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CDC7 inhibition impairs neuroendocrine transformation in lung and prostate tumors through MYC degradation

Signal Transduction and Targeted Therapy 2024年第8期9卷 3519-3532页

作者： Alvaro Quintanal-Villalonga Kenta Kawasaki Esther Redin Fathema Uddin Swanand Rakhade Vidushi Durani Amin Sabet Moniquetta Shafer Wouter R.Karthaus Samir Zaidi Yingqian A.Zhan Parvathy Manoj Harsha Sridhar Dennis Kinyua Hong Zhong Barbara P.Mello Metamia Ciampricotti Umesh K.Bhanot Irina Linkov Juan Qiu Radhika A.Patel Colm Morrsey Sanjoy Mehta Jesse Barnes Michael C.Haffner Nichlas D.Socci Richard P.Koche Elisa de Stanchina Sonia Molina-Pinelo Sohrab Salehi Helena A.Yu Joseph M.Chan Charles M.Rudin Department of Medicine Thoracic Oncology ServiceMemorial Sloan Kettering Cancer CenterNew YorkNYUSA cancer Biology and Genetics Program Sloan Kettering InstituteMemorial Sloan Kettering Cancer CenterNew YorkNYUSA Vagelos college of Physicians and Surgeons Columbia UniversityNew YorkNYUSA weill cornell Graduate School of medical Sciences Weill Cornell MedicineNew YorkNYUA Human Oncology and Pathogenesis Program Memorial Sloan Kettering Cancer CenterNew YorkNYUSA center for Epigenetics Research Memorial Sloan Kettering Cancer CenterNew YorkNYUSA Pathology Core Facilty Department of Pathology and Laboratory MedicineMSKCCNew YorkNYUSA Antitumor Assessment Core Memorial Sloan Kettering Cancer CenterNew YorkNYUSA Divisionsof Human Biology and Clinical Research Fred Hutchinon Cancer CenterSeattleWAUSA Deparmentof Urology University of WashingtonSeattleWAUSA Gene Editing&Screening Core Facility memorial sloan kettering cancer center New YorkNYUSA Department of Laboratory Medicine and Pathology University of WashingtonSeattleWAUSA Bioinfomatics CoreFacility Memorial Soan Kettering Cancer CenterNew YorkNYUSA Institute of Biomedicine of Seille(Bis) HURCSCUniversidad de SevillaSevilleSpain Computational Oncology Department of Epidemiology and BiostatisticsMemorial Sloan Kettering Cancer CenterNew YorkNYUSA Well cornell medical college New York NYUSA Present address:Swiss Institute for Experimental cancer Research(ISREC) School of Life SciencesEPFLLausanneSwitzerland

Neuroendocrine(NE)transformation is a mechanism of resistance to targeted therapy in lung and prostate adenocarcinomas leading to poor *** to date,even if patients at high risk of transformation can be identified by the occurrence of Tumor Protein P53(TP53)and Retinoblastoma Transcriptional Corepressor 1(RB1)mutations in their tumors,no therapeutic strategies are available to prevent or delay histological *** of the cell cycle kinase Cell Division Cycle 7(CDC7)occurred in tumors during the initial steps of NE transformation,already after TP53/RB1 co-inactivation,leading to induced sensitivity to the CDC7 inhibitor ***7 inhibition suppressed NE transdifferentiation and extended response to targeted therapy in in vivo models of NE transformation by inducing the proteasome-mediated degradation of the MYC Proto-Oncogen(MYC),implicated in stemness and histological *** overexpression of a degradation-resistant MYC isoform reestablished the NE transformation phenotype observed on targeted therapy,even in the presence of ***7 inhibition also markedly extended response to standard cytotoxics(cisplatin,irinotecan)in lung and prostate small cell carcinoma *** results nominate CDC7 inhibition as a therapeutic strategy to constrain lineage plasticity,as well as to effectively treat NE tumors de novo or after *** simurosertib clinical efficacy trials are ongoing,this concept could be readily translated for patients at risk oftransformation.

关键词： tumors markedly transformation

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Role of(～(18)F)2-fluoro-2-deoxyglucose positron emission tomography in upper gastrointestinal malignancies

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World Journal of Gastroenterology 2011年第46期17卷 5059-5074页

作者： Elizabeth C Smyth Manish A Shah Department of Gastrointestinal Oncology Weill Cornell Medical CollegeMemorial Sloan-Kettering Cancer Center Department of Gastrointestinal Oncology Weill Cornell Medical CollegeNew York-Presbyterian Hospital

The role of whole-body FDG [(～(18)F)2-fluoro-2-deoxy-glucose] positron emission tomography(PET)scan-ning as an imaging modality in the management of patients with malignancy has evolved enormously over the past two ***-PET has demonstrated signifi cant effi cacy in the staging,prognostication and detection of occult metastatic disease in malignancies of the gastrointestinal tract,in addition to assessment of the response to cytotoxic chemotherapy in a more timely manner than has traditionally been possible by more conventional imaging *** sensitivity and specif icity of FDG-PET for the detection and staging of malignancy depend not only on the site and size of the primary tumor and metastases,but also on histologi-cal cell type,reflecting underlying disparities in glucose *** metabolic response to neo-adjuvant chemotherapy or to chemo-radiotherapy in cancers of the gastro-esophageal junction or stomach has been demonstrated in several prospective studies to correlate signifi cantly with both the histological tumor response to treatment and with consequent improvements in overall *** may offer a future paradigm ofpersonalized treatment based on the PET response to ***-PET has been less successful in efforts to screen for and detect recurrent upper gastro-intestinal malignancies,and in the detection of low vol-ume metastatic peritoneal *** to improve the accuracy of PET include the use of novel radiotrac-ers such as(～(18)F)FLT(3-deoxy-3-fluorothymidine)or 11C-choline,or fusion PET-CT with concurrent high-res-olution computed *** review focuses on the role of FDG-PET scanning in staging and response assessment in malignancies of the upper gastrointesti-nal tract,specif ically gastric,esophageal and pancreas carcinoma.

关键词： Positron emission tomography Gastric cancer Esophageal cancer Pancreas cancer

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Association of previously irradiated stable brain metastases with outcomes of atezolizumab-treated non-small cell lung cancer: A pooled analysis of individual patient data from three randomized trials

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cancer Communications 2024年第2期44卷 278-281页

作者： Tiantian Guo Yue Zhou Fei Liang Zezhou Wang Vincent Bourbonne Lukas Käsmann Nora Sundahl Abraham Jing-Ching Wu Jianjiao Ni Zhengfei Zhu Department of Radiation Oncology Fudan University Shanghai Cancer CenterShanghaiP.R.China Department of Oncology Shanghai Medical CollegeFudan UniversityShanghaiP.R.China Shanghai Clinical Research center for Radiation Oncology ShanghaiP.R.China Shanghai Key Laboratory of Radiation Oncology ShanghaiP.R.China Department of Biostatistics Zhongshan HospitalFudan UniversityShanghaiP.R.China Department of cancer Prevention Fudan University Shanghai Cancer CenterShanghaiP.R.China Radiation Oncology Department University HospitalBrestFrance Department of Radiation Oncology University HospitalLMU MunichMunichGermany Department of Radiation Oncology AZ GroeningeKortrijkBelgium Department of Radiation Oncology Memorial Sloan Kettering Cancer CenterNew YorkNew YorkUSA Institute of Thoracic Oncology Fudan UniversityShanghaiP.R.China

Dear Editor:Brain metastasis(BM)has long been recognized as a prognostic factor associated with poor prognosis for non-small cell lung cancer(NSCLC)in the era of con-ventional chemotherapy and targeted therapy[1].In the era of immunotherapy,controversial findings have been reported regarding the prognostic significance of BM in patients with NSCLC treated with programmed death-1/programmed death-ligand 1(PD-1/PD-L1)inhibitors.

关键词： chemotherapy NSCLC metastasis death

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Geriatric assessment for oncologists

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cancer Biology & Medicine 2015年第4期12卷 261-274页

作者： Beatriz Korc-Grodzicki Holly M.Holmes Armin Shahrokni memorial sloan kettering cancer center Weill Cornell Medical CollegeNew York Division of Geriatric and Palliative Medicine The University of Texas Health Science Center at Houston

The world is experiencing aging of its population. Age-specific incidence rates of cancer are higher and cancer is now recognized as a part of aging. Treating older patients can be challenging. The clinical behavior of some tumors changes with age and the aging process itself brings physiological changes leading to decline in the function of organs. It is essential to identify those patients with longer life expectancy, potentially more likely to benefit from aggressive treatment vs. those that are more vulnerable to adverse outcomes. A primary determination when considering therapy for an older cancer patient is a patient's physiologic, rather than chronologic age. In order to differentiate amongst patients of the same age, it is useful to determine if a patient is fit or frail. Frail older adults have multiple chronic conditions and difficulties maintaining independence. They may be more vulnerable to therapy toxicities, and may not have substantial lasting benefits from therapy. Geriatric assessment(GA) may be used as a tool to determine reversible deficits and devise treatment strategies to mitigate such deficits. GA is also used in treatment decision making by clinicians, helping to risk stratify patients prior to potentially high-risk therapy. An important practical aspect of GA is the feasibility of incorporating it into a busy oncology practice. Key considerations in performing the GA include: available resources, patient population, GA tools to use, and who will be responsible for using the GA results and develop care plans. Challenges in implementing GA in clinical practice will be discussed.

关键词： Geriatric oncology geriatric assessment(GA) frailty

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A good gut feeling on Sarm1-mediated axon degeneration

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Protein & Cell 2021年第8期12卷 596-598页

作者： Victoria E.von Saucken David J.Simon Department of Biochemistry Weill Cornell Medical College Tri-Institutional MD-Ph D Program Weill Cornell Medicine Rockefeller University Memorial Sloan Kettering Cancer Center

Axons,the cable-l ike projections of neurons,experience a wide range of stressors throughout their *** result of any one of these challenges can be catastrophic,promoting degeneration of the *** degeneration is an active signaling process observed in traumatic brain injury,chemotherapy-induced peripheral neuropathies,and neurodegen erative disease (Simon and Watkins,2018;Coleman and Hoeke,2020).As a result,tremendous efforts have been made to identify biological targets that can be harnessed to block axon degeneration to treat these *** promising candidate is Sarm1 (sterile alpha and TIR motif containing protein 1),a member of the Myd88 immune adaptor protein family that itself has no clear role in innate immunity.

关键词： SARM1 ACTIVATION TRIGGERS DEATH

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AML1-ETO driven acute leukemia:insights into pathogenesis and potential therapeutic approaches

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Frontiers of Medicine 2012年第3期6卷 248-262页

作者： Megan A.Hatlen Lan Wang Stephen D.Nimer Molecular Pharmacology and Chemistry Program Sloan-Kettering InstituteMemorial Sloan-Kettering Cancer CenterNew YorkNY 10065USA weill cornell medical college New YorkNY 10065USA

The AML1-ETO fusion transcription factor is generated by the t(8;21)translocation,which is present in approximately 4%-12% of adult and 12%-30% of pediatric acute myeloid leukemia(AML)*** human and mouse models of AML have demonstrated that AML1-ETO is insufficient for leukemogenesis in the absence of secondary *** this review,we discuss the pathogenetic insights that have been gained from identifying the various events that can cooperate with AML1-ETO to induce AML in *** also discuss potential therapeutic strategies for t(8;21)positive AML that involve targeting the fusion protein itself,the proteins that bind to it,or the genes that it *** published studies suggest that a targeted therapy for t(8;21)positive AML is feasible and may be coming sometime soon.

关键词： AML1-ETO mouse model leukemia t(8,21) pathway hits mutation hematopoiesis Kasumi-1 CD34^(+)

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Driver mutations of cancer epigenomes

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Protein & Cell 2014年第4期5卷 265-296页

作者： David M. Roy Logan A. Walsh Timothy A. Chan Human Oncology and Pathogenesis Program Memorial Sloan-Kettering Cancer Center New York NY 10065 USA weill cornell/Rockefeller/sloan-kettering Tri-lnstitutional MD-PhD Program New York NY 10065 USA Department of Radiation Oncology Memorial Sloan-Kettering Cancer Center New York NY 10065 USA

Epigenetic alterations are associated with all aspects of cancer, from tumor initiation to cancer progression and metastasis. It is now well understood that both losses and gains of DNA methylation as well as altered chro- matin organization contribute significantly to cancer- associated phenotypes. More recently, new sequencing technologies have allowed the identification of driver mutations in epigenetic regulators, providing a mecha- nistic link between the cancer epigenome and genetic alterations. Oncogenic activating mutations are now known to occur in a number of epigenetic modifiers （i.e. IDHll2, EZH2, DNMT3A）, pinpointing epigenetic path- ways that are involved in tumorigenesis. Similarly, investigations into the role of inactivating mutations in chromatin modifiers （i.e. KDM6A, CREBBPIEP300, SMARCB1） implicate many of these genes as tumor suppressors. Intriguingly, a number of neoplasms are defined by a plethora of mutations in epigenetic regu- lators, including renal, bladder, and adenoid cystic car- cinomas. Particularly striking is the discovery of frequent histone H3.3 mutations in pediatric glioma, a particularly aggressive neoplasm that has long remained poorly understood. cancer epigenetics is a relatively new, promising frontier with much potential for improving cancer outcomes. Already, therapies such as 5-azacytidine and decitabine have proven that targeting epigenetic alterations in cancer can lead to tangible benefits. Understanding how genetic alterations give rise to the cancer epigenome will offer new possibilities for developing better prognostic and therapeutic strategies.

关键词： chromatin cancer epigenetics mutations,methylation

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Pylephlebitis and liver abscess mimicking hepatocellular carcinoma

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Hepatobiliary & Pancreatic Diseases International 2003年第2期2卷 537-541页

作者： KarenT.Brown RipalT.Gandhi AnneM.Covey LynnA.Brody GeorgeI.Getrajdman the Department of Radiology Memorial Sloan-Kettering Cancer Center Weill Medical College of Cornell University 1275 York Avenue New York NY 10021 USA

OBJECTIVE: To characterize the clinical and radiographic findings in patients with pylephlebitis and liver abscess with an emphasis on the findings that help to differentiate this disorder from portal vein occlusion associated with hepatocellular carcinoma. METHODS: We analyzed the clinical findings and radiographic images of four patients with pylephlebitis and liver abscess(es) who had been misdiagnosed as having hepatocellular carcinoma with portal vein thrombosis. Their medical records were reviewed in terms of clinical presentation, physical findings, laboratory data, treatment, and follow up. RESULTS: All patients undergoing color duplex ultrasonography had an echogenic thrombus within an expanded portal vein with negative color-flow findings within the thrombus. Contrast enhanced CT in all the patients demonstrated portal vein thrombosis associated with 'liver masses'. An intra-abdominal site of infection responsible for the subsequent ascending infection of the portal vein and liver was not identified in any patient on initial CT scan. At presentation, all patients were febrile and three of them had an elevated white blood cell count as well. All patients showed abnormalities of liver function. CONCLUSIONS: Liver abscess(es) associated with pylephlebitis may mimic hepatocellular carcinoma with portal vein thrombosis. Clinical features that help to distinguish the two entities include presence or absence of fever, elevated white blood cell count, elevated alpha-fetoprotein, cirrhosis, and risk factors for hepatocellular carcinoma.

关键词： pylephlehitis liver abscess portal vein thrombosis hepatoma hepatocellular carcinoma

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Exercise and cancer Prevention: Current Evidence and Future Directions

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Journal of Science in Sport and Exercise 2020年第3期2卷 190-200页

作者： Lee W.Jones Department of Medicine Memorial Sloan Kettering Cancer Center1275 York AvenueNew YorkNY 10065USA weill cornell medical college New YorkNYUSA

Establishment of the strong putative relationship between exercise and risk of virtually all non-communicable diseases prompted several research groups over the past two decades to investigate a question of significant public health concern:whether exercise lowers the risk of certain forms of *** this Opinion review I first overview studies of exercise in cancer prevention summarizing evidence from observational studies and available clinical *** the final section,I consider the next steps in the continued development of exercise as a cancer prevention strategy.

关键词： cancer Exercise Oncology Physical activity Primary prevention

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A targetable pathway to eliminate TRA-1-60^(+)/TRA-1-81^(+)chemoresistant cancer cells

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Journal of Molecular Cell Biology 2023年第6期15卷 25-39页

作者： Lei Tan Xiaohua Duan Pratyusha Mutyala Ting Zhou Sadaf Amin Tuo Zhang Brian Herbst Gokce Askan Tomer Itkin Zhaoying Xiang Fabrizio Michelassi Michael D.Lieberman Christine AIacobuzio-Donahue Steven DLeach Todd Evans Shuibing Chen Department of Surgery Weill Cornell MedicineNew YorkNY 10065USA center for Energy Metabolism and Reproduction Institute of Biomedicine and BiotechnologyShenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhen 518055China center for Genomic Health Weill Cornell MedicineNew YorkNY 10065USA The SKI Stem Cell Research Facility The Center for Stem Cell Biology and Developmental Biology ProgramMemorial Sloan Kettering Cancer CenterNew YorkNY 10065USA Genomic Resource Core Facility Weill Cornell Medical CollegeNew YorkNY 10065USA Rubenstein center for Pancreatic cancer Research Memorial Sloan Kettering Cancer CenterNew YorkNY 10065USA Division of Regenerative Medicine Hartman Institute for Therapeutic Organ RegenerationAnsary Stem Cell InstituteDepartment of MedicineWeill Cornell MedicineNew YorkNY 10065USA Dartmouth cancer center Darmouth CollegeHanoverNH 03755USA

Chemoresistance is a primary cause of treatment failure in pancreatic *** cell surface markers specifically expressed in chemoresistant cancer cells(CCCs)could facilitate targeted therapies to overcome *** performed an antibody-based screen and found that TRA-1-60 and TRA-1-81,two‘stemness’cell surface markers,are highly enriched in ***-more,TRA-1-60^(+)/TRA-1-81^(+)cells are chemoresistant compared to TRA-1-60^(-)/TRA-1-81^(-)*** profiling identified UGT1A10,shown to be both necessary and sufficient to maintain TRA-1-60/TRA-1-81 expression and *** a high-content chemical screen,we identified Cymarin,which downregulates UGT1A10,eliminates TRA-1-60/TRA-1-81 expression,and increases chemosensitivity both in vitro and in ***,TRA-1-60/TRA-1-81 expression is highly specific in primary cancer tissue and positively correlated with chemoresistance and short survival,which highlights their potentiality for targeted ***,we discovered a novel CCC surface marker regulated by a pathway that promotes chemoresistance,as well as a leading drug candidate to target this pathway.

关键词： pancreatic cancer TRA-1-60/TRA-1-81 chemoresistance UGT1A10 Cymarin

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