journal
MENU ▼
Read by QxMD icon Read
search

Cancer Cell

journal
https://www.readbyqxmd.com/read/28648284/common-molecular-subtypes-among-asian-hepatocellular-carcinoma-and-cholangiocarcinoma
#1
Jittiporn Chaisaingmongkol, Anuradha Budhu, Hien Dang, Siritida Rabibhadana, Benjarath Pupacdi, So Mee Kwon, Marshonna Forgues, Yotsawat Pomyen, Vajarabhongsa Bhudhisawasdi, Nirush Lertprasertsuke, Anon Chotirosniramit, Chawalit Pairojkul, Chirayu U Auewarakul, Thaniya Sricharunrat, Kannika Phornphutkul, Suleeporn Sangrajrang, Maggie Cam, Ping He, Stephen M Hewitt, Kris Ylaya, Xiaolin Wu, Jesper B Andersen, Snorri S Thorgeirsson, Joshua J Waterfall, Yuelin J Zhu, Jennifer Walling, Holly S Stevenson, Daniel Edelman, Paul S Meltzer, Christopher A Loffredo, Natsuko Hama, Tatsuhiro Shibata, Robert H Wiltrout, Curtis C Harris, Chulabhorn Mahidol, Mathuros Ruchirawat, Xin W Wang
Intrahepatic cholangiocarcinoma (ICC) and hepatocellular carcinoma (HCC) are clinically disparate primary liver cancers with etiological and biological heterogeneity. We identified common molecular subtypes linked to similar prognosis among 199 Thai ICC and HCC patients through systems integration of genomics, transcriptomics, and metabolomics. While ICC and HCC share recurrently mutated genes, including TP53, ARID1A, and ARID2, mitotic checkpoint anomalies distinguish the C1 subtype with key drivers PLK1 and ECT2, whereas the C2 subtype is linked to obesity, T cell infiltration, and bile acid metabolism...
June 6, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28625481/chromatin-accessibility-landscape-of-cutaneous-t-cell-lymphoma-and-dynamic-response-to-hdac-inhibitors
#2
Kun Qu, Lisa C Zaba, Ansuman T Satpathy, Paul G Giresi, Rui Li, Yonghao Jin, Randall Armstrong, Chen Jin, Nathalie Schmitt, Ziba Rahbar, Hideki Ueno, William J Greenleaf, Youn H Kim, Howard Y Chang
Here, we define the landscape and dynamics of active regulatory DNA in cutaneous T cell lymphoma (CTCL) by ATAC-seq. Analysis of 111 human CTCL and control samples revealed extensive chromatin signatures that distinguished leukemic, host, and normal CD4(+) T cells. We identify three dominant patterns of transcription factor (TF) activation that drive leukemia regulomes, as well as TF deactivations that alter host T cells in CTCL patients. Clinical response to histone deacetylase inhibitors (HDACi) is strongly associated with a concurrent gain in chromatin accessibility...
June 1, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28609660/snapshot-immune-checkpoint-inhibitors
#3
Gabriel Abril-Rodriguez, Antoni Ribas
Immunotherapy has changed the landscape of cancer treatment. Checkpoint blockade therapies unleash breaks in the immune system and induce long-lasting responses. However, a significant number of patients do not respond (innate resistance), and a subset progress after responding (acquired resistance). A better understanding of the molecular mechanisms underlying checkpoint blockade therapies will facilitate the design of novel strategies to treat and prevent resistance. To view this SnapShot, open or download the PDF...
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28609659/development-of-peptidomimetic-inhibitors-of-the-erg-gene-fusion-product-in-prostate-cancer
#4
Xiaoju Wang, Yuanyuan Qiao, Irfan A Asangani, Bushra Ateeq, Anton Poliakov, Marcin Cieślik, Sethuramasundaram Pitchiaya, Balabhadrapatruni V S K Chakravarthi, Xuhong Cao, Xiaojun Jing, Cynthia X Wang, Ingrid J Apel, Rui Wang, Jean Ching-Yi Tien, Kristin M Juckette, Wei Yan, Hui Jiang, Shaomeng Wang, Sooryanarayana Varambally, Arul M Chinnaiyan
No abstract text is available yet for this article.
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28609658/a-systems-biology-approach-identifies-fut8-as-a-driver-of-melanoma-metastasis
#5
Praveen Agrawal, Barbara Fontanals-Cirera, Elena Sokolova, Samson Jacob, Christopher A Vaiana, Diana Argibay, Veronica Davalos, Meagan McDermott, Shruti Nayak, Farbod Darvishian, Mireia Castillo, Beatrix Ueberheide, Iman Osman, David Fenyö, Lara K Mahal, Eva Hernando
Association of aberrant glycosylation with melanoma progression is based mainly on analyses of cell lines. Here we present a systems-based study of glycomic changes and corresponding enzymes associated with melanoma metastasis in patient samples. Upregulation of core fucosylation (FUT8) and downregulation of α-1,2 fucosylation (FUT1, FUT2) were identified as features of metastatic melanoma. Using both in vitro and in vivo studies, we demonstrate FUT8 is a driver of melanoma metastasis which, when silenced, suppresses invasion and tumor dissemination...
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28609657/ack1-tnk2-regulates-histone-h4-tyr88-phosphorylation-and-ar-gene-expression-in-castration-resistant-prostate-cancer
#6
Kiran Mahajan, Pavani Malla, Harshani R Lawrence, Zhihua Chen, Chandan Kumar-Sinha, Rohit Malik, Sudhanshu Shukla, Jongphil Kim, Domenico Coppola, Nicholas J Lawrence, Nupam P Mahajan
The androgen receptor (AR) is critical for the progression of prostate cancer to a castration-resistant (CRPC) state. AR antagonists are ineffective due to their inability to repress the expression of AR or its splice variant, AR-V7. Here, we report that the tyrosine kinase ACK1 (TNK2) phosphorylates histone H4 at tyrosine 88 upstream of the AR transcription start site. The WDR5/MLL2 complex reads the H4-Y88-phosphorylation marks and deposits the transcriptionally activating H3K4-trimethyl marks promoting AR transcription...
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28609656/kupffer-cell-derived-tnf-triggers-cholangiocellular-tumorigenesis-through-jnk-due-to-chronic-mitochondrial-dysfunction-and-ros
#7
Detian Yuan, Shan Huang, Emanuel Berger, Lei Liu, Nina Gross, Florian Heinzmann, Marc Ringelhan, Tracy O Connor, Mira Stadler, Michael Meister, Julia Weber, Rupert Öllinger, Nicole Simonavicius, Florian Reisinger, Daniel Hartmann, Rüdiger Meyer, Maria Reich, Marco Seehawer, Valentina Leone, Bastian Höchst, Dirk Wohlleber, Simone Jörs, Marco Prinz, Duncan Spalding, Ulrike Protzer, Tom Luedde, Luigi Terracciano, Matthias Matter, Thomas Longerich, Percy Knolle, Thomas Ried, Verena Keitel, Fabian Geisler, Kristian Unger, Einat Cinnamon, Eli Pikarsky, Norbert Hüser, Roger J Davis, Darjus F Tschaharganeh, Roland Rad, Achim Weber, Lars Zender, Dirk Haller, Mathias Heikenwalder
Intrahepatic cholangiocarcinoma (ICC) is a highly malignant, heterogeneous cancer with poor treatment options. We found that mitochondrial dysfunction and oxidative stress trigger a niche favoring cholangiocellular overgrowth and tumorigenesis. Liver damage, reactive oxygen species (ROS) and paracrine tumor necrosis factor (Tnf) from Kupffer cells caused JNK-mediated cholangiocellular proliferation and oncogenic transformation. Anti-oxidant treatment, Kupffer cell depletion, Tnfr1 deletion, or JNK inhibition reduced cholangiocellular pre-neoplastic lesions...
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28609655/mll2-not-mll1-plays-a-major-role-in-sustaining-mll-rearranged-acute-myeloid-leukemia
#8
Yufei Chen, Konstantinos Anastassiadis, Andrea Kranz, A Francis Stewart, Kathrin Arndt, Claudia Waskow, Akihiko Yokoyama, Kenneth Jones, Tobias Neff, Yoo Lee, Patricia Ernst
The MLL1 histone methyltransferase gene undergoes many distinct chromosomal rearrangements to yield poor-prognosis leukemia. The remaining wild-type allele is most commonly, but not always, retained. To what extent the wild-type allele contributes to leukemogenesis is unclear. Here we show, using rigorous, independent animal models, that endogenous MLL1 is dispensable for MLL-rearranged leukemia. Potential redundancy was addressed by co-deleting the closest paralog, Mll2. Surprisingly, Mll2 deletion alone had a significant impact on survival of MLL-AF9-transformed cells, and additional Mll1 loss further reduced viability and proliferation...
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28609654/intertumoral-heterogeneity-within-medulloblastoma-subgroups
#9
Florence M G Cavalli, Marc Remke, Ladislav Rampasek, John Peacock, David J H Shih, Betty Luu, Livia Garzia, Jonathon Torchia, Carolina Nor, A Sorana Morrissy, Sameer Agnihotri, Yuan Yao Thompson, Claudia M Kuzan-Fischer, Hamza Farooq, Keren Isaev, Craig Daniels, Byung-Kyu Cho, Seung-Ki Kim, Kyu-Chang Wang, Ji Yeoun Lee, Wieslawa A Grajkowska, Marta Perek-Polnik, Alexandre Vasiljevic, Cecile Faure-Conter, Anne Jouvet, Caterina Giannini, Amulya A Nageswara Rao, Kay Ka Wai Li, Ho-Keung Ng, Charles G Eberhart, Ian F Pollack, Ronald L Hamilton, G Yancey Gillespie, James M Olson, Sarah Leary, William A Weiss, Boleslaw Lach, Lola B Chambless, Reid C Thompson, Michael K Cooper, Rajeev Vibhakar, Peter Hauser, Marie-Lise C van Veelen, Johan M Kros, Pim J French, Young Shin Ra, Toshihiro Kumabe, Enrique López-Aguilar, Karel Zitterbart, Jaroslav Sterba, Gaetano Finocchiaro, Maura Massimino, Erwin G Van Meir, Satoru Osuka, Tomoko Shofuda, Almos Klekner, Massimo Zollo, Jeffrey R Leonard, Joshua B Rubin, Nada Jabado, Steffen Albrecht, Jaume Mora, Timothy E Van Meter, Shin Jung, Andrew S Moore, Andrew R Hallahan, Jennifer A Chan, Daniela P C Tirapelli, Carlos G Carlotti, Maryam Fouladi, José Pimentel, Claudia C Faria, Ali G Saad, Luca Massimi, Linda M Liau, Helen Wheeler, Hideo Nakamura, Samer K Elbabaa, Mario Perezpeña-Diazconti, Fernando Chico Ponce de León, Shenandoah Robinson, Michal Zapotocky, Alvaro Lassaletta, Annie Huang, Cynthia E Hawkins, Uri Tabori, Eric Bouffet, Ute Bartels, Peter B Dirks, James T Rutka, Gary D Bader, Jüri Reimand, Anna Goldenberg, Vijay Ramaswamy, Michael D Taylor
While molecular subgrouping has revolutionized medulloblastoma classification, the extent of heterogeneity within subgroups is unknown. Similarity network fusion (SNF) applied to genome-wide DNA methylation and gene expression data across 763 primary samples identifies very homogeneous clusters of patients, supporting the presence of medulloblastoma subtypes. After integration of somatic copy-number alterations, and clinical features specific to each cluster, we identify 12 different subtypes of medulloblastoma...
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28609653/aberrant-glycosylation-in-cancer-a-novel-molecular-mechanism-controlling-metastasis
#10
Ana Magalhães, Henrique O Duarte, Celso A Reis
Glycosylation alterations are involved in several steps of human cancer pathogenesis. In this issue of Cancer Cell, Agrawal et al. identified the glycosyltransferase FUT8 as a previously unrecognized mediator of melanoma metastasis, establishing core fucosylation as a potential therapeutic target for prevention and treatment of metastatic tumors.
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28609652/paradoxical-effects-of-mll-paralogs-in-mll-rearranged-leukemia
#11
Michael J Thirman
Conflicting data exist on the requirement for wild-type MLL1 in MLL-rearranged leukemia. In this issue of Cancer Cell, Chen et al. describe complementary approaches demonstrating that MLL1 is dispensable for MLL-fusion-mediated leukemogenesis. They also observe an unexpected role for MLL2 in MLL-rearranged leukemia cells and identify potential therapeutic targets.
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28609651/from-one-to-many-further-refinement-of-medulloblastoma-subtypes-offers-promise-for-personalized-therapy
#12
Abhishek Bavle, D Williams Parsons
There is significant intertumoral heterogeneity within the four molecular subgroups of medulloblastoma. In this issue of Cancer Cell, Cavalli et al. apply similarity network fusion to gene expression and DNA methylation data to identify 12 medulloblastoma subtypes with distinct molecular and clinical profiles, making an important step toward molecularly tailored therapy.
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28552327/inhibition-of-b-cell-receptor-signaling-by-ibrutinib-in-primary-cns-lymphoma
#13
Michail S Lionakis, Kieron Dunleavy, Mark Roschewski, Brigitte C Widemann, John A Butman, Roland Schmitz, Yandan Yang, Diane E Cole, Christopher Melani, Christine S Higham, Jigar V Desai, Michele Ceribelli, Lu Chen, Craig J Thomas, Richard F Little, Juan Gea-Banacloche, Sucharita Bhaumik, Maryalice Stetler-Stevenson, Stefania Pittaluga, Elaine S Jaffe, John Heiss, Nicole Lucas, Seth M Steinberg, Louis M Staudt, Wyndham H Wilson
Primary CNS lymphoma (PCNSL) harbors mutations that reinforce B cell receptor (BCR) signaling. Ibrutinib, a Bruton's tyrosine kinase (BTK) inhibitor, targets BCR signaling and is particularly active in lymphomas with mutations altering the BCR subunit CD79B and MYD88. We performed a proof-of-concept phase Ib study of ibrutinib monotherapy followed by ibrutinib plus chemotherapy (DA-TEDDi-R). In 18 PCNSL patients, 94% showed tumor reductions with ibrutinib alone, including patients having PCNSL with CD79B and/or MYD88 mutations, and 86% of evaluable patients achieved complete remission with DA-TEDDi-R...
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28552326/ibrutinib-in-pcnsl-the-curious-cases-of-clinical-responses-and-aspergillosis
#14
Christian Grommes, Anas Younes
In this issue of Cancer Cell, Lionakis et al. demonstrate that the combination of temozolomide, etoposide, doxorubicin, dexamethasone, rituximab, and the Bruton tyrosine kinase (BTK) inhibitor ibrutinib induced frequent responses in patients with primary central nervous system lymphoma but was associated with significant toxicity, including pulmonary and cerebral aspergillosis infections.
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28528867/a-pan-cancer-proteogenomic-atlas-of-pi3k-akt-mtor-pathway-alterations
#15
Yiqun Zhang, Patrick Kwok-Shing Ng, Melanie Kucherlapati, Fengju Chen, Yuexin Liu, Yiu Huen Tsang, Guillermo de Velasco, Kang Jin Jeong, Rehan Akbani, Angela Hadjipanayis, Angeliki Pantazi, Christopher A Bristow, Eunjung Lee, Harshad S Mahadeshwar, Jiabin Tang, Jianhua Zhang, Lixing Yang, Sahil Seth, Semin Lee, Xiaojia Ren, Xingzhi Song, Huandong Sun, Jonathan Seidman, Lovelace J Luquette, Ruibin Xi, Lynda Chin, Alexei Protopopov, Thomas F Westbrook, Carl Simon Shelley, Toni K Choueiri, Michael Ittmann, Carter Van Waes, John N Weinstein, Han Liang, Elizabeth P Henske, Andrew K Godwin, Peter J Park, Raju Kucherlapati, Kenneth L Scott, Gordon B Mills, David J Kwiatkowski, Chad J Creighton
Molecular alterations involving the PI3K/AKT/mTOR pathway (including mutation, copy number, protein, or RNA) were examined across 11,219 human cancers representing 32 major types. Within specific mutated genes, frequency, mutation hotspot residues, in silico predictions, and functional assays were all informative in distinguishing the subset of genetic variants more likely to have functional relevance. Multiple oncogenic pathways including PI3K/AKT/mTOR converged on similar sets of downstream transcriptional targets...
June 12, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28486110/ablation-of-key-oncogenic-pathways-by-rita-reactivated-p53-is-required-for-efficient-apoptosis
#16
Vera V Grinkevich, Fedor Nikulenkov, Yao Shi, Martin Enge, Wenjie Bao, Alena Maljukova, Angela Gluch, Alexander Kel, Olle Sangfelt, Galina Selivanova
No abstract text is available yet for this article.
May 8, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28486109/tumor-residing-batf3-dendritic-cells-are-required-for-effector-t-cell-trafficking-and-adoptive-t-cell-therapy
#17
Stefani Spranger, Daisy Dai, Brendan Horton, Thomas F Gajewski
Effector T cells have the capability of recognizing and killing cancer cells. However, whether tumors can become immune resistant through exclusion of effector T cells from the tumor microenvironment is not known. By using a tumor model resembling non-T cell-inflamed human tumors, we assessed whether adoptive T cell transfer might overcome failed spontaneous priming. Flow cytometric assays combined with intra-vital imaging indicated failed trafficking of effector T cells into tumors. Mechanistically, this was due to the absence of CXCL9/10, which we found to be produced by CD103(+) dendritic cells (DCs) in T cell-inflamed tumors...
May 8, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28486108/trib3-promotes-apl-progression-through-stabilization-of-the-oncoprotein-pml-rar%C3%AE-and-inhibition-of-p53-mediated-senescence
#18
Ke Li, Feng Wang, Wen-Bin Cao, Xiao-Xi Lv, Fang Hua, Bing Cui, Jiao-Jiao Yu, Xiao-Wei Zhang, Shuang Shang, Shan-Shan Liu, Jin-Mei Yu, Ming-Zhe Han, Bo Huang, Ting-Ting Zhang, Xia Li, Jian-Dong Jiang, Zhuo-Wei Hu
Acute promyelocytic leukemia (APL) is driven by the oncoprotein PML-RARα, which antagonizes myeloid differentiation and promotes APL-initiating cell self-renewal. Combined all-trans retinoic acid (ATRA) with arsenic trioxide (As2O3) or chemotherapy dramatically improves the prognosis of APL patients. Here we report that expression of pseudokinase Tribble 3 (TRIB3) associates positively with APL progression and therapeutic resistance. The elevated TRIB3 expression promotes APL by interacting with PML-RARα and suppressing its sumoylation, ubiquitylation, and degradation...
May 8, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28486107/rasgrp3-mediates-mapk-pathway-activation-in-gnaq-mutant-uveal-melanoma
#19
Xu Chen, Qiuxia Wu, Philippe Depeille, Peirong Chen, Sophie Thornton, Helen Kalirai, Sarah E Coupland, Jeroen P Roose, Boris C Bastian
Constitutive activation of Gαq signaling by mutations in GNAQ or GNA11 occurs in over 80% of uveal melanomas (UMs) and activates MAPK. Protein kinase C (PKC) has been implicated as a link, but the mechanistic details remained unclear. We identified PKC δ and ɛ as required and sufficient to activate MAPK in GNAQ mutant melanomas. MAPK activation depends on Ras and is caused by RasGRP3, which is significantly and selectively overexpressed in response to GNAQ/11 mutation in UM. RasGRP3 activation occurs via PKC δ- and ɛ-dependent phosphorylation and PKC-independent, DAG-mediated membrane recruitment, possibly explaining the limited effect of PKC inhibitors to durably suppress MAPK in UM...
May 8, 2017: Cancer Cell
https://www.readbyqxmd.com/read/28486106/hippo-signaling-suppresses-cell-ploidy-and-tumorigenesis-through-skp2
#20
Shihao Zhang, Qinghua Chen, Qingxu Liu, Yuxi Li, Xiufeng Sun, Lixin Hong, Suyuan Ji, Chengyan Liu, Jing Geng, Weiji Zhang, Zhonglei Lu, Zhen-Yu Yin, Yuanyuan Zeng, Kwang-Huei Lin, Qiao Wu, Qiyuan Li, Keiko Nakayama, Keiich I Nakayama, Xianming Deng, Randy L Johnson, Liang Zhu, Daming Gao, Lanfen Chen, Dawang Zhou
Polyploidy can lead to aneuploidy and tumorigenesis. Here, we report that the Hippo pathway effector Yap promotes the diploid-polyploid conversion and polyploid cell growth through the Akt-Skp2 axis. Yap strongly induces the acetyltransferase p300-mediated acetylation of the E3 ligase Skp2 via Akt signaling. Acetylated Skp2 is exclusively localized to the cytosol, which causes hyper-accumulation of the cyclin-dependent kinase inhibitor p27, leading to mitotic arrest and subsequently cell polyploidy. In addition, the pro-apoptotic factors FoxO1/3 are overly degraded by acetylated Skp2, resulting in polyploid cell division, genomic instability, and oncogenesis...
May 8, 2017: Cancer Cell
journal
journal
39886
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"