BioEssays

Cover image for Vol. 39 Issue 7

Edited By: Andrew Moore

Online ISSN: 1521-1878

Cancer

Cancer

Cancer is a very heterogeneous disease, and this special collection takes a look at a wide variety of its features: from the mechanisms of metastasis, through a comparison of cancer cells with stem cells all the way to therapeutic opportunities. We hope you enjoy exploring these different aspects.



For primer literature of relevance to the articles below, see the Encyclopedia of Life SciencesELS_Logoentries Cell Biology of Cancer and Cancer Genetics.



Cancer: Time for a new theory and new clinical approaches?
Debating Cancer: the Paradox in Cancer Research

Edited by Henry H. Heng, World Scientific Publishing Co., Hackensack, 2016 ISBN: 978-9814520843, hardcover, 464 pages, US$ ca. 112.

Adam S. Wilkins*

BioEssays 2017, 39, No. 2, 0–0 [Thoughts & Opinion]


A tale of TALE, PREP1, PBX1, and MEIS1: Interconnections and competition in cancer

A tale of TALE, PREP1, PBX1, and MEIS1: Interconnections and competition in cancer

Francesco Blasi*, Chiara Bruckmann, Dmitry Penkov, Leila Dardaei

TALE proteins PREP1 and MEIS1 have opposite functions in tumors (tumor suppressor v. oncogene). To this end both need to dimerize with PBX1 but dimerization is mutually exclusive, hence they compete. PREP1-PBX1 and MEIS1-PBX1 dimers recognize specific DNA sequences and this accounts for their individual peculiar functions.

BioEssays 2017, 39, No. 5, 0 [Prospects & Overviews]


Alternating pH landscapes shape epithelial cancer initiation and progression: Focus on pancreatic cancer

Alternating pH landscapes shape epithelial cancer initiation and progression: Focus on pancreatic cancer

Stine F. Pedersen*, Ivana Novak, Frauke Alves, Albrecht Schwab, Luis A. Pardo*

Cells in organs performing net acid-base transport, like the pancreatic ductal and gastric epithelia, survive in an extraordinarily large and variable extracellular pH gradient. This renders epithelial and stromal cells pre-adapted to the heterogeneous extracellular pH in the tumor microenvironment and may thereby contribute to the development of epithelial cancers.

BioEssays 2017, 39, No. 6, 0 [Insights & Perspectives]


Long non-coding RNAs in cancer metabolism

Long non-coding RNAs in cancer metabolism

Zhen-Dong Xiao, Li Zhuang, Boyi Gan*

Altered cellular metabolism is a hallmark of cancer. The metabolic network is regulated by a myriad of metabolic enzymes. In this “Recently in press” mini-review, we discuss the emerging roles of long non-coding RNAs, the type of non-coding genes that are often described as the “dark matter” in our genome, in cancer metabolism.

BioEssays 2016, 38, No. 10, 991–996 [Prospects & Overviews]


Enhancer deregulation in cancer and other diseases

Enhancer deregulation in cancer and other diseases

Hans-Martin Herz*

Enhancer deregulation underlies various diseases. It can be caused by mutations in enhancer-associated chromatin-modifying factors such as UTX/KDM6A, MLL3/KMT2C, and MLL4/KMT2D or alternatively by mutations or genomic alterations of disease, or cancer gene enhancers. Both cases result in altered enhancer activity of disease-relevant genes such as tumor suppressor or oncogenes.

BioEssays 2016, 38, No. 10, 1003–1015 [Prospects & Overviews]


mTORC2 activity in brain cancer: Extracellular nutrients are required to maintain oncogenic signaling

mTORC2 activity in brain cancer: Extracellular nutrients are required to maintain oncogenic signaling

Kenta Masui*, Noriyuki Shibata, Webster K. Cavenee, Paul S. Mischel*

We propose that in glioblastoma, and possibly other cancers, abundant glucose or acetate, which are readily available to tumor cells in their native environment, facilitate biochemical modification of a core component of the growth factor receptor signaling pathway, mTOR complex 2, driving growth and rendering tumors resistant to drugs that target upstream components of growth factor signaling pathways.

BioEssays 2016, 38, No. 9, 839–844 [Insights & Perspectives]


Transmissible cancers in an evolutionary context

Transmissible cancers in an evolutionary context

Beata Ujvari*, Anthony T. Papenfuss, Katherine Belov

Transmissible cancers are ideal to investigate the evolutionary arms race between cancer cells and their surrounding environment. While all three contagious cancers show ongoing adaptations to selective forces, canine transmissible venereal tumour has reached an evolutionary stalemate with its host, while devil facial tumor disease and clam leukaemia are still in a more dynamic phase of their evolution.

BioEssays 2016, 38, No. S1, 0–0 [Prospects & Overviews]


Mutations and deletions of PRC2 in prostate cancer

Mutations and deletions of PRC2 in prostate cancer

Payal Jain, Luciano Di Croce*

PRC2 in cancer can be mutated leading to activation/inactivation associated with gain or loss of H3K27me3. Overexpressed EZH2 acquires new targets and silences tumor suppressors and miRNAs. Phosphorylated EZH2 can acquire non-histone substrates. Lastly, PRC2 associated factors can be mutated or affected in cancer modulating PRC2 binding accordingly.

BioEssays 2016, 38, No. 5, 446–454 [Prospects & Overviews]


Targeting MYC in cancer therapy: RNA processing offers new opportunities

Targeting MYC in cancer therapy: RNA processing offers new opportunities

Cheryl M. Koh*, Arianna Sabò*, Ernesto Guccione*

Cancer cells express high levels of MYC:MAX, and Myc/MYC abundance can be directly targeted for cancer therapy (1). Additionally, MYC-overexpressing cells have an increased dependence on core MYC-regulated functions, compared to normal cells. These functions therefore present potential points of synthetic lethality that may be exploited in anti-cancer therapies (2).

BioEssays 2016, 38, No. 3, 266–275 [Prospects & Overviews]


Host manipulation by cancer cells: Expectations, facts, and therapeutic implications

Host manipulation by cancer cells: Expectations, facts, and therapeutic implications

Tazzio Tissot, Audrey Arnal, Camille Jacqueline, Robert Poulin, Thierry Lefèvre, Frédéric Mery, François Renaud, Benjamin Roche, François Massol, Michel Salzet, Paul Ewald, Aurélie Tasiemski, Beata Ujvari, Frédéric Thomas*

Cancer cell lineages able to manipulate phenotypic traits in their host in a way that favors their proliferation should be favored by oncogenic selection. However, the extent of this phenomenon remains underappreciated. We review this issue in the light of the parasitological concepts developed during the last few decades.

BioEssays 2016, 38, No. 3, 276–285 [Prospects & Overviews]


Human and primate-specific microRNAs in cancer: Evolution, and significance in comparison with more distantly-related research models

Human and primate-specific microRNAs in cancer: Evolution, and significance in comparison with more distantly-related research models

Costas Koufaris*

The human miRNAome can be divided into miRNAs that are widely conserved, those that are primate-specific, and those that are human-specific. The latter two categories can also contribute to tumor development and complicate the study of human cancers in non-primate animal models.

BioEssays 2016, 38, No. 3, 286–294 [Prospects & Overviews]


Targeting tumor suppressor genes for cancer therapy

Targeting tumor suppressor genes for cancer therapy

Yunhua Liu, Xiaoxiao Hu, Cecil Han, Liana Wang, Xinna Zhang, Xiaoming He, Xiongbin Lu*

Driver mutations that cause loss-of-function in tumor suppressor genes had been thought of as undruggable because of technical difficulties or mechanistic complexity. Recent advances in cancer genomics, drug design and development, and bioinformatic tools have revealed new therapeutic opportunities for targeting tumor suppressor mutations.

BioEssays 2015, 37, No. 12, 1277–1286 [Insights & Perspectives]


Tumor-induced solid stress activates ß-catenin signaling to drive malignant behavior in normal, tumor-adjacent cells

Tumor-induced solid stress activates ß-catenin signaling to drive malignant behavior in normal, tumor-adjacent cells

Guanqing Ou, Valerie Marie Weaver*

Mechanical cues are important mediators of cell behavior in cancer. Manipulating the solid stress experienced by murine colon cells in vivo implicated mechanically driven ß-catenin activation and proliferation in tumor-adjacent cells as one mechanism by which tumor-induced mechanical changes can propagate the malignant behavior of a tissue.

BioEssays 2015, 37, No. 12, 1293–1297 [Prospects & Overviews]


Tumor-derived microvesicles in the tumor microenvironment: How vesicle heterogeneity can shape the future of a rapidly expanding field

Tumor-derived microvesicles in the tumor microenvironment: How vesicle heterogeneity can shape the future of a rapidly expanding field

James W. Clancy, Christopher J. Tricarico, Crislyn D'Souza-Schorey*

Microvesicle heterogeneity can impact tumor-stromal signaling: tumor-derived microvesicles (TMVs) represent a novel mechanism of intercellular communication that significantly impacts the tumor microenvironment. Microvesicles are released directly into the extracellular space where they participate in multiple cargo-dependent, pro-tumorigenic roles. Here we speculate on the implications to tumor cell signaling that may result from heterogeneity within the TMV pool.

BioEssays 2015, 37, No. 12, 1309–1316 [Prospects & Overviews]


Mouse models of colorectal cancer as preclinical models

Mouse models of colorectal cancer as preclinical models

Rebecca E. McIntyre*, Simon J.A. Buczacki, Mark J. Arends, David J. Adams

Colorectal cancer is a heterogeneous disease, both genetically and epigenetically. Furthermore, tumour behaviour is strongly influenced by the micro-environment. Mouse modelling provides useful tools for validating therapeutic targets and providing mechanistic insights within the context of tumour diversity. Here we review the current repertoire of mouse models of colorectal cancer.

BioEssays 2015, 37, No. 8, 909–920 [Prospects & Overviews]


Bad luck and cancer: Does evolution spin the wheel of fortune?

Bad luck and cancer: Does evolution spin the wheel of fortune?

Benjamin Roche*, Beata Ujvari, Frédéric Thomas

Cancer is a complex disease, with sophisticated cellular mechanisms as the targets of evolutionary processes driven by random genetic and epigenetic mutations. Oncogenesis is evolutionarily linked to stem cell numbers/mutations and organ/body size; therefore, inter-disciplinary frameworks across different scales (cellular, tissue, organs and species) are necessary to decipher cancer progression.

BioEssays 2015, 37, No. 6, 586–587 [Thoughts & Opinion]


Gut microbial metabolism and colon cancer: Can manipulations of the microbiota be useful in the management of gastrointestinal health?

Gut microbial metabolism and colon cancer: Can manipulations of the microbiota be useful in the management of gastrointestinal health?

Antoaneta Belcheva*, Thergiory Irrazabal, Alberto Martin*

Microbial metabolism is essential in the maintenance of colonic homeostasis. Microbially-produced metabolites contribute to colon cancer development. Disrupting microbiota leads to dysbiosis and changes in the metabolic profile. Understanding the mechanisms through which metabolites drive cancer development is an essential step towards better management and treatment of colon cancer.

BioEssays 2015, 37, No. 4, 403–412 [Prospects & Overviews]


MAPping the Ndc80 loop in cancer: A possible link between Ndc80/Hec1 overproduction and cancer formation

MAPping the Ndc80 loop in cancer: A possible link between Ndc80/Hec1 overproduction and cancer formation

Ngang Heok Tang*, Takashi Toda*

Mitotic chromosome mis-segregation leads to aneuploidy, the hallmark of cancer. Ndc80 kinetochore protein promotes cancer formation upon overproduction for some unknown reason. Here we propose that rather than a gain-of-function by overproduced Ndc80, abnormal sequestration of its binding proteins via the Ndc80 internal loop may exert causative impacts on tumourigenesis.

BioEssays 2015, 37, No. 3, 248–256 [Insights & Perspectives]


Do age-associated DNA methylation changes increase the risk of malignant transformation?

Do age-associated DNA methylation changes increase the risk of malignant transformation?

Wolfgang Wagner*, Carola I. Weidner, Qiong Lin

Age-predictors based on specific DNA-methylation (DNAm) changes reflect biological aging. The global changes in DNAm pattern may also trigger aberrant DNAm – so called epimutations – that can initiate tumor formation in the elderly. The figure is adopted from Waddington's “epigenetic landscape” (The Strategy of The Genes. London, Allan & Unwin 1957).

BioEssays 2015, 37, No. 1, 20–24 [Insights & Perspectives]


Lysine methylation in cancer: SMYD3-MAP3K2 teaches us new lessons in the Ras-ERK pathway

Lysine methylation in cancer: SMYD3-MAP3K2 teaches us new lessons in the Ras-ERK pathway

Paula Colón-Bolea, Piero Crespo*

Lysine methylation is traditionally associated with histones and epigenetics. Recently, lysine methyltransferases involved in methylation of non-histone substrates have been frequently found deregulated in tumours. Now methyltransferase SMYD3 has been identified as an enhancer of Ras-driven cancer via methylation of MAP3K2, which prevents it from binding to the phosphatase PP2A, thereby mitigating its negative regulation of Ras-ERK1/2 signals, hence promoting tumourigenesis.

BioEssays 2014, 36, No. 12, 1162–1169 [Prospects & Overviews]


How does oncogene transformation render tumor cells hypersensitive to nutrient deprivation?

How does oncogene transformation render tumor cells hypersensitive to nutrient deprivation?

Gabriel Leprivier, Poul H. Sorensen*

Oncogene activation leads to hypersensitivity to nutrient deprivation by deregulation of specific metabolic pathways. Novel mechanisms underlying this phenotype are emerging, such as altered control of mRNA translation elongation by inhibition of the eEF2 kinase (eEF2K). The adaptive mechanisms used to circumvent oncogene-mediated cell death under nutrient deprivation are described.

BioEssays 2014, 36, No. 11, 1082–1090 [Prospects & Overviews]


Targeting cancer's weaknesses (not its strengths): Therapeutic strategies suggested by the atavistic model

Targeting cancer's weaknesses (not its strengths): Therapeutic strategies suggested by the atavistic model

Charles H. Lineweaver*, Paul C. W. Davies, Mark D. Vincent

In the atavistic model of cancer progression, tumor cell dedifferentiation is interpreted as a reversion to phylogenetically earlier capabilities. Phylostratigraphy can then help predict which capabilities cancer cells have lost, and these predictions can be translated into new target-the-weaknesses therapies. Our most detailed example involves the immune system.

BioEssays 2014, 36, No. 9, 827–835 [Insights & Perspectives]


From promotion to management: The wide impact of bacteria on cancer and its treatment

From promotion to management: The wide impact of bacteria on cancer and its treatment

Ernesto Perez-Chanona, Christian Jobin*

The intestinal microbiota plays an essential role in the maintenance of intestinal homeostasis, and disrupted microbial functions are often associated with intestinal pathology such as colorectal cancer (CRC). New findings demonstrate that the microbiota also influence the anti-tumor efficacy of chemotherapeutic drugs, suggesting a novel role for microbes in cancer management.

BioEssays 2014, 36, No. 7, 658–664 [Prospects & Overviews]


Evolutionarily conserved stress responses as potential anticancer therapeutic targets? (Comment on DOI 10.1002/bies.201300170)

Mark Vincent*

BioEssays 2014, 36, No. 6, 544–545 [Idea to watch]


Stress-induced cellular adaptive strategies: Ancient evolutionarily conserved programs as new anticancer therapeutic targets

Stress-induced cellular adaptive strategies: Ancient evolutionarily conserved programs as new anticancer therapeutic targets

Arcadi Cipponi, David M. Thomas*

Resistance to anticancer therapies is partly due to the mutagenic capacity of malignant cells, accelerating adaptation to selective pressures. Since similar phenomena have been observed in prokaryotes and primitive eukaryotes, we hypothesize that evolutionarily conserved mechanisms may regulate hypermutability in cancer cells in response to environmental stress, including drug therapy.

BioEssays 2014, 36, No. 6, 552–560 [Insights & Perspectives]

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