Olga Aprelikova

National Cancer Institute

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Gadisetti V.R. Chandramouli

National Cancer Institute

John I. Risinger

Michigan State University

James R. Vasselli

Clovis Oncology (United States)

Joseph Riss

University of California, Los Angeles

John N. Weinstein

The University of Texas MD Anderson Cancer Center

Maxwell P. Lee

National Institutes of Health

Jodi K. Maranchie

University of Pittsburgh

Howard H. Yang

Google (United States)

Kurt W. Kohn

National Cancer Institute

David E. Kleiner

National Cancer Institute

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National Cancer Institute

112

National Institutes of Health

108

Center for Cancer Research

Harvard University

Frederick National Laboratory for Cancer Research

Memorial Sloan Kettering Cancer Center

Cornell University

Science Applications International Corporation (United States)

Johns Hopkins University

University of North Carolina at Chapel Hill

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Data from Melanoma Antigen-11 Inhibits the Hypoxia-Inducible Factor Prolyl Hydroxylase 2 and Activates Hypoxic Response

Olga Aprelikova Silvia Pandolfi Sean Tackett Mark Ferreira Konstantin Salnikow

<div>Abstract<p>Activation of hypoxia-inducible factors (HIF), responsible for tumor angiogenesis and glycolytic switch, is regulated by reduced oxygen availability. Normally, HIF-α proteins are maintained at low levels, controlled by site-specific hydroxylation carried out by HIF prolyl hydroxylases (PHD) and subsequent proteasomal degradation via the von Hippel-Lindau ubiquitin ligase. Using a yeast two-hybrid screen, we identified an interaction between melanoma antigen-11 (MAGE-11) cancer-testis antigen and the major HIF-α hydroxylating enzyme PHD2. The interaction was confirmed by a pull-down assay, coimmunoprecipitation, and colocalization in both normoxic and hypoxic conditions. Furthermore, MAGE-9, the closest homologue of MAGE-11, was also found to interact with PHD2. MAGE-11 inhibited PHD activity without affecting protein levels. This inhibition was accompanied by stabilization of ectopic or endogenous HIF-1α protein. Knockdown of MAGE-11 by small interfering RNA results in decreased hypoxic induction of HIF-1α and its target genes. Inhibition of PHD by MAGE-11, and following activation of HIFs, is a novel tumor-associated HIF regulatory mechanism. This finding provides new insights into the significance of MAGE expression in tumors and may provide valuable tools for therapeutic intervention because of the restricted expression of the MAGE gene family in cancers, but not in normal tissues. [Cancer Res 2009;69(2):616–24]</p></div>

Hypoxia

Hypoxia-Inducible Factors

Hypoxia-Inducible Factor 1

10.1158/0008-5472.c.6498755.v1

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Impaired meiotic DNA-damage repair and lack of crossing-over during spermatogenesis in BRCA1 full-length isoform deficient mice

Development (2003)

Xiaoling Xu Olga Aprelikova Peter B. Møens Chu‐Xia Deng Priscilla A. Furth

Breast tumor suppressor gene 1 (BRCA1) plays an essential role in maintaining genomic integrity. Here we show that mouse Brca1 is required for DNA-damage repair and crossing-over during spermatogenesis. Male Brca1(Delta11/Delta11)p53(+/-) mice that carried a homozygous deletion of Brca1 exon 11 and a p53 heterozygous mutation had significantly reduced testicular size and no spermatozoa in their seminiferous tubules. During spermatogenesis, homologous chromosomes from the mutant mice synapsed and advanced to the pachytene stage but failed to progress to the diplotene stage. Our analyses revealed that the Brca1 mutation affected cellular localization of several DNA damage-repair proteins. This included prolonged association of gammaH2AX with sites of DNA damage, reduced sex body formation, diminished Rad51 foci and absence of Mlh1 foci in the pachytene stage. Consequently, chromosomes from mutant mice did not form chiasmata, a point that connects exchanging homologous chromosomes. Brca1-mutant spermatocytes also exhibited decreased RNA expression levels of several genes that are involved in DNA-damage repair, including RuvB-like DNA helicase, XPB, p62 and TFIID. Of note, the premature termination of spermatogenesis at the pachytene stage was accompanied by increased apoptosis by both p53-dependent and p53-independent mechanisms. Thus, our study revealed an essential role of Brca1 in DNA-damage repair and crossing-over of homologous chromosomes during spermatogenesis.

10.1242/dev.00410

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Supplementary Table S8 from Cancers as Wounds that Do Not Heal: Differences and Similarities between Renal Regeneration/Repair and Renal Cell Carcinoma

Joseph Riss Chand Khanna Seongjoon Koo Gadisetti V.R. Chandramouli Howard H. Yang

Supplementary Table S8 from Cancers as Wounds that Do Not Heal: Differences and Similarities between Renal Regeneration/Repair and Renal Cell Carcinoma

Table (database)

10.1158/0008-5472.22364417.v1

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Supplementary Table S5B from Cancers as Wounds that Do Not Heal: Differences and Similarities between Renal Regeneration/Repair and Renal Cell Carcinoma

Joseph Riss Chand Khanna Seongjoon Koo Gadisetti V.R. Chandramouli Howard H. Yang

Supplementary Table S5B from Cancers as Wounds that Do Not Heal: Differences and Similarities between Renal Regeneration/Repair and Renal Cell Carcinoma

Table (database)

10.1158/0008-5472.22364426

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Two human FLT4 receptor tyrosine kinase isoforms with distinct carboxy terminal tails are produced by alternative processing of primary transcripts.

PubMed (1993)

Katri Pajusola Olga Aprelikova Elina Armstrong S. W. Morris Kari Alitalo

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Cancers as Wounds that Do Not Heal: Differences and Similarities between Renal Regeneration/Repair and Renal Cell Carcinoma

Cancer Research (2006)

Joseph Riss Chand Khanna Seongjoon Koo Gadisetti V.R. Chandramouli Howard H. Yang

Abstract Cancers have been described as wounds that do not heal, suggesting that the two share common features. By comparing microarray data from a model of renal regeneration and repair (RRR) with reported gene expression in renal cell carcinoma (RCC), we asked whether those two processes do, in fact, share molecular features and regulatory mechanisms. The majority (77%) of the genes expressed in RRR and RCC were concordantly regulated, whereas only 23% were discordant (i.e., changed in opposite directions). The orchestrated processes of regeneration, involving cell proliferation and immune response, were reflected in the concordant genes. The discordant gene signature revealed processes (e.g., morphogenesis and glycolysis) and pathways (e.g., hypoxia-inducible factor and insulin-like growth factor-I) that reflect the intrinsic pathologic nature of RCC. This is the first study that compares gene expression patterns in RCC and RRR. It does so, in particular, with relation to the hypothesis that RCC resembles the wound healing processes seen in RRR. However, careful attention to the genes that are regulated in the discordant direction provides new insights into the critical differences between renal carcinogenesis and wound healing. The observations reported here provide a conceptual framework for further efforts to understand the biology and to develop more effective diagnostic biomarkers and therapeutic strategies for renal tumors and renal ischemia. (Cancer Res 2006; 66(14): 7216-24)

Kidney cancer

10.1158/0008-5472.can-06-0040

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783: Gene Expression Analysis of the Effects of 5-Aza- 2'-Deoxycytidine On Hypermethylated VHL Clear-Cell Kidney Cancer

The Journal of Urology (2004)

Wade G. Alleman Gadisetti V.R. Chandramouli Olga Aprelikova Ray Tabios W. Marston Linehan

You have accessJournal of UrologyDiscussed Poster, Monday, May 10, 2004, 8:00 am - 12:00 pm1 Apr 2004783: Gene Expression Analysis of the Effects of 5-Aza- 2'-Deoxycytidine On Hypermethylated VHL Clear-Cell Kidney Cancer Wade Alleman, Gadisetti Chandramouli, Olga Aprelikova, Ray Tabios, W.Marston Linehan, and James Vasselli Wade AllemanWade Alleman More articles by this author , Gadisetti ChandramouliGadisetti Chandramouli More articles by this author , Olga AprelikovaOlga Aprelikova More articles by this author , Ray TabiosRay Tabios More articles by this author , W.Marston LinehanW.Marston Linehan More articles by this author , and James VasselliJames Vasselli More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)38032-7AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "783: Gene Expression Analysis of the Effects of 5-Aza- 2'-Deoxycytidine On Hypermethylated VHL Clear-Cell Kidney Cancer." The Journal of Urology, 171(4S), p. 207 © 2016 by American Urological AssociationFiguresReferencesRelatedDetails Volume 171Issue 4SApril 2004Page: 207 Advertisement Copyright & Permissions© 2016 by American Urological AssociationMetricsAuthor Information Wade Alleman More articles by this author Gadisetti Chandramouli More articles by this author Olga Aprelikova More articles by this author Ray Tabios More articles by this author W.Marston Linehan More articles by this author James Vasselli More articles by this author Expand All Advertisement PDF downloadLoading ...

Kidney cancer

10.1016/s0022-5347(18)38032-7

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Supplementary Figure 3A Gene List from Gene Expression Profiles Associated with Response to Chemotherapy in Epithelial Ovarian Cancers

Amir A. Jazaeri Christopher S. Awtrey Gadisetti V.R. Chandramouli Yao Eric Chuang Javed Khan

10.1158/1078-0432.22441185.v1

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Supplementary Materials from Cancers as Wounds that Do Not Heal: Differences and Similarities between Renal Regeneration/Repair and Renal Cell Carcinoma

Joseph Riss Chand Khanna Seongjoon Koo Gadisetti V.R. Chandramouli Howard H. Yang

<p>Figure 4, Tables 4-8, supplementary text</p>

10.1158/0008-5472.22364435

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Supplementary Figure S4 from Cancers as Wounds that Do Not Heal: Differences and Similarities between Renal Regeneration/Repair and Renal Cell Carcinoma

Joseph Riss Chand Khanna Seongjoon Koo Gadisetti V.R. Chandramouli Howard H. Yang

Supplementary Figure S4 from Cancers as Wounds that Do Not Heal: Differences and Similarities between Renal Regeneration/Repair and Renal Cell Carcinoma

Kidney cancer

10.1158/0008-5472.22364438.v1

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