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1. The epigenetic evolution of glioma is determined by the IDH1 mutation status and treatment regimen

Author

Malta, Tathiane M., primary, Sabedot, Thais S., additional, Morosini, Natalia S., additional, Datta, Indrani, additional, Garofano, Luciano, additional, Vallentgoed, Wies R., additional, Varn, Frederick S., additional, Aldape, Kenneth, additional, D'Angelo, Fulvio, additional, Bakas, Spyridon, additional, Barnholtz-Sloan, Jill S., additional, Gan, Hui K., additional, Hasanain, Mohammad, additional, Hau, Ann-Christin, additional, Johnson, Kevin C., additional, Cazacu, Simona, additional, deCarvalho, Ana C., additional, Khasraw, Mustafa, additional, Kocakavuk, Emre, additional, Kouwenhoven, Mathilde C.M., additional, Migliozzi, Simona, additional, Niclou, Simone P., additional, Niers, Johanna M., additional, Ormond, D. Ryan., additional, Paek, Sun Ha, additional, Reifenberger, Guido, additional, Sillevis Smitt, Peter A., additional, Smits, Marion, additional, Stead, Lucy F., additional, van den Bent, Martin J., additional, Van Meir, Erwin G., additional, Walenkamp, Annemiek, additional, Weiss, Tobias, additional, Weller, Michael, additional, Westerman, Bart A., additional, Ylstra, Bauke, additional, Wesseling, Pieter, additional, Lasorella, Anna, additional, French, Pim J., additional, Poisson, Laila M., additional, Consortium, The GLASS, additional, Verhaak, Roel G.W., additional, Iavarone, Antonio, additional, and Noushmehr, Houtan, additional

Published
2023
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3. Abstract 127: Single-cell methylation sequencing data reveals succinct metastatic migration histories and tumor progression models

Author

Li, Xuan C., primary, Liu, Yuelin, additional, Mehrabadi, Farid Rashidi, additional, Schäffer, Alejandro A., additional, Pratt, Drew, additional, Crawford, David R., additional, Malikić, Salem, additional, Molloy, Erin K., additional, Gopalan, Vishaka, additional, Mount, Stephen M., additional, Ruppin, Eytan, additional, Aldape, Kenneth, additional, and Sahinalp, S. Cenk, additional

Published
2023
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4. Abstract 3523: A systematic comparison of molecular features shared by H3K27-altered diffuse midline gliomas and posterior fossa A ependymomas

Author

Pun, Matthew, primary, Pratt, Drew, additional, Nano, Patricia R., additional, Joshi, Piyush K., additional, Jiang, Li, additional, Englinger, Bernhard, additional, Rao, Arvind, additional, Cieslik, Marcin, additional, Chinnaiyan, Arul M., additional, Aldape, Kenneth, additional, Pfister, Stefan, additional, Filbin, Mariella G., additional, Bhaduri, Aparna, additional, and Venneti, Sriram, additional

Published
2023
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5. Abstract 4512: My Pediatric and Adult Rare Tumor Network (MyPART): integrating longitudinal, clinical, molecular, and patient-reported outcomes for rare tumors

Author

Ahmed, Shadin, primary, Raygada, Margarita, additional, Lockridge, Robin, additional, Malone, Mary Frances Wedekind, additional, Rivero, Jaydira Del, additional, Glod, John W., additional, Thomas, Barbara J., additional, Bernstein, Donna, additional, Miettinen, Markku M., additional, Xi, Liqiang, additional, Kim, Jung, additional, Tygagi, Manoj, additional, Raffeld, Mark, additional, Aldape, Kenneth, additional, Malayeri, Ashkan A., additional, Sandler, Abby B., additional, Widemann, Brigitte C., additional, and Reilly, Karlyne M., additional

Published
2023
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6. Abstract 4355: Prediction of cancer treatment response from histopathology images for a broad set of treatments and indications

Author

Hoang, Danh-Tai, primary, Dinstag, Gal, additional, Hermida, Leandro C., additional, Ben-Zvi, Doreen S., additional, Elis, Efrat, additional, Caley, Katherine, additional, Sinha, Sanju, additional, Sinha, Neelam, additional, Dampier, Christopher H., additional, Beker, Tuvik, additional, Aldape, Kenneth, additional, Aharonov, Ranit, additional, Stone, Eric A., additional, and Ruppin, Eytan, additional

Published
2023
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7. Abstract 957: Prediction of patient response to targeted and immunotherapies from the tumor transcriptome in a wide set of indications and clinical trials

Author

Dinstag, Gal, primary, Shulman, Eldad D., additional, Elis, Efrat, additional, Ben-Zvi, Doreen S., additional, Tirosh, Omer, additional, Maimon, Eden, additional, Meilijson, Isaac, additional, Elalouf, Emmanuel, additional, Temkin, Boris, additional, Vitkovsky, Philipp, additional, Schiff, Eyal, additional, Hoang, Danh-Tai, additional, Sinha, Sanju, additional, Nair, Nishanth Ulhas, additional, Sang-Lee, Joo, additional, Schäffer, Alejandro A., additional, Ronai, Ze'ev, additional, Juric, Dejan, additional, Apolo, Andrea B., additional, Dahut, William L., additional, Lipkowitz, Stanley, additional, Berger, Raanan, additional, Kurzrock, Razelle, additional, Papanicolau-Sengos, Antonios, additional, Karzai, Fatima, additional, Gilbert, Mark R., additional, Aldape, Kenneth, additional, Rajagopal, Padma S., additional, Beker, Tuvik, additional, Ruppin, Eytan, additional, and Aharonov, Ranit, additional

Published
2023
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10. Abstract 1889: Next-generation neuropathology - Improving diagnostic accuracy for brain tumors using DNA methylation array-based molecular profiling

Author

Jones, David T. W., primary, Capper, David, additional, Sill, Martin, additional, Hovestadt, Volker, additional, Schweizer, Leonille, additional, Fischer, Roger, additional, Schick, Matthias, additional, Bewerunge-Hudler, Melanie, additional, Benner, Axel, additional, Zagzag, David, additional, Lichter, Peter, additional, Karajannis, Matthias A., additional, Aldape, Kenneth D., additional, Korshunov, Andrey, additional, Deimling, Andreas von, additional, and Pfister, Stefan M., additional

Published
2014
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11. Abstract 4276: T200: a high depth targeted exome sequencing platform to identify actionable alterations in FFPE solid tumor samples

Author

Ken Chen, Song Ping, John de Groot, Funda Meric-Bernstam, Aldape Kenneth, Lan Zhang, Mark J. Routbort, John Mendelsohn, Kenna M. Shaw, Chacha Horombe, Ezzeddine Nader, Raja Luthra, Yong Mao, Karina Eterovic, Lin-ya Tang, Michael Davies, Stacy L. Moulder, Scott Kopetz, Gordon B. Mills, Zhang Qingxiu, and Hao Zhao

Subjects
Genetics, Cancer Research, Cancer, Ion semiconductor sequencing, Biology, medicine.disease, medicine.disease_cause, Loss of heterozygosity, Oncology, medicine, Copy-number variation, KRAS, Indel, Exome sequencing, Reference genome
Abstract

Background: We developed and established a high depth targeted sequencing platform of 202 genes (all exons) to identify actionable DNA alterations in tumor samples. We aimed a minimum of 500x depth and defined actionable if the aberration had a direct link to an available clinical treatment or clinical trial. Our platform was optimized for FFPE specimens and low input DNA while the data analysis pipeline was designed to detect low frequency mutations and copy number alterations. Over 500 tumor samples and matched normal were analyzed using this platform. Methods: Libraries were made from a minimum of 170 ng of FFPE DNA (tumors) or blood DNA (matched normal). Capture of 202 genes (over 5,000 exons) was performed using Nimblegen probes to a minimum of 50x fold enrichment. Captured libraries were sequenced using Illumina HiSeq2000. Duplicate reads were removed from the raw data and the reads were mapped hg19 reference genome. We used VarScan2 for calling somatic, germline and loss of heterozygosity SNVs and short indels. Copy number variation was also reported when significant gain/loss on an exon was detected. Additionally, we used other tolls to annotate the functional consequence of the SNVs, such as CanDrA to predict if an SNV is driver or passenger event. Results: We sequenced over 500 tumor samples and their normal match (blood). The mean coverage for most of samples was over 1500x, which allowed us to detect low frequency mutations (5% or higher) with accuracy. The most common disease sites analyzed where we found genetic alterations were: breast, colon, brain, ovary, endometrial, skin, lung, prostate, head and neck, sarcoma, kidney and stomach. About 98% of all tumors analyzed had at least one somatic alteration (SNVs or copy number) and although the vast majority of the samples analyzed were derived from FFPE blocks, the number of samples that failed was less than 5%. Among the most common genes mutated are several “actionable genes” such as BRAF, EGFR and KRAS. The samples tested in this platform were also tested on ion torrent Ampliseq 46 gene panel (46 overlapping genes) in a CLIA certified laboratory at MD Anderson Cancer Center with a very high level of concordance. Conclusion: With a very low level of failure and high depth provided, our results indicate that this platform can be used for FFPE tumor samples with high level of accuracy and sensitivity, showing that this platform is reliable to be implemented in clinical settings. Citation Format: Karina Eterovic, Ken Chen, Hao Zhao, Funda Meric-Bernstam, Raja Luthra, Aldape Kenneth, Mark Routbort, Scott Kopetz, Michael Davies, John de Groot, Stacy Moulder, Yong Mao, Chacha Horombe, Lin-ya Tang, Song Ping, Zhang Qingxiu, Ezzeddine Nader, Lan Zhang, Kenna M. Shaw, John Mendelsohn, Gordon B. Mills. T200: a high depth targeted exome sequencing platform to identify actionable alterations in FFPE solid tumor samples. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4276. doi:10.1158/1538-7445.AM2014-4276

Published
2014

26. Abstract 1144: Micro RNA profiling of intracranial germ cell tumors

Author

Terashima, Keita, primary, Shen, Jianhe J., additional, Luan, Joseph, additional, Yu, Alexander, additional, Suzuki, Tomonari, additional, Nishikawa, Ryo, additional, Matsutani, Masao, additional, Nakamura, Hideo, additional, Kinjo, Sayano, additional, Natsume, Atsushi, additional, Wakabayashi, Toshihiko, additional, Allen, Jeffrey C., additional, Aldape, Kenneth D., additional, Adesina, Adekunle M., additional, Man, Tsz-Kwong, additional, and Lau, Ching C., additional

Published
2011
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28. Abstract 1789: NFKBIA deletion in malignant gliomas

Author

Bredel, Markus, primary, Yadav, Ajay, additional, Renfrow, Jaclyn, additional, Scholtens, Denise, additional, Chandler, James, additional, Bredel, Claudia, additional, Tagge, Michael, additional, Lukac, Paul, additional, Robe, Pierre, additional, Vogel, Hannes, additional, Scheck, Adrienne, additional, Aldape, Kenneth, additional, Chakravarti, Arnab, additional, and Harsh, Griffith, additional

Published
2010
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33. Reversing HOXA9 Oncogene Activation by PI3K Inhibition: Epigenetic Mechanism and Prognostic Significance in Human Glioblastoma

Author

Costa, Bruno M., primary, Smith, Justin S., additional, Chen, Ying, additional, Chen, Justin, additional, Phillips, Heidi S., additional, Aldape, Kenneth D., additional, Zardo, Giuseppe, additional, Nigro, Janice, additional, James, C. David, additional, Fridlyand, Jane, additional, Reis, Rui M., additional, and Costello, Joseph F., additional

Published
2010
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35. Her-2 Overexpression Increases the Metastatic Outgrowth of Breast Cancer Cells in the Brain

Author

Palmieri, Diane, primary, Bronder, Julie L., additional, Herring, Jeanne M., additional, Yoneda, Toshiyuki, additional, Weil, Robert J., additional, Stark, Andreas M., additional, Kurek, Raffael, additional, Vega-Valle, Eleazar, additional, Feigenbaum, Lionel, additional, Halverson, Douglas, additional, Vortmeyer, Alexander O., additional, Steinberg, Seth M., additional, Aldape, Kenneth, additional, and Steeg, Patricia S., additional

Published
2007
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36. Distinct Genetic Signatures among Pilocytic Astrocytomas Relate to Their Brain Region Origin

Author

Sharma, Mukesh K., primary, Mansur, David B., additional, Reifenberger, Guido, additional, Perry, Arie, additional, Leonard, Jeffrey R., additional, Aldape, Kenneth D., additional, Albin, Meredith G., additional, Emnett, Ryan J., additional, Loeser, Simon, additional, Watson, Mark A., additional, Nagarajan, Rakesh, additional, and Gutmann, David H., additional

Published
2007
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37. Serum IgE, Tumor Epidermal Growth Factor Receptor Expression, and Inherited Polymorphisms Associated with Glioma Survival

Author

Wrensch, Margaret, primary, Wiencke, John K., additional, Wiemels, Joe, additional, Miike, Rei, additional, Patoka, Joe, additional, Moghadassi, Michelle, additional, McMillan, Alex, additional, Kelsey, Karl T., additional, Aldape, Kenneth, additional, Lamborn, Kathleen R., additional, Parsa, Andrew T., additional, Sison, Jennette D., additional, and Prados, Michael D., additional

Published
2006
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38. FoxM1B Is Overexpressed in Human Glioblastomas and Critically Regulates the Tumorigenicity of Glioma Cells

Author

Liu, Mingguang, primary, Dai, Bingbing, additional, Kang, Shin-Hyuk, additional, Ban, Kechen, additional, Huang, Feng-Ju, additional, Lang, Frederick F., additional, Aldape, Kenneth D., additional, Xie, Tong-xin, additional, Pelloski, Christopher E., additional, Xie, Keping, additional, Sawaya, Raymond, additional, and Huang, Suyun, additional

Published
2006
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40. Integrated Array-Comparative Genomic Hybridization and Expression Array Profiles Identify Clinically Relevant Molecular Subtypes of Glioblastoma

Author

Nigro, Janice M., primary, Misra, Anjan, additional, Zhang, Li, additional, Smirnov, Ivan, additional, Colman, Howard, additional, Griffin, Chandi, additional, Ozburn, Natalie, additional, Chen, Mingang, additional, Pan, Edward, additional, Koul, Dimpy, additional, Yung, W.K. Alfred, additional, Feuerstein, Burt G., additional, and Aldape, Kenneth D., additional

Published
2005
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42. Polymorphisms of DNA Repair Genes and Risk of Glioma

Author

Wang, Li-E, primary, Bondy, Melissa L., additional, Shen, Hongbing, additional, El-Zein, Randa, additional, Aldape, Kenneth, additional, Cao, Yumei, additional, Pudavalli, Vinay, additional, Levin, Victor A., additional, Yung, W. K. Alfred, additional, and Wei, Qingyi, additional

Published
2004
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43. Src Family Kinases as Novel Therapeutic Targets to Treat Breast Cancer Brain Metastases.

Author

Siyuan Zhang, Wen-Chien Huang, Lin Zhang, Chenyu Zhang, Lowery, Frank J., Zhaoxi Ding, Hua Guo, Hai Wang, Suyun Huang, Sahin, Aysegul A., Aldape, Kenneth D., Steeg, Patricia S., and Dihua Yu

Subjects
*BREAST cancer treatment, *CANCER invasiveness, *CELL lines, *BRAIN cancer, *CELL cycle
Abstract

Despite better control of early-stage disease and improved overall survival of patients with breast cancer, the incidence of life-threatening brain metastases continues to increase in some of these patients. Unfortunately, other than palliative treatments there is no effective therapy for this condition. In this study, we reveal a critical role for Src activation in promoting brainmetastasis in a preclinical model of breast cancer and we show how Src-targeting combinatorial regimens can treat HER2+ brain metastases in this model. We found that Src was hyperactivated in brain-seeking breast cancer cells derived from human cell lines or from patients' brain metastases. Mechanistically, Src activation promoted tumor cell extravasation into the brain parenchyma via permeabilization of the blood--brain barrier. When combined with the EGFR/HER2 dual-targeting drug lapatinib, an Src-targeting combinatorial regimen prevented outgrowth of disseminated breast cancer cells through the induction of cell-cycle arrest. More importantly, this combinatorial regimen inhibited the outgrowth of established experimental brain metastases, prolonging the survival of metastases-bearing mice. Our results provide a rationale for clinical evaluation of Src-targeting regimens to treat patients with breast cancer suffering from brain metastasis. [ABSTRACT FROM AUTHOR]

Published
2013
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44. Caveolin-1 Upregulation Mediates Suppression of Primary Breast Tumor Growth and Brain Metastases by Stat3 Inhibition.

Author

Wen-Tai Chiu, Hsueh-Te Lee, Feng-Ju Huang, Aldape, Kenneth D., Yao, Jun, Steeg, Patricia S., Cheng-Yang Chou, Zhimin Lu, Keping Xie, and Suyun Huang

Subjects
*BREAST cancer, *TUMOR growth, *CANCER invasiveness, *METASTASIS, *CANCER cells
Abstract

Stat3 activation has been implicated as an important driver of brain metastasis in breast cancer, but the critical targets of Stat3 in this process are yet to be fully defined. In this study, we identified the lipid raft organizing protein Caveolin-1 (Cav-1) as a critical genetic target of Stat3 in this process. In human breast cancers, we found that activated Stat3 correlated with attenuation of Cav-1 in brain metastases relative to primary tumors. Cav-1 promoter activity and gene expression were increased by overexpressing an activated form of Stat3 but decreased by attenuation of Stat3 activity or expression. We identified putative Stat3- binding elements in the Cav-1 promoter and showed a direct repression of Cav-1 transcription by Stat3. Reciprocally, we showed that strategies to increase or decrease Cav-1 expression were sufficient to attenuate or promote breast cancer cell invasion. Furthermore, increased expression of Cav-1 phenocopied the effects of Stat3 activation in blocking primary tumor growth and abrogating formation of brain metastases. Collectively, our findings provide clinical and mechanistic evidence that Cav-1 is a critical target for suppression by Stat3 in driving invasion and metastasis of breast cancer cells. Cancer Res; 71(14); 4932-43. ©2011 AACR. [ABSTRACT FROM AUTHOR]

Published
2011
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45. Chromosome 7 gain compensates for chromosome 10 loss in glioma.

Author

Nair NU, Schaffer AA, Gertz EM, Cheng K, Zerbib J, Sahu AD, Leor G, Shulman ED, Aldape KD, Ben-David U, and Ruppin E

Abstract

The co-occurrence of chromosome 10 loss and chromosome 7 gain in gliomas is the most frequent loss-gain co-aneuploidy pair in human cancers. This phenomenon has been investigated since the late 1980s without resolution. Expanding beyond previous gene-centric studies, we investigated the co-occurrence in a genome-wide manner taking an evolutionary perspective. Mining of large-scale tumor aneuploidy data confirmed the previous finding of a small-scale longitudinal study that the most likely order is chromosome 10 loss followed by chromosome 7 gain. Extensive analysis of genomic and transcriptomic data from both patients and cell lines revealed that this co-occurrence can be explained by functional rescue interactions that are highly enriched on chromosome 7, which could potentially compensate for any detrimental consequences arising from the loss of chromosome 10. Transcriptomic data from various normal, non-cancerous human brain tissues were analyzed to assess which tissues may be most predisposed to tolerate compensation of chromosome 10 loss by chromosome 7 gain. The analysis indicated that the pre-existing transcriptomic states in the cortex and frontal cortex, where gliomas arise, are more favorable than other brain regions for compensation by rescuer genes that are active on chromosome 7. Collectively, these findings suggest that the phenomenon of chromosome 10 loss and chromosome 7 gain in gliomas is orchestrated by a complex interaction of many genes residing within these two chromosomes and provide a plausible reason why this co-occurrence happens preferentially in cancers originating in certain regions of the brain.

Published
2024
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46. The Epigenetic Evolution of Glioma Is Determined by the IDH1 Mutation Status and Treatment Regimen.

Author

Malta TM, Sabedot TS, Morosini NS, Datta I, Garofano L, Vallentgoed W, Varn FS, Aldape K, D'Angelo F, Bakas S, Barnholtz-Sloan JS, Gan HK, Hasanain M, Hau AC, Johnson KC, Cazacu S, deCarvalho AC, Khasraw M, Kocakavuk E, Kouwenhoven MCM, Migliozzi S, Niclou SP, Niers JM, Ormond DR, Paek SH, Reifenberger G, Sillevis Smitt PA, Smits M, Stead LF, van den Bent MJ, Van Meir EG, Walenkamp A, Weiss T, Weller M, Westerman BA, Ylstra B, Wesseling P, Lasorella A, French PJ, Poisson LM, Verhaak RGW, Iavarone A, and Noushmehr H

Subjects
Humans, Epigenesis, Genetic, Epigenomics, Mutation, Neoplasm Recurrence, Local genetics, Tumor Microenvironment, Brain Neoplasms pathology, Glioma pathology, Isocitrate Dehydrogenase genetics, Isocitrate Dehydrogenase metabolism
Abstract

Tumor adaptation or selection is thought to underlie therapy resistance in glioma. To investigate longitudinal epigenetic evolution of gliomas in response to therapeutic pressure, we performed an epigenomic analysis of 132 matched initial and recurrent tumors from patients with IDH-wildtype (IDHwt) and IDH-mutant (IDHmut) glioma. IDHwt gliomas showed a stable epigenome over time with relatively low levels of global methylation. The epigenome of IDHmut gliomas showed initial high levels of genome-wide DNA methylation that was progressively reduced to levels similar to those of IDHwt tumors. Integration of epigenomics, gene expression, and functional genomics identified HOXD13 as a master regulator of IDHmut astrocytoma evolution. Furthermore, relapse of IDHmut tumors was accompanied by histologic progression that was associated with survival, as validated in an independent cohort. Finally, the initial cell composition of the tumor microenvironment varied between IDHwt and IDHmut tumors and changed differentially following treatment, suggesting increased neoangiogenesis and T-cell infiltration upon treatment of IDHmut gliomas. This study provides one of the largest cohorts of paired longitudinal glioma samples with epigenomic, transcriptomic, and genomic profiling and suggests that treatment of IDHmut glioma is associated with epigenomic evolution toward an IDHwt-like phenotype., Significance: Standard treatments are related to loss of DNA methylation in IDHmut glioma, resulting in epigenetic activation of genes associated with tumor progression and alterations in the microenvironment that resemble treatment-naïve IDHwt glioma., (©2023 The Authors; Published by the American Association for Cancer Research.)

Published
2024
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