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Cancers, Volume 4, Issue 4 (December 2012), Pages 969-1348

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Research

Jump to: Review, Other

Open AccessArticle Do Non-Genomically Encoded Fusion Transcripts Cause Recurrent Chromosomal Translocations?
Cancers 2012, 4(4), 1036-1049; doi:10.3390/cancers4041036
Received: 26 July 2012 / Revised: 14 September 2012 / Accepted: 9 October 2012 / Published: 18 October 2012
Cited by 3 | PDF Full-text (733 KB) | HTML Full-text | XML Full-text
Abstract
We among others have recently demonstrated that normal cells produce “fusion mRNAs”. These fusion mRNAs do not derive from rearranged genomic loci, but rather they are derived from “early-terminated transcripts” (ETTs). Premature transcriptional termination takes place in intronic sequences that belong to “breakpoint
[...] Read more.
We among others have recently demonstrated that normal cells produce “fusion mRNAs”. These fusion mRNAs do not derive from rearranged genomic loci, but rather they are derived from “early-terminated transcripts” (ETTs). Premature transcriptional termination takes place in intronic sequences that belong to “breakpoint cluster regions”. One important property of ETTs is that they exhibit an unsaturated splice donor site. This results in: (1) splicing to “cryptic exons” present in the final intron; (2) Splicing to another transcript of the same gene (intragenic trans-splicing), resulting in “exon repetitions”; (3) splicing to a transcript of another gene (intergenic trans-splicing), leading to “non-genomically encoded fusion transcripts” (NGEFTs). These NGEFTs bear the potential risk to influence DNA repair processes, since they share identical nucleotides with their DNA of origin, and thus, could be used as “guidance RNA” for DNA repair processes. Here, we present experimental data about four other genes. Three of them are associated with hemato-malignancies (ETV6, NUP98 and RUNX1), while one is associated with solid tumors (EWSR1). Our results demonstrate that all genes investigated so far (MLL, AF4, AF9, ENL, ELL, ETV6, NUP98, RUNX1 and EWSR1) display ETTs and produce transpliced mRNA species, indicating that this is a genuine property of translocating genes. Full article
(This article belongs to the Special Issue Leukemia)
Open AccessArticle Mouse Lymphoblastic Leukemias Induced by Aberrant Prdm14 Expression Demonstrate Widespread Copy Number Alterations Also Found in Human ALL
Cancers 2012, 4(4), 1050-1066; doi:10.3390/cancers4041050
Received: 26 July 2012 / Revised: 2 October 2012 / Accepted: 9 October 2012 / Published: 18 October 2012
PDF Full-text (968 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Aberrant expression and activation of oncogenes in somatic cells has been associated with cancer initiation. Required for reacquisition of pluripotency in the developing germ cell, PRDM14 initiates lymphoblastic leukemia when misexpressed in murine bone marrow. Activation of pluripotency in somatic cells can lead
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Aberrant expression and activation of oncogenes in somatic cells has been associated with cancer initiation. Required for reacquisition of pluripotency in the developing germ cell, PRDM14 initiates lymphoblastic leukemia when misexpressed in murine bone marrow. Activation of pluripotency in somatic cells can lead to aneuploidy and copy number alterations during iPS cell generation, and we hypothesized that PRDM14-induced lymphoblastic leukemias would demonstrate significant chromosomal damage. High-resolution oligo array comparative genomic hybridization demonstrated infrequent aneuploidy but frequent amplification and deletion, with amplifications occurring in a 5:1 ratio with deletions. Many deletions (i.e., Cdkn2a, Ebf1, Pax5, Ikzf1) involved B-cell development genes and tumor suppressor genes, recapitulating deletions occurring in human leukemia. Pathways opposing senescence were frequently deactivated via Cdkn2a deletion or Tbx2 amplification, with corollary gene expression. Additionally, gene expression studies of abnormal pre-leukemic B-precursors showed downregulation of genes involved in chromosomal stability (i.e., Xrcc6) and failure to upregulate DNA repair pathways. We propose a model of leukemogenesis, triggered by pluripotency genes like Prdm14, which involves ongoing DNA damage and failure to activate non-homologous end-joining secondary to aberrant gene expression. Full article
(This article belongs to the Special Issue Leukemia)
Open AccessArticle Annotating Cancer Variants and Anti-Cancer Therapeutics in Reactome
Cancers 2012, 4(4), 1180-1211; doi:10.3390/cancers4041180
Received: 8 October 2012 / Revised: 31 October 2012 / Accepted: 2 November 2012 / Published: 8 November 2012
Cited by 82 | PDF Full-text (1361 KB) | HTML Full-text | XML Full-text
Abstract
Reactome describes biological pathways as chemical reactions that closely mirror the actual physical interactions that occur in the cell. Recent extensions of our data model accommodate the annotation of cancer and other disease processes. First, we have extended our class of protein modifications
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Reactome describes biological pathways as chemical reactions that closely mirror the actual physical interactions that occur in the cell. Recent extensions of our data model accommodate the annotation of cancer and other disease processes. First, we have extended our class of protein modifications to accommodate annotation of changes in amino acid sequence and the formation of fusion proteins to describe the proteins involved in disease processes. Second, we have added a disease attribute to reaction, pathway, and physical entity classes that uses disease ontology terms. To support the graphical representation of “cancer” pathways, we have adapted our Pathway Browser to display disease variants and events in a way that allows comparison with the wild type pathway, and shows connections between perturbations in cancer and other biological pathways. The curation of pathways associated with cancer, coupled with our efforts to create other disease-specific pathways, will interoperate with our existing pathway and network analysis tools. Using the Epidermal Growth Factor Receptor (EGFR) signaling pathway as an example, we show how Reactome annotates and presents the altered biological behavior of EGFR variants due to their altered kinase and ligand-binding properties, and the mode of action and specificity of anti-cancer therapeutics. Full article
(This article belongs to the Special Issue System Biology in Cancer Research)
Open AccessArticle dNTP Supply Gene Expression Patterns after P53 Loss
Cancers 2012, 4(4), 1212-1224; doi:10.3390/cancers4041212
Received: 27 October 2012 / Revised: 27 October 2012 / Accepted: 15 November 2012 / Published: 20 November 2012
Cited by 3 | PDF Full-text (204 KB) | HTML Full-text | XML Full-text
Abstract
Loss of the transcription factor p53 implies mRNA losses of target genes such as the p53R2 subunit of human ribonucleotide reductase (RNR). We hypothesized that other genes in the dNTP supply system would compensate for such p53R2 losses and looked for this in
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Loss of the transcription factor p53 implies mRNA losses of target genes such as the p53R2 subunit of human ribonucleotide reductase (RNR). We hypothesized that other genes in the dNTP supply system would compensate for such p53R2 losses and looked for this in our own data and in data of the Gene Expression Omnibus (GEO). We found that the de novo dNTP supply system compensates for p53R2 losses with increases in RNR subunit R1, R2, or both. We also found compensatory increases in cytosolic deoxycytidine kinase (dCK) and thymidine kinase 1 (TK1) and in mitochondrial deoxyguanosine kinase (dGK), all of the salvage dNTP supply system; in contrast, the remaining mitochondrial salvage enzyme thymidine kinase 2 (TK2) decreased with p53 loss. Thus, TK2 may be more dedicated to meeting mitochondrial dNTP demands than dGK which may be more obligated to assist cytosolic dNTP supply in meeting nuclear DNA dNTP demands. Full article
Open AccessArticle Nuclear DNA-Content in Mesenchymal Lesions in Dogs: Its Value as Marker of Malignancy and Extent of Genomic Instability
Cancers 2012, 4(4), 1300-1317; doi:10.3390/cancers4041300
Received: 25 October 2012 / Revised: 16 November 2012 / Accepted: 26 November 2012 / Published: 3 December 2012
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Abstract
DNA-aneuploidy may reflect the malignant nature of mesenchymal proliferations and herald gross genomic instability as a mechanistic factor in tumor genesis. DNA-ploidy and -index were determined by flow cytometry in canine inflammatory or neoplastic mesenchymal tissues and related to clinico-pathological features, biological behavior
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DNA-aneuploidy may reflect the malignant nature of mesenchymal proliferations and herald gross genomic instability as a mechanistic factor in tumor genesis. DNA-ploidy and -index were determined by flow cytometry in canine inflammatory or neoplastic mesenchymal tissues and related to clinico-pathological features, biological behavior and p53 gene mutational status. Half of all sarcomas were aneuploid. Benign mesenchymal neoplasms were rarely aneuploid and inflammatory lesions not at all. The aneuploidy rate was comparable to that reported for human sarcomas with significant variation amongst subtypes. DNA-ploidy status in canines lacked a relation with histological grade of malignancy, in contrast to human sarcomas. While aneuploidy was related to the development of metastases in soft tissue sarcomas it was not in osteosarcomas. No relation amongst sarcomas was found between ploidy status and presence of P53 gene mutations. Heterogeneity of the DNA index between primary and metastatic sarcoma sites was present in half of the cases examined. Hypoploidy is more common in canine sarcomas and hyperploid cases have less deviation of the DNA index than human sarcomas. The variation in the presence and extent of aneuploidy amongst sarcoma subtypes indicates variation in genomic instability. This study strengthens the concept of interspecies variation in the evolution of gross chromosomal aberrations during cancer development. Full article
(This article belongs to the Special Issue Soft Tissue and Bone Sarcoma) Print Edition available
Open AccessArticle Azithromycin Synergistically Enhances Anti-Proliferative Activity of Vincristine in Cervical and Gastric Cancer Cells
Cancers 2012, 4(4), 1318-1332; doi:10.3390/cancers4041318
Received: 25 September 2012 / Revised: 16 November 2012 / Accepted: 30 November 2012 / Published: 4 December 2012
Cited by 3 | PDF Full-text (919 KB) | HTML Full-text | XML Full-text
Abstract
In this study, the anti-proliferative and anticancer activity of azithromycin (AZM) was examined. In the presence of AZM, cell growth was inhibited more effectively in Hela and SGC-7901 cancer cells, relative to transformed BHK-21 cells. The respective 50% inhibition of cell growth (IC
[...] Read more.
In this study, the anti-proliferative and anticancer activity of azithromycin (AZM) was examined. In the presence of AZM, cell growth was inhibited more effectively in Hela and SGC-7901 cancer cells, relative to transformed BHK-21 cells. The respective 50% inhibition of cell growth (IC50) values for Hela, SGC-7901 and BHK-21 were 15.66, 26.05 and 91.00 µg/mL at 72 h post incubation, indicative of a selective cytotoxicity against cancer cells. Cell apoptosis analysis using Hoechst nuclear staining and annexin V-FITC binding assay further demonstrated that AZM was capable of inducing apoptosis in both cancer cells and transformed cells. The apoptosis induced by AZM was partly through a caspase-dependent mechanism with an up-regulation of apoptotic protein cleavage PARP and caspase-3 products, as well as a down-regulation of anti-apoptotic proteins, Mcl-1, bcl-2 and bcl-X1. More importantly, a combination of AZM and a low dose of the common anti-cancer chemotherapeutic agent vincristine (VCR), produced a selectively synergistic effect on apoptosis of Hela and SGC-7901 cells, but not BHK-21 cells. In the presence of 12.50 μg/mL of VCR, the respective IC50 values of Hela, SGC-7901 and BHK-21 cells to AZM were reduced to 9.47 µg/mL, 8.43 µg/mL and 40.15 µg/mL at 72 h after the incubation, suggesting that the cytotoxicity of AZM had a selective anti-cancer effect on cancer over transformed cells in vitro. These results imply that AZM may be a potential anticancer agent for use in chemotherapy regimens, and it may minimize side effects via reduction of dosage and enhancing the effectiveness common chemotherapeutic drugs. Full article

Review

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Open AccessReview Estrogen Signaling in Lung Cancer: An Opportunity for Novel Therapy
Cancers 2012, 4(4), 969-988; doi:10.3390/cancers4040969
Received: 4 July 2012 / Revised: 9 August 2012 / Accepted: 10 September 2012 / Published: 25 September 2012
Cited by 7 | PDF Full-text (190 KB) | HTML Full-text | XML Full-text
Abstract
Lung cancer is the leading cause of cancer death in U.S. and represents a major public health burden. Epidemiologic data have suggested that lung cancer in women may possess different biological characteristics compared to men, as evidenced by a higher proportion of never-smokers
[...] Read more.
Lung cancer is the leading cause of cancer death in U.S. and represents a major public health burden. Epidemiologic data have suggested that lung cancer in women may possess different biological characteristics compared to men, as evidenced by a higher proportion of never-smokers among women with lung cancer. Emerging data indicate that female hormones such as estrogen and progesterone play a significant role in lung carcinogenesis. It has been reported that estrogen and progesterone receptors are expressed in lung cancer cell lines as well as in patient-derived tumors. Hormone related risk factors such as hormone replacement therapy have been implicated in lung carcinogenesis and several preclinical studies show activity of anti-estrogen therapy in lung cancer. In this review, we summarize the emerging evidence for the role of reproductive hormones in lung cancer and implications for lung cancer therapy. Full article
(This article belongs to the Special Issue Hormones and Carcinogenesis)
Open AccessReview Cancer Stem Cells, EMT, and Developmental Pathway Activation in Pancreatic Tumors
Cancers 2012, 4(4), 989-1035; doi:10.3390/cancers4040989
Received: 10 September 2012 / Revised: 2 October 2012 / Accepted: 9 October 2012 / Published: 12 October 2012
Cited by 11 | PDF Full-text (532 KB) | HTML Full-text | XML Full-text
Abstract
Pancreatic cancer is a disease with remarkably poor patient survival rates. The frequent presence of metastases and profound chemoresistance pose a severe problem for the treatment of these tumors. Moreover, cross-talk between the tumor and the local micro-environment contributes to tumorigenicity, metastasis and
[...] Read more.
Pancreatic cancer is a disease with remarkably poor patient survival rates. The frequent presence of metastases and profound chemoresistance pose a severe problem for the treatment of these tumors. Moreover, cross-talk between the tumor and the local micro-environment contributes to tumorigenicity, metastasis and chemoresistance. Compared to bulk tumor cells, cancer stem cells (CSC) have reduced sensitivity to chemotherapy. CSC are tumor cells with stem-like features that possess the ability to self-renew, but can also give rise to more differentiated progeny. CSC can be identified based on increased in vitro spheroid- or colony formation, enhanced in vivo tumor initiating potential, or expression of cell surface markers. Since CSC are thought to be required for the maintenance of a tumor cell population, these cells could possibly serve as a therapeutic target. There appears to be a causal relationship between CSC and epithelial-to-mesenchymal transition (EMT) in pancreatic tumors. The occurrence of EMT in pancreatic cancer cells is often accompanied by re-activation of developmental pathways, such as the Hedgehog, WNT, NOTCH, and Nodal/Activin pathways. Therapeutics based on CSC markers, EMT, developmental pathways, or tumor micro-environment could potentially be used to target pancreatic CSC. This may lead to a reduction of tumor growth, metastatic events, and chemoresistance in pancreatic cancer. Full article
Open AccessReview High Resolution Fluorescence Imaging of Cancers Using Lanthanide Ion-Doped Upconverting Nanocrystals
Cancers 2012, 4(4), 1067-1105; doi:10.3390/cancers4041067
Received: 13 August 2012 / Revised: 20 September 2012 / Accepted: 15 October 2012 / Published: 22 October 2012
Cited by 24 | PDF Full-text (2057 KB) | HTML Full-text | XML Full-text
Abstract
During the last decade inorganic luminescent nanoparticles that emit visible light under near infrared (NIR) excitation (in the biological window) have played a relevant role for high resolution imaging of cancer. Indeed, semiconductor quantum dots (QDs) and metal nanoparticles, mostly gold nanorods (GNRs),
[...] Read more.
During the last decade inorganic luminescent nanoparticles that emit visible light under near infrared (NIR) excitation (in the biological window) have played a relevant role for high resolution imaging of cancer. Indeed, semiconductor quantum dots (QDs) and metal nanoparticles, mostly gold nanorods (GNRs), are already commercially available for this purpose. In this work we review the role which is being played by a relatively new class of nanoparticles, based on lanthanide ion doped nanocrystals, to target and image cancer cells using upconversion fluorescence microscopy. These nanoparticles are insulating nanocrystals that are usually doped with small percentages of two different rare earth (lanthanide) ions: The excited donor ions (usually Yb3+ ion) that absorb the NIR excitation and the acceptor ions (usually Er3+, Ho3+ or Tm3+), that are responsible for the emitted visible (or also near infrared) radiation. The higher conversion efficiency of these nanoparticles in respect to those based on QDs and GNRs, as well as the almost independent excitation/emission properties from the particle size, make them particularly promising for fluorescence imaging. The different approaches of these novel nanoparticles devoted to "in vitro" and "in vivo" cancer imaging, selective targeting and treatment are examined in this review. Full article
(This article belongs to the Special Issue Nanotechnology and Cancer Therapeutics)
Open AccessReview RGD-Binding Integrins in Prostate Cancer: Expression Patterns and Therapeutic Prospects against Bone Metastasis
Cancers 2012, 4(4), 1106-1145; doi:10.3390/cancers4041106
Received: 23 August 2012 / Revised: 9 October 2012 / Accepted: 22 October 2012 / Published: 26 October 2012
Cited by 17 | PDF Full-text (714 KB) | HTML Full-text | XML Full-text
Abstract
Prostate cancer is the third leading cause of male cancer deaths in the developed world. The current lack of highly specific detection methods and efficient therapeutic agents for advanced disease have been identified as problems requiring further research. The integrins play a vital
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Prostate cancer is the third leading cause of male cancer deaths in the developed world. The current lack of highly specific detection methods and efficient therapeutic agents for advanced disease have been identified as problems requiring further research. The integrins play a vital role in the cross-talk between the cell and extracellular matrix, enhancing the growth, migration, invasion and metastasis of cancer cells. Progression and metastasis of prostate adenocarcinoma is strongly associated with changes in integrin expression, notably abnormal expression and activation of the β3 integrins in tumour cells, which promotes haematogenous spread and tumour growth in bone. As such, influencing integrin cell expression and function using targeted therapeutics represents a potential treatment for bone metastasis, the most common and debilitating complication of advanced prostate cancer. In this review, we highlight the multiple ways in which RGD-binding integrins contribute to prostate cancer progression and metastasis, and identify the rationale for development of multi-integrin antagonists targeting the RGD-binding subfamily as molecularly targeted agents for its treatment. Full article
(This article belongs to the Special Issue Adhesion and Integrins)
Open AccessReview Chemoprevention of Breast Cancer: The Paradox of Evidence versus Advocacy Inaction
Cancers 2012, 4(4), 1146-1160; doi:10.3390/cancers4041146
Received: 31 July 2012 / Revised: 23 September 2012 / Accepted: 19 October 2012 / Published: 29 October 2012
Cited by 4 | PDF Full-text (506 KB) | HTML Full-text | XML Full-text
Abstract
Women who are at high risk of breast cancer can be offered chemoprevention. Chemoprevention strategies have expanded over the past decade and include selective receptor modulator inhibitors and aromatase inhibitors. Physicians are expected to provide individualized risk assessments to identify high risk women
[...] Read more.
Women who are at high risk of breast cancer can be offered chemoprevention. Chemoprevention strategies have expanded over the past decade and include selective receptor modulator inhibitors and aromatase inhibitors. Physicians are expected to provide individualized risk assessments to identify high risk women who may be eligible for chemoprevention. It is prudent that physicians utilize a shared decision approach when counseling high risk women about their preventive options. Barriers and misperceptions however exist with patient and physician acceptance of chemoprevention and continue to impede uptake of chemoprevention as a strategy to reduce breast cancer risk. Programs to increase awareness and elucidate the barriers are critical for women to engage in cancer prevention and promote chemoprevention adherence. Full article
(This article belongs to the Special Issue Advances in Cancer Chemoprevention)
Open AccessReview The Development of Novel Therapies for the Treatment of Acute Myeloid Leukemia (AML)
Cancers 2012, 4(4), 1161-1179; doi:10.3390/cancers4041161
Received: 22 August 2012 / Revised: 29 September 2012 / Accepted: 17 October 2012 / Published: 2 November 2012
Cited by 3 | PDF Full-text (422 KB) | HTML Full-text | XML Full-text
Abstract
Acute myeloid leukemia (AML) is nearly always a fatal malignancy. For the past 40 years, the standard of care remains a combination of cytarabine and an anthracycline known as 7 + 3. This treatment regimen is troubled by both low survival rates (10%
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Acute myeloid leukemia (AML) is nearly always a fatal malignancy. For the past 40 years, the standard of care remains a combination of cytarabine and an anthracycline known as 7 + 3. This treatment regimen is troubled by both low survival rates (10% at 5 years) and deaths due to toxicity. Substantial new laboratory findings over the past decade have identified many cellular pathways that contribute to leukemogenesis. These studies have led to the development of novel agents designed to target these pathways. Here we discuss the molecular underpinnings and clinical benefits of these novel treatment strategies. Most importantly these studies demonstrate that clinical response is best achieved by stratifying each patient based on a detailed understanding of their molecular abnormalities. Full article
(This article belongs to the Special Issue Leukemia)
Open AccessReview Therapeutic Cancer Vaccines in Prostate Cancer: The Quest for Intermediate Markers of Response
Cancers 2012, 4(4), 1229-1246; doi:10.3390/cancers4041229
Received: 8 October 2012 / Revised: 9 November 2012 / Accepted: 14 November 2012 / Published: 22 November 2012
Cited by 2 | PDF Full-text (156 KB) | HTML Full-text | XML Full-text
Abstract
Despite recent advances in cancer immunotherapy, no prospectively validated intermediate biomarkers exist to predict response. These biomarkers are highly desirable given modern immunotherapy’s paradoxical pattern of clinical benefit; that is, improvement in overall survival without short-term change in progression. Immunotherapy clinical trials have
[...] Read more.
Despite recent advances in cancer immunotherapy, no prospectively validated intermediate biomarkers exist to predict response. These biomarkers are highly desirable given modern immunotherapy’s paradoxical pattern of clinical benefit; that is, improvement in overall survival without short-term change in progression. Immunotherapy clinical trials have evaluated biomarkers that may correlate with clinical outcomes. Many of them are performed on peripheral blood to evaluate the systemic response, such as tumor-targeted humoral and cellular immunity, and cytokine responses. Accumulating evidence suggests that immune infiltrates in tumors may suggest evidence for the therapy’s mechanism of action, and have greater potential for providing prognostic and predictive information. In addition, a non-immunologic biomarker, such as tumor growth kinetics, may explain this paradoxical pattern of clinical benefit, and predict survival in patients treated with an immunotherapy. Prospective assessment and validation of these and other intermediate markers would be required to better understand their potential clinical role. Full article
(This article belongs to the Special Issue Immune Responses to Human Prostate Cancer)
Open AccessReview Emerging Roles of ADAMTSs in Angiogenesis and Cancer
Cancers 2012, 4(4), 1252-1299; doi:10.3390/cancers4041252
Received: 22 October 2012 / Revised: 21 November 2012 / Accepted: 23 November 2012 / Published: 29 November 2012
Cited by 12 | PDF Full-text (1259 KB) | HTML Full-text | XML Full-text
Abstract
A Disintegrin-like And Metalloproteinase with ThromboSpondin motifs—ADAMTSs—are a multi-domain, secreted, extracellular zinc metalloproteinase family with 19 members in humans. These extracellular metalloproteinases are known to cleave a wide range of substrates in the extracellular matrix. They have been implicated in various physiological processes,
[...] Read more.
A Disintegrin-like And Metalloproteinase with ThromboSpondin motifs—ADAMTSs—are a multi-domain, secreted, extracellular zinc metalloproteinase family with 19 members in humans. These extracellular metalloproteinases are known to cleave a wide range of substrates in the extracellular matrix. They have been implicated in various physiological processes, such as extracellular matrix turnover, melanoblast development, interdigital web regression, blood coagulation, ovulation, etc. ADAMTSs are also critical in pathological processes such as arthritis, atherosclerosis, cancer, angiogenesis, wound healing, etc. In the past few years, there has been an explosion of reports concerning the role of ADAMTS family members in angiogenesis and cancer. To date, 10 out of the 19 members have been demonstrated to be involved in regulating angiogenesis and/or cancer. The mechanism involved in their regulation of angiogenesis or cancer differs among different members. Both angiogenesis-dependent and -independent regulation of cancer have been reported. This review summarizes our current understanding on the roles of ADAMTS in angiogenesis and cancer and highlights their implications in cancer therapeutic development. Full article
(This article belongs to the Special Issue Tumour Angiogenesis)
Figures

Open AccessReview Immunotherapy: Shifting the Balance of Cell-Mediated Immunity and Suppression in Human Prostate Cancer
Cancers 2012, 4(4), 1333-1348; doi:10.3390/cancers4041333
Received: 24 October 2012 / Revised: 29 November 2012 / Accepted: 5 December 2012 / Published: 11 December 2012
Cited by 1 | PDF Full-text (432 KB) | HTML Full-text | XML Full-text
Abstract
Active immunotherapy is dependent on the ability of the immune system to recognize and respond to tumors. Despite overwhelming evidence to support a cell-mediated immune response to prostate cancer, it is insufficient to eradicate the disease. This is likely due to a high
[...] Read more.
Active immunotherapy is dependent on the ability of the immune system to recognize and respond to tumors. Despite overwhelming evidence to support a cell-mediated immune response to prostate cancer, it is insufficient to eradicate the disease. This is likely due to a high level of suppression at the tumor site from a variety of sources, including immunosuppressive cells. Immune cells entering the tumor microenvironment may be inhibited directly by the tumor, stromal cells or other immune cells that have been induced to adopt a suppressive phenotype. The resurgence of interest in immunotherapy following the approval of sipuleucel-T and ipilimumab by the Food and Drug Administration has brought about new strategies for overcoming tumor-mediated suppression and bolstering anti-tumor responses. Improved understanding of the immune response to prostate cancer can lead to new combination therapies, such as the use of vaccine with small molecule and checkpoint inhibitors or other immunotherapies. Full article
(This article belongs to the Special Issue Immune Responses to Human Prostate Cancer)

Other

Jump to: Research, Review

Open AccessCommentary A Comment on Qi et al.: An Estimation of Radiobiological Parameters for Head-and-Neck and the Clinical Implications. Cancers, 2012, 4, 566-580
Cancers 2012, 4(4), 1225-1228; doi:10.3390/cancers4041225
Received: 28 September 2012 / Revised: 14 November 2012 / Accepted: 14 November 2012 / Published: 22 November 2012
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Abstract
Important results were shown as cell survival points in the two panels of the figure which is reproduced in this Comment letter. A curve was fitted assuming the mono-exponential recovery half-time of 17 ± 21 minutes. The wide error limits indicate that this
[...] Read more.
Important results were shown as cell survival points in the two panels of the figure which is reproduced in this Comment letter. A curve was fitted assuming the mono-exponential recovery half-time of 17 ± 21 minutes. The wide error limits indicate that this fit is not very good, but the notable feature of both panels is that the last four points are clearly continuing to rise, above the “fitted” curve. This indicates that there is a second, slower, component of repair or recovery and this Comment explores constructively the implications of that additional discovery. Full article
Open AccessCommentary Cancer Cachexia: Muscle Physiology and Exercise Training
Cancers 2012, 4(4), 1247-1251; doi:10.3390/cancers4041247
Received: 11 September 2012 / Revised: 17 November 2012 / Accepted: 21 November 2012 / Published: 29 November 2012
Cited by 4 | PDF Full-text (308 KB) | HTML Full-text | XML Full-text
Abstract
Cachexia in cancer patients is a condition marked by severe tissue wasting and a myriad of quality of life and health consequences. Cachexia is also directly linked to the issues of morbidity and survivability in cancer patients. Therapeutic means of mitigating cachexia and
[...] Read more.
Cachexia in cancer patients is a condition marked by severe tissue wasting and a myriad of quality of life and health consequences. Cachexia is also directly linked to the issues of morbidity and survivability in cancer patients. Therapeutic means of mitigating cachexia and its effects are thus critical in cancer patient treatment. We present a discussion on the use of physical exercise activities in the context of such treatment as a means to disruption the tissue wasting effects (i.e., muscle tissue losses via anorexigenic pro-inflammatory cytokines) of cachexia. In addition we propose a theoretical model (Exercise Anti-Cachectic Hypothetical—“EACH” model) as to how exercise training may promote a disruption in the cycle of events leading to advancing cachexia and in turn promote an enhanced functionality and thus improved quality of life in cancer patients. Full article
(This article belongs to the Special Issue System Biology in Cancer Research)

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