Targeting Therapy Resistance: When Glutamine Catabolism Becomes Essential.

abstract：:The receptor tyrosine kinase HER2 enhances tumor metastasis; however, its role in homing to metastatic organs is poorly understood. The chemokine receptor CXCR4 has recently been shown to mediate the movement of malignant cancer cells to specific organs. Here, we show that HER2 enhances the expression of CXCR4, which ...

journal_title：Cancer cell

authors： Li YM,Pan Y,Wei Y,Cheng X,Zhou BP,Tan M,Zhou X,Xia W,Hortobagyi GN,Yu D,Hung MC

更新日期：2004-11-01 00:00:00

abstract：:The Twist1 transcription factor is known to promote tumor metastasis and induce Epithelial-Mesenchymal Transition (EMT). Here, we report that Twist1 is capable of promoting the formation of invadopodia, specialized membrane protrusions for extracellular matrix degradation. Twist1 induces PDGFRα expression, which in tu...

journal_title：Cancer cell

authors： Eckert MA,Lwin TM,Chang AT,Kim J,Danis E,Ohno-Machado L,Yang J

更新日期：2011-03-08 00:00:00

abstract：:Pro-inflammatory cytokines produced in the tumor microenvironment lead to eradication of anti-tumor immunity and enhanced tumor cell survival. In the current study, we identified tumor necrosis factor alpha (TNF-α) as a major factor triggering cancer cell immunosuppression against T cell surveillance via stabilization...

journal_title：Cancer cell

authors： Lim SO,Li CW,Xia W,Cha JH,Chan LC,Wu Y,Chang SS,Lin WC,Hsu JM,Hsu YH,Kim T,Chang WC,Hsu JL,Yamaguchi H,Ding Q,Wang Y,Yang Y,Chen CH,Sahin AA,Yu D,Hortobagyi GN,Hung MC

更新日期：2016-12-12 00:00:00

abstract：:The life history of cancer cells encompasses a series of genetic missteps in which normal cells are progressively transformed into tumor cells that invade surrounding tissues and become malignant. Most prominent among the regulators disrupted in cancer cells are two tumor suppressors, the retinoblastoma protein (RB) a...

journal_title：Cancer cell

authors： Sherr CJ,McCormick F

更新日期：2002-08-01 00:00:00

abstract：:Transcription factor NF-kappaB has been implicated in cancer development due to its ability to upregulate expression of genes with potentially prooncogenic functions, such as cell cycle regulators and antiapoptotic proteins (Karin et al., 2002). A recent report by suggests that a structural motif, a death domain (DD),...

journal_title：Cancer cell

authors： Häcker H,Karin M

更新日期：2002-12-01 00:00:00

abstract：:Our understanding of Ewing's sarcoma development mediated by the EWS/FLI fusion protein has been limited by a lack of knowledge regarding the tumor cell of origin. To circumvent this, we analyzed the function of EWS/FLI in Ewing's sarcoma itself. By combining retroviral-mediated RNA interference with reexpression stud...

journal_title：Cancer cell

authors： Smith R,Owen LA,Trem DJ,Wong JS,Whangbo JS,Golub TR,Lessnick SL

更新日期：2006-05-01 00:00:00

abstract：:The transcription factor Meis1 drives myeloid leukemogenesis in the context of Hox gene overexpression but is currently considered undruggable. We therefore investigated whether myeloid progenitor cells transformed by Hoxa9 and Meis1 become addicted to targetable signaling pathways. A comprehensive (phospho)proteomic ...

journal_title：Cancer cell

authors： Mohr S,Doebele C,Comoglio F,Berg T,Beck J,Bohnenberger H,Alexe G,Corso J,Ströbel P,Wachter A,Beissbarth T,Schnütgen F,Cremer A,Haetscher N,Göllner S,Rouhi A,Palmqvist L,Rieger MA,Schroeder T,Bönig H,Müller-Tidow C

更新日期：2017-04-10 00:00:00

abstract：:Tumors constitute highly suppressive microenvironments in which infiltrating T cells are "exhausted" by inhibitory receptors such as PD-1. Here we identify TIGIT as a coinhibitory receptor that critically limits antitumor and other CD8(+) T cell-dependent chronic immune responses. TIGIT is highly expressed on human an...

journal_title：Cancer cell

authors： Johnston RJ,Comps-Agrar L,Hackney J,Yu X,Huseni M,Yang Y,Park S,Javinal V,Chiu H,Irving B,Eaton DL,Grogan JL

更新日期：2014-12-08 00:00:00

abstract：:Cancer cells reprogram their metabolism using different strategies to meet energy and anabolic demands to maintain growth and survival. Understanding the molecular and genetic determinants of these metabolic programs is critical to successfully exploit them for therapy. Here, we report that the oncogenic melanocyte li...

journal_title：Cancer cell

authors： Vazquez F,Lim JH,Chim H,Bhalla K,Girnun G,Pierce K,Clish CB,Granter SR,Widlund HR,Spiegelman BM,Puigserver P

更新日期：2013-03-18 00:00:00

abstract：:A recent report in Science from the Varmus laboratory (Podsypanina et al., 2008) puts an interesting twist on the origins of metastatic cells, suggesting that metastases can arise in ways that are very different from those widely believed. ...

journal_title：Cancer cell

authors： Weinberg RA

更新日期：2008-10-07 00:00:00

abstract：:MicroRNAs (miRNA) are mostly downregulated in cancer. However, the mechanism underlying this phenomenon and the precise consequence in tumorigenesis remain obscure. Here we show that ERK suppresses pre-miRNA export from the nucleus through phosphorylation of exportin-5 (XPO5) at T345/S416/S497. After phosphorylation b...

journal_title：Cancer cell

authors： Sun HL,Cui R,Zhou J,Teng KY,Hsiao YH,Nakanishi K,Fassan M,Luo Z,Shi G,Tili E,Kutay H,Lovat F,Vicentini C,Huang HL,Wang SW,Kim T,Zanesi N,Jeon YJ,Lee TJ,Guh JH,Hung MC,Ghoshal K,Teng CM,Peng Y,Croce CM

更新日期：2016-11-14 00:00:00

abstract：:The SH2-containing tyrosine phosphatase Shp2 (PTPN11) is required for growth factor and cytokine signaling. Germline Shp2 mutations cause Noonan Syndrome (NS), which is associated with increased risk of juvenile myelomonocytic leukemia (JMML). Somatic Shp2 mutations occur in sporadic JMML and other leukemias. We found...

journal_title：Cancer cell

authors： Mohi MG,Williams IR,Dearolf CR,Chan G,Kutok JL,Cohen S,Morgan K,Boulton C,Shigematsu H,Keilhack H,Akashi K,Gilliland DG,Neel BG

更新日期：2005-02-01 00:00:00

abstract：:Gene alterations play a prominent role in driving cancer initiation and progression. However, the genetic events that occur in normal cells prior to tumorigenesis are still unknown. Recent studies have started to map somatic mutations in normal human tissues, and here we discuss their implications for our understandin...

journal_title：Cancer cell

authors： Wijewardhane N,Dressler L,Ciccarelli FD

更新日期：2020-11-17 00:00:00

abstract：:We investigated the transcriptional and epigenetic repression of miR-29 by MYC, HDAC3, and EZH2 in mantle cell lymphoma and other MYC-associated lymphomas. We demonstrate that miR-29 is repressed by MYC through a corepressor complex with HDAC3 and EZH2. MYC contributes to EZH2 upregulation via repression of the EZH2 t...

journal_title：Cancer cell

authors： Zhang X,Zhao X,Fiskus W,Lin J,Lwin T,Rao R,Zhang Y,Chan JC,Fu K,Marquez VE,Chen-Kiang S,Moscinski LC,Seto E,Dalton WS,Wright KL,Sotomayor E,Bhalla K,Tao J

更新日期：2012-10-16 00:00:00

abstract：:It is widely accepted that metastasis is a late event in cancer progression. Here, however, we show that tumor cells can disseminate systemically from earliest epithelial alterations in HER-2 and PyMT transgenic mice and from ductal carcinoma in situ in women. Wild-type mice transplanted with single premalignant HER-2...

journal_title：Cancer cell

authors： Hüsemann Y,Geigl JB,Schubert F,Musiani P,Meyer M,Burghart E,Forni G,Eils R,Fehm T,Riethmüller G,Klein CA

更新日期：2008-01-01 00:00:00

abstract：:To identify regulatory drivers of prostate cancer malignancy, we have assembled genome-wide regulatory networks (interactomes) for human and mouse prostate cancer from expression profiles of human tumors and of genetically engineered mouse models, respectively. Cross-species computational analysis of these interactome...

journal_title：Cancer cell

authors： Aytes A,Mitrofanova A,Lefebvre C,Alvarez MJ,Castillo-Martin M,Zheng T,Eastham JA,Gopalan A,Pienta KJ,Shen MM,Califano A,Abate-Shen C

更新日期：2014-05-12 00:00:00

abstract：:Oncogene-induced senescence, e.g., in melanocytic nevi, terminates the expansion of pre-malignant cells via transcriptional silencing of proliferation-related genes due to decoration of their promoters with repressive trimethylated histone H3 lysine 9 (H3K9) marks. We show here that structurally distinct H3K9-active d...

journal_title：Cancer cell

authors： Yu Y,Schleich K,Yue B,Ji S,Lohneis P,Kemper K,Silvis MR,Qutob N,van Rooijen E,Werner-Klein M,Li L,Dhawan D,Meierjohann S,Reimann M,Elkahloun A,Treitschke S,Dörken B,Speck C,Mallette FA,Zon LI,Holmen SL,Peeper DS

更新日期：2018-02-12 00:00:00

abstract：:Advanced basal cell carcinomas (BCCs) frequently acquire resistance to Smoothened (SMO) inhibitors through unknown mechanisms. Here we identify SMO mutations in 50% (22 of 44) of resistant BCCs and show that these mutations maintain Hedgehog signaling in the presence of SMO inhibitors. Alterations include four ligand ...

journal_title：Cancer cell

authors： Atwood SX,Sarin KY,Whitson RJ,Li JR,Kim G,Rezaee M,Ally MS,Kim J,Yao C,Chang AL,Oro AE,Tang JY

更新日期：2015-03-09 00:00:00

abstract：:Constitutive activation of NF-κB signaling can promote oncogenesis, providing a rationale for anticancer strategies that inhibit NF-κB signaling. Two recent publications in Genes & Development provide evidence that, in contexts where prosurvival signals derive from other oncogenes, NF-κB activity instead enhances sens...

journal_title：Cancer cell

authors： Klein U,Ghosh S

更新日期：2011-11-15 00:00:00

abstract：:To identify FDA-approved agents targeting leukemic cells, we performed a chemical screen on two human leukemic cell lines and identified the antimicrobial tigecycline. A genome-wide screen in yeast identified mitochondrial translation inhibition as the mechanism of tigecycline-mediated lethality. Tigecycline selective...

journal_title：Cancer cell

authors： Skrtić M,Sriskanthadevan S,Jhas B,Gebbia M,Wang X,Wang Z,Hurren R,Jitkova Y,Gronda M,Maclean N,Lai CK,Eberhard Y,Bartoszko J,Spagnuolo P,Rutledge AC,Datti A,Ketela T,Moffat J,Robinson BH,Cameron JH,Wrana J,Eaves

更新日期：2011-11-15 00:00:00

abstract：:Ras and pRb are key regulators of a plethora of cellular processes, including proliferation, differentiation, and tumorigenesis. Adding to several previously established lines of communication between the two, in this issue of Cancer Cell, Shamma et al. resolve a new signaling network involved in cellular senescence a...

journal_title：Cancer cell

authors： Peeper DS

更新日期：2009-04-07 00:00:00

abstract：:Benign neurofibromas and malignant peripheral nerve sheath tumors are serious complications of neurofibromatosis type 1. The epidermal growth factor receptor is not expressed by normal Schwann cells, yet is overexpressed in subpopulations of Nf1 mutant Schwann cells. We evaluated the role of EGFR in Schwann cell tumor...

journal_title：Cancer cell

authors： Ling BC,Wu J,Miller SJ,Monk KR,Shamekh R,Rizvi TA,Decourten-Myers G,Vogel KS,DeClue JE,Ratner N

更新日期：2005-01-01 00:00:00

abstract：:Activating mutations in BRAF are the most common genetic alterations in melanoma. Inhibition of BRAF by small molecules leads to cell-cycle arrest and apoptosis. We show here that BRAF inhibition also induces an oxidative phosphorylation gene program, mitochondrial biogenesis, and the increased expression of the mitoc...

journal_title：Cancer cell

authors： Haq R,Shoag J,Andreu-Perez P,Yokoyama S,Edelman H,Rowe GC,Frederick DT,Hurley AD,Nellore A,Kung AL,Wargo JA,Song JS,Fisher DE,Arany Z,Widlund HR

更新日期：2013-03-18 00:00:00

abstract：:In this issue of Cancer Cell, Kumar et al. describe how CSF1R blockade induces not only an expected deprivation of tumor-associated macrophages, but also an accumulation of tumor-infiltrating polymorphonuclear mononuclear cells caused by Cxcl-1 released from cancer-associated fibroblasts. ...

journal_title：Cancer cell

authors： Greten TF

更新日期：2017-11-13 00:00:00

abstract：:Ependymoma is the third most common pediatric tumor with posterior fossa group A (PFA) being its most aggressive subtype. Ependymomas are generally refractory to chemotherapies and thus lack any effective treatment. Here, we report that elevated expression of CXorf67 (chromosome X open reading frame 67), which frequen...

journal_title：Cancer cell

authors： Han J,Yu M,Bai Y,Yu J,Jin F,Li C,Zeng R,Peng J,Li A,Song X,Li H,Wu D,Li L

更新日期：2020-12-14 00:00:00

abstract：:PIK3R1 (p85α regulatory subunit of PI3K) is frequently mutated across cancer lineages. Herein, we demonstrate that the most common recurrent PIK3R1 mutation PIK3R1(R348∗) and a nearby mutation PIK3R1(L370fs), in contrast to wild-type and mutations in other regions of PIK3R1, confers an unexpected sensitivity to MEK an...

journal_title：Cancer cell

authors： Cheung LW,Yu S,Zhang D,Li J,Ng PK,Panupinthu N,Mitra S,Ju Z,Yu Q,Liang H,Hawke DH,Lu Y,Broaddus RR,Mills GB

更新日期：2014-10-13 00:00:00

abstract：:In this issue of Cancer Cell, Haybaeck et al. unravel the role of lymphotoxin pathway in the development of hepatocellular carcinoma (HCC). Aberrant activation of this cascade in mice livers recapitulates the stages of fibrosis and inflammation that precedes human liver cancer, providing a novel family of potential th...

journal_title：Cancer cell

authors： Villanueva A,Savic R,Llovet JM

更新日期：2009-10-06 00:00:00

abstract：:Wnt/β-catenin signaling is essential for stem cell regulation and tumorigenesis, but its molecular mechanisms are not fully understood. Here, we report that FoxM1 is a downstream component of Wnt signaling and is critical for β-catenin transcriptional function in tumor cells. Wnt3a increases the level and nuclear tran...

journal_title：Cancer cell

authors： Zhang N,Wei P,Gong A,Chiu WT,Lee HT,Colman H,Huang H,Xue J,Liu M,Wang Y,Sawaya R,Xie K,Yung WK,Medema RH,He X,Huang S

更新日期：2011-10-18 00:00:00

abstract：:Recent genomic analyses of pediatric glioblastoma, a poorly understood tumor with dismal outcome, have identified mutations in histone H3 variants that affect critical amino acids in the tail. The findings extend discoveries of chromatin regulator inactivation and gain-of-function mutations by documenting alteration o...

journal_title：Cancer cell

authors： Rheinbay E,Louis DN,Bernstein BE,Suvà ML

更新日期：2012-03-20 00:00:00

abstract：:ERK pathway activation in cells expressing wild-type BRAF is a well-reported, clinically-relevant adverse effect of the otherwise impressive response of BRAF(V600E)-mutated melanomas to RAF inhibitors. In this issue of Cancer Cell, Holderfield and colleagues show that RAF autoinhibition underpins this paradox, further...

journal_title：Cancer cell

authors： Hey F,Pritchard C

更新日期：2013-05-13 00:00:00