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Beyond first-line chemotherapy for advanced pancreatic cancer:An expanding array of therapeutic options?

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World Journal of Gastroenterology 2014年第9期20卷 2224-2236页

作者： Evan J Walker Andrew H Ko University of California Helen Diller Family Comprehensive Cancer Center San Francisco CA 94115 United States

While an increasing number of therapeutic options are now available for the first-line treatment of locally advanced or metastatic pancreatic cancer,the optimal choice for treatment in the second-line setting and beyond is less well defined.A variety of cytotoxic agents,either alone or in combination,have been evaluated,although primarily in the context of small single-arm or retrospective *** regimens have been associated with median progression-free survival rates in the range of 2-4 mo and overall survival rates between 4-8mo,highlighting the very poor prognosis of patients who are candidates for such *** therapies studied in this chemotherapy-refractory setting,meanwhile,have produced even worse efficacy *** the current article,we review the clinical evidence for treatment of refractory disease,primarily in patients who have progressed on front-line gemcitabine-based *** the process,we highlight the limitations of the available data to date as well as some of the challenges in designing appropriate clinical trials in this salvage setting,including how to select an appropriate control arm given the absence of a wellestablished reference standard,and the importance of incorporating predictive biomarkers and quality of life measures whenever possible into study design.

关键词： Pancreatic cancer Refractory Second-line chemotherapy Gemcitabine

Molecular markers as therapeutic targets in lung cancer

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Chinese Journal of Cancer 2013年第2期32卷 59-62页

作者： Hsin-Hui Tseng Biao He Thoracic Oncology Program.Department of Surgery Helen Diller Family Comprehensive Cancer CenterUniversity of California

Lung cancer is responsible for 29% of cancer deaths in the United States and has very low 5-year survival rates of approximately 11% in men and 15% in *** the early diagnosis of lung cancer may increase the survival rate with adequate treatment,advanced lung cancers are often metastasized and receive limited benefit from therapeutic *** conventional treatments for lung cancer reach their limitations,researchers have attempted to discover novel drug therapies aimed at specific targets contributing to the progression of *** advances in systems biology have enabled the molecular biology of lung carcinogenesis to be *** understanding of the physiologic processes of tumor development provide a means to design more effective and specific drugs with less toxicity,thereby accelerating the delivery of new drug therapies to the patient's bedside.

关键词：治疗方案肺癌分子标记靶点药物治疗肿瘤发生分子生物学系统生物学

Therapeutic targets in the pancreatic adenocarcinoma microenvironment: past challenges and opportunities for the future

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Journal of Cancer Metastasis and Treatment 2021年第1期7卷 448-465页

作者： Erica S.Tsang Margaret A.Tempero Helen Diller family comprehensive Cancer Center University of California San FranciscoSan FranciscoCA 94158USA

Pancreatic ductal adenocarcinoma(PDAC)remains a leading cause of cancer-related mortality,with cytotoxic chemotherapy still the mainstay of *** effective therapeutic agents alone,successful drug delivery is *** PDAC,the tumor microenvironment represents a physical barrier that limits in vivo drug delivery and *** this review,we highlight therapeutic targets in the tumor microenvironment,focusing on past challenges and opportunities for the *** discussed include the Hedgehog pathway,angiogenesis,hyaluronic acid,cancer-associated fibroblasts and associated cytokines,among *** the obstacles in successfully recapitulating promising lab results to practice-changing clinical results,many important lessons have been learned to improve clinical trial design within a highly engaged and motivated scientific *** collaborative efforts and the collective optimism will continue to propel the momentum forward to overcome these barriers and ultimately improve patient outcomes.

关键词： Pancreatic cancer PDAC tumor microenvironment pancreatic stroma

Moving from late to early stage disease: lessons learned from erlotinib in pancreatic cancer

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Hepatobiliary Surgery and Nutrition 2018年第5期7卷 406-408页

作者： Andrew H. Ko Division of Hematology/Oncology Gastrointestinal Oncology Program Helen Diller Family Comprehensive Cancer Center University of California San Francisco San Francisco CA USA

At the time the CONKO-005 trial was originally conceived, there was an inherent rationale to its design;it represented the next logical step in trying to move the needle in the treatment of early-stage pancreatic aden... 详细信息

关键词： needle adenocarcinoma rational

Effects and mechanisms of silibinin on human hepatocellular carcinoma xenografts in nude mice

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World Journal of Gastroenterology 2009年第16期15卷 1943-1950页

作者： Wei Cui Fan Gu Ke-Qin Hu Division of Gastroenterology and Chao family comprehensive Cancer Center University of California Orange School of Medicine Orange CA 92868 United States Department of Surgery Nanfang Hospital Southern Medical University Guangzhou 510515 Guangdong Province China

AIM:To investigate the in vivo effects and mechanisms of silibinin on the growth of hepatocellular carcinoma (HCC) xenografts in nude ***: Nude mice bearing HuH7 xenografts were used to assess the anti-HCC effects and mechanisms of ***: Silibinin resulted in a potent dosedependent reduction of HuH7 xenografts in association with a significant decrease in Ki-67 and α-fetoprotein production, nuclear NF-κB content, polo-like kinase 1, Rb phosphorylation, and E2F1/DP1 complex, but increased p27/CDK4 complex and checkpoint kinase 1 expression, suggesting that the in vivo effects of silibinin are mediated by inhibiting G1-S transition of the cell cycle. Silibinin-induced apoptosis of HuH7 xenografts was associated with inhibited survivin phosphorylation. Silibinin-reduced growth of HuH7 xenografts was associated with decreased p-ERK, increased PTEN expression and the activity of silibinin was correlated with decreased p-Akt production, indicating involvement of PTEN/PI3K/Akt and ERK pathways in its in vivo anti-HCC effects. Silibinin-reduced growth of HuH7 xenografts was also associated with a significant increase in AC-H3 and AC-H4 expression and the production of superoxide dismutase (SOD)-***: Silibinin reduces HCC xenograft growth through the inhibition of cell proliferation, cell cycle progression and PTEN/P-Akt and ERK signaling, inducing cell apoptosis, and increasing histone acetylation and SOD-1 expression.

关键词： Apoptosis Cell cycle Chemoprevention Hepatocellular carcinoma Histone acetylation Silibinin

Long noncoding RNAs in prostate cancer： overview and clinical implications

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Asian Journal of Andrology 2016年第4期18卷 568-574页

作者： Bhavna Malik Felix Y Feng Department of Radiation Oncology University of Michigan Ann Arbor Michigan USA Department of Radiation Oncology Urology and Medicine University of California at San Francisco USA Helen Diller family comprehensive Cancer Center University of California at San Francisco USA

Prostate cancer is the second most common cause of cancer mortality among men in the United States. While many prostate cancers are indolent, an important subset of patients experiences disease recurrence after conventional therapy and progresses to castration-resistant prostate cancer （CRPC）, which is currently incurable. Thus, there is a critical need to identify biomarkers that will distinguish indolent from aggressive disease, as well as novel therapeutic targets for the prevention or treatment of CRPC. In recent years, long noncoding RNAs （IncRNAs） have emerged as an important class of biological molecules. LncRNAs are polyadenylated RNA species that share many similarities with protein-coding genes despite the fact that they are noncoding （not translated into proteins）. They are usually transcribed by RNA polymerase II and exhibit the same epigenetic signatures as protein-coding genes. LncRNAs have also been implicated in the development and progression of variety of cancers, including prostate cancer. While a large number of IncRNAs exhibit tissue- and cancer-specific expression, their utility as diagnostic and prognostic biomarkers is just starting to be explored. In this review, we highlight recent findings on the functional role and molecular mechanisms of IncRNAs in the progression of prostate cancer and evaluate their use as potential biomarkers and therapeutic targets.

关键词： biomarker long noncoding RNAs (IncRNAs) prostate cancer

Short hairpin RNA-mediated knockdown of nuclear factor erythroid 2-like 3 exhibits tumor-suppressing effects in hepatocellular carcinoma cells

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World Journal of Gastroenterology 2019年第10期25卷 1210-1222页

作者： Miao-Mei Yu Yue-Hua Feng Lu Zheng Jun Zhang Guang-Hua Luo comprehensive Laboratory the Third Affiliated Hospital of Soochow University

BACKGROUND Hepatocellular carcinoma(HCC) is one of the most common malignant tumors with high mortality-to-incidence ratios. Nuclear factor erythroid 2-like 3(NFE2 L3), also known as NRF3, is a member of the cap ‘n' collar basic-region leucine zipper family of transcription factors. NFE2 L3 is involved in the regulation of various biological processes, whereas its role in HCC has not been *** To explore the expression and biological function of NFE2 L3 in *** We analyzed the expression of NFE2 L3 in HCC tissues and its correlation with clinicopathological parameters based on The Cancer Genome Atlas(TCGA) data portal. Short hairpin RNA(shRNA) interference technology was utilized to knock down NFE2 L3 in vitro. Cell apoptosis, clone formation, proliferation, migration,and invasion assays were used to identify the biological effects of NFE2 L3 in BEL-7404 and SMMC-7721 cells. The expression of epithelial-mesenchymal transition(EMT) markers was examined by Western blot *** TCGA analysis showed that NFE2 L3 expression was significantly positively correlated with tumor grade, T stage, and pathologic stage. The qPCR and Western blot results showed that both the mRNA and protein levels of NFE2 L3 were significantly decreased after shRNA-mediated knockdown in BEL-7404 and SMMC-7721 cells. The shRNA-mediated knockdown of NFE2 L3 could induce apoptosis and inhibit the clone formation and cell proliferation of SMMC-7721 and BEL-7404 cells. NFE2 L3 knockdown also significantly suppressed the migration, invasion, and EMT of the two cell *** Our study showed that shRNA-mediated knockdown of NFE2 L3 exhibited tumor-suppressing effects in HCC cells.

关键词： Nuclear factor erythroid 2-like 3 Hepatocellular carcinoma The Cancer Genome Atlas Short hairpin RNA Epithelial-mesenchymal transition

Proinflammatory cytokine TNFα promotes HPV-associated oral carcinogenesis by increasing cancer stemness

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International Journal of Oral Science 2020年第1期12卷 40-49页

作者： Hannah SHong Jonathan Akhavan Sung Hee Lee Reuben HKim Mo KKang No-Hee Park Ki-Hyuk Shin The Shapiro family Laboratory of Viral Oncology and Aging Research UCLA School of DentistryLos AngelesCAUSA UCLA Jonsson comprehensive Cancer Center Los AngelesCAUSA Department of Medicine David Geffen School of Medicine at UCLALos AngelesCAUSA

High-risk human papillomaviruses(HPVs) are involved in the development of several human cancers, including oropharyngeal squamous cell carcinomas. However, many studies have demonstrated that HPV alone is not sufficient for the oncogenic transformation of normal human epithelial cells, indicating that additional cofactors are required for the oncogenic conversion of HPV-infected cells. Inasmuch as chronic inflammation is also closely associated with carcinogenesis, we investigated the effect of chronic exposure to tumor necrosis factor α(TNFα), the major proinflammatory cytokine, on oncogenesis in two immortalized oral keratinocyte cell lines, namely, HPV16-immortalized and human telomerase reverse transcriptase(h TERT)-immortalized cells. TNFαtreatment led to the acquisition of malignant growth properties in HPV16-immortalized cells, such as(1) calcium resistance,(2)anchorage independence, and(3) increased cell proliferation in vivo. Moreover, TNFα increased the cancer stem cell-like population and stemness phenotype in HPV16-immortalized cells. However, such transforming effects were not observed in h TERTimmortalized cells, suggesting an HPV-specific role in TNFα-promoted oncogenesis. We also generated h TERT-immortalized cells that express HPV16 E6 and E7. Chronic TNFα exposure successfully induced the malignant growth and stemness phenotype in the E6-expressing cells but not in the control and E7-expressing cells. We further demonstrated that HPV16 E6 played a key role in TNFα-induced cancer stemness via suppression of the stemness-inhibiting micro RNAs mi R-203 and mi R-200 c. Overexpression of mi R-203 and mi R-200 c suppressed cancer stemness in TNFα-treated HPV16-immortalized cells. Overall, our study suggests that chronic inflammation promotes cancer stemness in HPV-infected cells, thereby promoting HPV-associated oral carcinogenesis.

关键词： carcinogenesis cytokine cancer

Kavalactone yangonin induces autophagy and sensitizes bladder cancer cells to flavokawain A and docetaxel via inhibition of the mTOR pathway

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The Journal of Biomedical Research 2017年第5期31卷 408-418页

作者： Zhongbo Liu U-Syn Ha Ke Yu Chunli Wu Noriko Yokoyama Xiaolin Zi Departments of Urology University of CaliforniaIrvine Orange CA 92868 USA. Pharmacology University of CaliforniaIrvine Orange CA 92868 USA. Chao family comprehensive Cancer Center University of CaliforniaIrvine Orange CA 92868 USA.

Consumption of kava(Piper methysticum Forst) has been linked to reduced cancer risk in the South Pacific *** are major bioactive components in kava root extracts, which have recently demonstrated anti-cancer activities. However, molecular mechanisms of kavalactones' anti-cancer action remain largely unknown. We have identified two kavalactones, yangonin and 5' 6'-dehydrokawain, as potent inducers of autophagic cell death in bladder cancer cells. The effect of yangonin inducing autophagy is associated with increased expression of beclin and *** addition, yangonin increases the expression of LKB1 and decreases the phosphorylation of Akt, PRAS40, rpS6,p70S6 K and 4E-BP1, leading to increased binding of 4E-BP1 to m7 GTP. The growth inhibitory effects of yangonin were attenuated in TSC1 or LKB1 knockout mouse embryonic fibroblasts, suggesting that TSC1 and LKB1 expression may contribute to optimal growth inhibition by yangonin. Furthermore, yangonin reduces the viability of bladder cancer cell lines derived from different stages of human bladder cancer, and acts synergistically with apoptosis-inducing agents such as docetaxel and flavokawain A. Our results support a novel anti-bladder cancer mechanism by yangonin and further studies are needed to assess the potential use of yangonin for bladder cancer prevention and treatment

关键词： yangonin bladder cancer autophagy mTOR