癌症研究进展 (ACR) 涵盖了一段非凡的发现时期，其中包括生物学革命的开始。癌症研究进展 (ACR) 涵盖了一段非凡的发现时期，其中包括生物学革命的开始。第一本 ACR 卷出版于 WATSON 和 CRICK 报道生物学中心法则 DNA 双螺旋的那一年。在前 100 卷中，发现了一些帮助塑造这场革命的人的许多贡献，他们在癌症研究中取得了许多显着的发现，并由此发展而来。

Advances in Cancer Research covers significant advancements in the field of cancer research, marking the beginning of a biological revolution. The first volume was published in the same year that Watson and Crick reported the double helix structure of DNA. In the first 100 volumes, numerous contributions from scientists who shaped this revolution led to significant discoveries in cancer research, driving the development of the field.

《Advances in Cancer Research》涵盖了癌症研究领域的重大进展，标志着生物学革命的开端。第一卷的出版恰逢沃森和克里克报道DNA双螺旋结构的那一年。在前100卷中，许多为这场革命做出贡献的科学家们在癌症研究中取得了显著的发现，这些发现推动了该领域的发展。

Advances in Cancer Research

Despite the recent introduction of new effective systemic agents, the survival of patients with hepatocellular carcinoma (HCC) at advanced stages remains dismal. This underscores the need for new therapies, which has spurred extensive research on the identification of the main drivers of pathway de-regulation as a source of novel therapeutic targets. Frequently altered pathways in HCC involve growth factor receptors (e.g., VEGFR, FGFR, TGFA, EGFR, IGFR) and/or its cytoplasmic intermediates (e.g., PI3K-AKT-mTOR, RAF/ERK/MAPK) as well as key pathways in cell differentiation (e.g., Wnt/β-catenin, JAK/STAT, Hippo, Hedgehog, Notch). Somatic mutations, chromosomal aberrations and epigenetic changes are common mechanisms for pathway deregulation in HCC. Aberrant pathway activation has also been explored as a biomarker to predict response to specific therapies, but currently, these strategies are not implemented when deciding systemic therapies in HCC patients. Beyond the well-established molecular cascades, there are numerous emerging signaling pathways also deregulated in HCC (e.g., tumor microenvironment, non-coding RNA, intestinal microbiota), which have opened new avenues for therapeutic exploration.

Teresa Garcia-Lezana

Juan Luis Lopez-Canovas

Augusto Villanueva

Advances in cancer research

Adv Cancer Res

Signaling pathways in hepatocellular carcinoma.

肝细胞癌中的信号通路

Cholangiocarcinoma is associated with several different risk factors, many of which have known genetic associations. Advances in our understanding of the human genome have translated to the development of gene specific and whole genome assays for identifying gene variants and other alterations associated with cancer development. An improved understanding of the inherited genetic variants associated with risk of cholangiocarcinoma has the potential to improve our understanding of the basic biology of cholangiocarcinoma, enhance the performance of risk stratification models for identifying individuals at highest risk for cholangiocarcinoma, and identifying genetic variants associated with predisposition to cholangiocarcinoma in families with multiple affected individuals. It is increasingly recognized that major cancer-causing mutations or other gene alterations associated with familial risk of multiple cancers can also occur as germline events in individuals with apparently sporadically occurring cancer. In this chapter we review the major risk factors for cholangiocarcinoma as well as known gene variants associated with these risk factors, gene variants that have been associated with cholangiocarcinoma as the result of interrogation of candidate genes known to be associated with putative cancer causing pathways in cholangiocarcinoma, as well as the prevalence of major cancer causing genetic aberrations shown to be inherited in the germline of patients with sporadically developed cholangiocarcinoma. There has not yet been any large-scale genome wide association study of cholangiocarcinoma, and the results from such a study are eagerly anticipated.

Mikayla A Schmidt

Lewis R Roberts

Understanding the genetic basis for cholangiocarcinoma.

理解胆管癌的遗传基础。

Tumor growth and metastasis can be promoted by a small sub-population of cancer cells, termed cancer stem-like cells (CSCs). While CSCs possess capability in self-renewing and differentiating, the hierarchy of CSCs during tumor growth is highly plastic. This plasticity in CSCs fate and function can be regulated by signals from the tumor microenvironment. One emerging pathway in CSCs that connects the alteration in microenvironment and signaling network in cancer cells is the hexosamine biosynthetic pathway (HBP). The final product of HBP, UDP-N-acetylglucosamine (UDP-GlcNAc), is utilized for glycosylating of membrane and secreted proteins, but also nuclear and cytoplasmic proteins by the post-translational modification O-GlcNAcylation. O-GlcNAcylation and its enzyme, O-GlcNAc transferase (OGT), are upregulated in nearly all cancers and been linked to regulate many cancer cell phenotypes. Recent studies have begun to connect OGT and O-GlcNAcylation to regulation of CSCs. In this review, we will discuss the emerging role of OGT and O-GlcNAcylation in regulating fate and plasticity of CSCs, as well as the potential in targeting OGT/O-GlcNAcylation in CSCs.

Giang Le Minh

Mauricio J Reginato

Role of O-GlcNAcylation on cancer stem cells: Connecting nutrient sensing to cell plasticity.

O-GlcNA酰化在癌症干细胞中的作用：连接营养感应与细胞可塑性。

Cutaneous malignant melanoma is one of the few major cancers that continue to exhibit a positive rate of increase in the developed world. A wealth of epidemiological data has undisputedly implicated ultraviolet radiation (UVR) from sunlight and artificial sources as the major risk factor for melanomagenesis. However, the molecular mechanisms of this cause-and-effect relationship remain murky and understudied. Recent efforts on multiple fronts have brought unprecedented expansion of our knowledge base on this subject and it is now clear that melanoma is caused by a complex interaction between genetic predisposition and environmental exposure, primarily to UVR. Here we provide an overview of the effects of the macroenvironment (UVR) on the skin microenvironment and melanocyte-specific intrinsic (mostly genetic) landscape, which conspire to produce one of the deadliest malignancies.

Xuan Mo

Sarah Preston

M Raza Zaidi

Macroenvironment-gene-microenvironment interactions in ultraviolet radiation-induced melanomagenesis.

紫外线辐射诱导黑色素瘤发生中的宏观环境-基因-微环境相互作用。

The incidence and mortality associated with colorectal cancer (CRC) diagnosed in patients under the age of 50 have been steadily increasing. The exact etiology of these epidemiologic trends is unclear. This chapter will provide a comprehensive review on the topic of early age onset colorectal cancer (EAO-CRC), defined as colorectal cancer (CRC) diagnosed in patients under the age of 50. Topics reviewed will include the epidemiology of EAO-CRC around the world, clinical and pathological features of EAO-CRC in contrast to later age onset CRC (CRC diagnosed on those over the age of 50) and the observed molecular and somatic characteristics. This chapter will review the etiologies to EAO-CRC and the established, as well as proposed risk factors for disease. Evidence-based approaches to prevention, early detection, treatment and survivorship will be presented.

Abbreviation	Adv. Cancer. Res.
Journal Impact	5.62

ISSN	0065-230X, 2162-5557
h-index	109

Publication Information	Publisher: Academic Press Inc.，Publishing cycle: Irregular，Journal Type: book-series，Open Access Journals: No
Basic data	Year of publication: 1969，Proportion of original research papers: 0.00%，Self Citation Rate:N.A.， Gold OA Rate: 0.00%
Average review cycle	网友分享经验：约稿?周期不定
Average recruitment ratio	网友分享经验：较难

Advances in Cancer Research

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Signaling pathways in hepatocellular carcinoma.

Understanding the genetic basis for cholangiocarcinoma.

Role of O-GlcNAcylation on cancer stem cells: Connecting nutrient sensing to cell plasticity.

Macroenvironment-gene-microenvironment interactions in ultraviolet radiation-induced melanomagenesis.

Early age onset colorectal cancer.

PFKP: More than phosphofructokinase

Role of O-GlcNAcylation on cancer stem cells: Connecting nutrient sensing to cell plasticity.

Understanding the genetic basis for cholangiocarcinoma.

Chemotherapy induced gastrointestinal toxicities

Predictive value of collagen in cancer