced chronic atrophic gastritis or acid suppressing drugs) and gastrin producing tumors (gastrinomas). There is now accumulating evidence that altered local and plasma concentrations of gastrin may play a role during the development of various gastric tumors. In the absence of H pylori infection, marked hypergastrinemia frequently results in the development of gastric enterochromaffi n cell-like neuroendocrine tumors and surgery to remove the cause of hypergastrinemia may lead to tumor resolution in this condition. In animal models such as transgenic INS-GAS mice, hypergastrinemia has also been shown to act as a cofactor with Helicobacter infection during gastric adenocarcinoma development. However, it is currently unclear as to what extent gastrin also modulates human gastric adenocarcinoma development. Therapeutic approaches targeting hypergastrinemia,such as immunization with G17DT, have been evaluated for the treatment of gastric adenocarcinoma, with some promising results. Although the mild hypergastrinemia associated with proton pump inhibitor drug use has been shown to cause ECL-cell hyperplasia and to increase H pylori-induced gastric atrophy, there is currently no convincing evidence that this class of agents contributes towards the development of gastric neuroendocrine tumors or gastric adenocarcinomas in human subjects.

Patients with brain metastases from gastrointestinal tract cancer treated with whole brain radiation therapy:Prognostic factors and survival

AIM: To identify the prognostic factors with regard to survival for patients with brain metastasis from primary tumors of the gastrointestinal tract. METHODS: Nine hundred and sixteen patients with brain metastases, treated with whole brain radiation therapy (WBRT) between January 1985 and December 2000 at the Department of Radiation Oncology, University Hospital Freiburg, were analyzed retrospectively. RESULTS: Fifty-seven patients presented with a primary tumor of the gastrointestinal tract (esophagus: n=0, stomach: n=10, colorectal: n=47). Twenty-six patients had a solitary brain metastasis, 31 patients presented with multiple brain metastases. Surgical resection was performed in 25 patients. WBRT was applied with daily fractions of 2 Gray (Gy) or 3Gy to a total dose of 50Gy or 30Gy, respectively. The interval between diagnoses of the primary tumors and brain metastases was 22.6mo vs 8.0mo for patients with primary tumors of the colon/rectum vs other primary tumors, respectively (P<0.01, log-rank). Median overall survival for all patients with brain metastases (n=916) was 3.4mo and 3.2mo for patients with gastrointestinal neoplasms. Patients with gastrointestinal primary tumors presented significantly more often with a solitary brain metastasis than patients with other primary tumors (P<0.05, log-rank). In patients with gastrointestinal neoplasms (n=57), the median overall survival was 5.8 mo for patients with solitary brain metastasis vs 2.7mo for patients with multiple brain metastases (P<0.01, log-rank). The median overall survival for patients with a Karnofsky performance status (KPS) ≥70 was 5.5mo vs 2.1mo for patients with KPS <70 (P<0.01, log-rank). At multivariate analysis (Cox Model) the performance status and the number of brain metastases were identified as independent prognostic factors for overall survival. CONCLUSION: Brain metastases occur late in the course of gastrointestinal tumors. Pretherapeutic variables like KPS and the number of brain metastases have a profound influence on treatment outcome.

Modern management of rectal cancer: A 2006 update

The goal of this review is to outline some of the important surgical issues surrounding the management of patients with early (T1/T2 and NO), as well as locally advanced (T3/T4 and/or N1) rectal cancer. Surgery for rectal cancer continues to develop towards the ultimate goals of improved local control and overall survival, maintaining quality of life, and preserving sphincter, genitourinary, and sexual function. Information concerning the depth of tumor penetration through the rectal wall, lymph node involvement, and presence of distant metastatic disease is of crucial importance when planning a curative rectal cancer resection. Preoperative staging is used to determine the indication for neoadjuvant therapy as well as the indication for local excision versus radical cancer resection. Local excision is likely to be curative in most patients with a primary tumor which is limited to the submucosa (T1N0M0), without high-risk features and in the absence of metastatic disease. In appropriate patients, minimally invasive procedures, such as local excision, TEM, and laparoscopic resection allow for improved patient comfort, shorter hospital stays, and earlier return to preoperative activity level. Once the tumor invades the muscularis propria (T2), radical rectal resection in acceptable operative candidates is recommended. In patients with transmural and/or node positive disease (T3/T4 and/or N1) with no distant metastases, preoperative chemoradiation followed by radical resection according to the principles of TME has become widely accepted. During the planning and conduct of a radical operation for a locally advanced rectal cancer, a number of surgical management issues are considered, including: (1) total mesorectal excision (TME); (2) autonomic nerve preservation (ANP); (3) circumferential resection margin (CRM); (4) distal resection margin; (5) sphincter preservation and options for restoration of bowel continuity; (6) laparoscopic approaches; and (7) postoperative quality of life.

Low intensity ultrasound-induced apoptosis in human gastric carcinoma cells

AIM： To investigate the low intensity ultrasound （US）- induced apoptosis in human gastric carcinoma cells and its potential mechanism and to suggest a new therapeutic approach to gastric carcinoma. METHODS： Human SGC-7901 gastric carcinoma cells were cultured in vitro and irradiated by low intensity US for 10 min at different intensities with different incubation times after irradiation. Morphologic changes were examined under microscope with trypan blue staining and then the percentage of early apoptotic cells was detected by flow cytometry （FCM） with double staining of fiuorescein isothiocyanate （FITC）- Annexin V/propidium iodide （PI）. Two-dimensional electrophoresis （2DE） was used to get the protein profile and some proteins differently expressed after US irradiation were identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry （MALDI-TOF-MS）. Functional analysis was performed to investigate the mechanism of US-induced cell apoptosis. RESULTS： The percentage of apoptotic cells increased about 10% after US irradiation （12.0 W/cm^2, 12 h culture）, The percentage of early apoptosis and secondary necrosis in the US-irradiated cells increased with the increased US intensity. Moreover, apoptotic cells increased with the increased culture time after US irradiation and reached its maximum at about 12 h.Several new proteins appeared after US irradiation and were up or down regulated more than 2 times. Some heat shock proteins （HSPs） were found to be associated with the signal process simulating the apoptosis of cells. CONCLUSION： Low intensity US could induce apoptosis in human gastric carcinoma cells. US-induced apoptosis is related to US intensity/culture time. US-induced apoptosis may be caspases-dependent and endoplasmic reticulum （ER） stress-triggered apoptosis may also contribute to it. Proteomic experimental system is useful in finding the protein alteration in carcinoma cells after US irradiation, helping to develop a new cancer therapy.

Cancer metabolic reprogramming: importance, main features, and potentials for precise targeted anti-cancer therapies

Cancer cells are well documented to rewire their metabolism and energy production networks to support and enable rapid proliferation, continuous growth, survival in harsh conditions, invasion, metastasis, and resistance to cancer treatments. Since Dr. Otto Warhurg＇s discovery about altered cancer cell metabolism in 1930, thousands of studies have shed light on various aspects of cancer metabolism with a common goal to find new ways for effectively eliminating tumor cells by targeting their energy metabolism. This review highlights the importance of the main features of cancer metabolism, summarizes recent remarkable advances in this field, and points out the potentials to translate these scientific findings into life-saving diagnosis and therapies to help cancer patients.

Role of ErbB family receptor tyrosine kinases in intrahepatic cholangiocarcinoma

Aberrant expression and signaling of epidermal growth factor receptor (ErbB) family receptor tyrosine kinases, most notably that of ErbB2 and ErbB1, have been implicated in the molecular pathogenesis of intrahepatic cholangiocarcinoma. Constitutive overexpression of ErbB2 and/or ErbB1 in malignant cholangiocytes has raised interest in the possibility that agents which selectively target these receptors could potentially be effective in cholangiocarcinoma therapy. However, current experience with such ErbB-directed therapies have at best produced only modest responses in patients with biliary tract cancers. This review provides a comprehensive and critical analysis of both preclinical and clinical studies aimed at assessing the role of altered ErbB2 and/or ErbB1 expression, genetic modifications, and dysregulated signaling on cholangiocarcinoma development and progression. Specific limitations in experimental approaches that have been used to assess human cholangiocarcinoma specimens for ErbB2 and/or ErbB1 overexpression and gene amplification are discussed. In addition, current rodent models of intrahepatic cholangiocarcinogenesis associated with constitutive ErbB2 overexpression are reviewed. Select interactive relationships between ErbB2 or ErbB1 with other relevant molecular signaling pathways associated with intrahepatic cholangiocarcinoma development and progression are also detailed, including those linking ErbB receptors to bile acid, cyclooxygenase-2,interleukin-6/gp130, transmembrane mucins, hepatocyte growth factor/Met, and vascular endothelial growth factor signaling. Lastly, various factors that can limit therapeutic efficacy of ErbB-targeted agents against cholangiocarcinoma are considered.

Long-term outcomes of hepatectomy vs percutaneous ablation for treatment of hepatocellular carcinoma≤4 cm

AIM： To determine which treatment modality - hepatectomy or percutaneous ablation - is more beneficial for patients with small hepatocellular carcinoma （HCC） （≤4 cm） in terms of long-term outcomes. METHODS： A retrospective analysis of 149 patients with HCC ≤ 4 cm was conducted. Eighty-five patients underwent partial hepatectomy （anatomic in 47 and nonanatomic in 38） and 64 underwent percutaneous ablation （percutaneous ethanol injection in 37, radiofrequency ablation in 21, and microwave coagulation in 6）. The median follow-up period was 69 mo. RESULTS： Hepatectomy was associated with larger tumor size （P〈0.001）, whereas percutaneous ablation was significantly associated with impaired hepatic functional reserve. Local recurrence was less frequent following hepatectomy （P〈0.0001）. Survival was better following hepatectomy （median survival time： 122 mo） than following percutaneous ablation （median survival time： 66 mo; P= 0.0123）. When tumor size was divided into ≤ 2 cm vs 〉 2 cm, the favorable effects of hepatectomy on long-term survival was seen only in patients with tumors 〉2 cm （P= 0.0001）. The Cox proportional hazards regression model revealed that hepatoctomy （P= 0.006） and tumors ≤ 2 cm （P=0.017） were independently associated with better survival. CONCLUSION： Hepatectomy provides both better local control and better long-term survival for patients with HCC ≤4 cm compared with percutaneous ablation. Of the patients with HCC ≤4 cm, those with tumors 〉 2 cm are good candidates for hepatectomy, provided that the hepatic functional reserve of the patient permits resection.

Development and characterization of multidrug resistant human hepatocarcinoma cell line in nude mice

AIM： To establish a multidrug resistant （MDR） cell subline from the human hepatocardnoma cell line （HepG2） in nude mice. METHODS： HepG2 cell cultures were incubated with increasing concentrations of adriamycin （ADM） to develop an ADM-resistant cell subline （HepG2/ADM） with crossresistance to other chemotherapeutic agents. Twenty male athymic BALB/c-nu/nu mice were randomized into HepG2/nude and HepG2/ADM/nude groups （10 in each group）. A cell suspension （either HepG2 or HepG2/ADM） was injected subcutaneously into mice in each group. Tumor growth was recorded, and animals were sacrificed 4-5 wk after cell implantation. Tumors were prepared for histology, and viable tumor was dispersed into a single-cell suspension. The IC50 values for a number of chemotherapeutic agents were determined by 2, 3-bis （2-methoxy-4-nitro-5-sulfophenyl）-2H-tetrazolium-5-carboxanilide inner salt （MTT） assay. Rhodamine-123 retention/efflux and the level of resistance-associated proteins were determined by flow cytometry. The mRNA expression of mdr1, mrp and Irp genes was detected using reverse transcriptase polymerase chain reaction （RT-PCR） in HepG2/nude and HepG2/ADM/nude groups. RESULTS： The appearances of HepG2/nude cells were slightly different from those of HepG2/ADM/nude cells. Similar tumor growth curves were determined in both groups. A cross-resistance to ADM, vincristine, cisplatin and 5-fluorouracil was seen in HepG2/ADM/nude group. The levels of P-glycoprotein and multidrug resistanceassociated proteins were significantly increased. The mRNA expression levels of mdrl, mrp and/rp were higher in HepG2/ADM/nude cells. CONCLUSION： ADM-resistant HepG2 subline in nude mice has a cross resistance to chemotherapeutic drugs. It may be used as an in vivo model to investigate the mechanisms of MDR, and explore the targeted approaches to overcoming MDR.