Vitamin D receptor polymorphisms and survival in patients with cutaneous melanoma: a population-based study
Factors known to affect melanoma survival include age at presentation, sex and tumor characteristics. Polymorphisms also appear to modulate survival following diagnosis. Result from other studies suggest that vitamin D receptor (VDR) polymorphisms (SNPs) impact survival in patients with glioma, renal cell carcinoma, lung, breast, prostate and other cancers; however, a comprehensive study of VDR polymorphisms and melanoma-specific survival is lacking. We aimed to investigate whether VDR genetic variation influences survival in patients with cutaneous melanoma. The analysis involved 3566 incident single and multiple primary ...
Source: Carcinogenesis - January 5, 2016 Category: Cancer & Oncology Authors: Orlow, I., Reiner, A. S., Thomas, N. E., Roy, P., Kanetsky, P. A., Luo, L., Paine, S., Armstrong, B. K., Kricker, A., Marrett, L. D., Rosso, S., Zanetti, R., Gruber, S. B., Anton-Culver, H., Gallagher, R. P., Dwyer, T., Busam, K., Begg, C. B., Berwick, M. Tags: Original Manuscript Source Type: research
Dickkopf-3 regulates prostate epithelial cell acinar morphogenesis and prostate cancer cell invasion by limiting TGF-{beta}-dependent activation of matrix metalloproteases
Dickkopf-3 (Dkk-3) is a secreted protein whose expression is downregulated in many types of cancer. Endogenous Dkk-3 is required for formation of acini in 3D cultures of prostate epithelial cells, where it inhibits transforming growth factor (TGF)-β/Smad signaling. Here, we examined the effects of Dkk-3 on the expression and activity of matrix metalloproteases (MMPs), which mediate the effects of TGF-β on extracellular matrix disassembly during tissue morphogenesis and promote invasion of tumor cells. Silencing of Dkk-3 in prostate epithelial cells resulted in increased expression and enzyme activity of MMP-2 and...
Source: Carcinogenesis - January 5, 2016 Category: Cancer & Oncology Authors: Romero, D., Al-Shareef, Z., Gorrono-Etxebarria, I., Atkins, S., Turrell, F., Chhetri, J., Bengoa-Vergniory, N., Zenzmaier, C., Berger, P., Waxman, J., Kypta, R. Tags: Original Manuscript Source Type: research
A cryptic paracentric inversion of MSH2 exons 2-6 causes Lynch syndrome
We present a 38-year-old male with a clinicopathological and family history consistent with Lynch syndrome, including loss of MSH2 expression in his tumor. Germline testing revealed normal MSH2 coding sequence, splice sites and exon copy number, however, cDNA sequencing identified an aberrant MSH2 transcript lacking exons 2–6. An inversion PCR on germline DNA identified an ~18kb unbalanced, paracentric inversion within MSH2, with breakpoints in a long terminal repeat in intron 1 and an Alu repeat in intron 6. The 3' end of the inversion had a 1.2 kb deletion and an 8 bp insertion at the junction with intron 6. Screen...
Source: Carcinogenesis - January 5, 2016 Category: Cancer & Oncology Authors: Liu, Q., Hesson, L. B., Nunez, A. C., Packham, D., Williams, R., Ward, R. L., Sloane, M. A. Tags: Original Manuscript Source Type: research
Cancer prevention as part of precision medicine: 'plenty to be done
Cancer burden worldwide is projected to rise from 14 million new cases in 2012 to 24 million in 2035. Although the greatest increases will be in developing countries, where cancer services are already hard pressed, even the richest nations will struggle to meet demands of increasing patient numbers and spiralling treatment costs. No country can treat its way out of the cancer problem. Consequently, cancer control must combine improvements in treatment with greater emphasis on prevention and early detection. Cancer prevention is founded on describing the burden of cancer, identifying the causes and evaluating and implementi...
Source: Carcinogenesis - January 5, 2016 Category: Cancer & Oncology Authors: Stewart, B. W., Bray, F., Forman, D., Ohgaki, H., Straif, K., Ullrich, A., Wild, C. P. Tags: Review Source Type: research
Editorial
(Source: Carcinogenesis)
Source: Carcinogenesis - January 5, 2016 Category: Cancer & Oncology Authors: Harris, C. C. Tags: Editorial Source Type: research
Table_of_Contents
(Source: Carcinogenesis)
Source: Carcinogenesis - January 5, 2016 Category: Cancer & Oncology Tags: Cover / Standing Material Source Type: research
Subscriptions
(Source: Carcinogenesis)
Source: Carcinogenesis - January 5, 2016 Category: Cancer & Oncology Tags: Cover / Standing Material Source Type: research
Instructions_to_Authors
(Source: Carcinogenesis)
Source: Carcinogenesis - January 5, 2016 Category: Cancer & Oncology Tags: Cover / Standing Material Source Type: research
Front_Cover
(Source: Carcinogenesis)
Source: Carcinogenesis - January 5, 2016 Category: Cancer & Oncology Tags: Cover / Standing Material Source Type: research
Editorial_Board
(Source: Carcinogenesis)
Source: Carcinogenesis - January 5, 2016 Category: Cancer & Oncology Tags: Cover / Standing Material Source Type: research
Back_Cover
(Source: Carcinogenesis)
Source: Carcinogenesis - January 5, 2016 Category: Cancer & Oncology Tags: Cover / Standing Material Source Type: research
Editor-in-Chiefs Note - Thank you to Reviewers
(Source: Carcinogenesis)
Source: Carcinogenesis - November 28, 2015 Category: Cancer & Oncology Tags: List of referees Source Type: research
The retinoic acid derivative, ABPN, inhibits pancreatic cancer through induction of Nrdp1
Combination chemotherapy for the treatment of pancreatic cancer commonly employs gemcitabine with an EGFR inhibitor such as erlotinib. Here, we show that the retinoic acid derivative, ABPN, exhibits more potent anticancer effects than erlotinib, while exhibiting less toxicity toward noncancerous human control cells. Low micromolar concentrations of ABPN induced apoptosis in BxPC3 and HPAC pancreatic cancer cell lines, concomitant with a reduction in phosphorylated EGFR as well as decreased ErbB3, Met and BRUCE protein levels. The degradation of ErbB3 is a result of proteasomal degradation, possibly due to the ABPN-dependen...
Source: Carcinogenesis - November 28, 2015 Category: Cancer & Oncology Authors: Byun, S., Shin, S. H., Lee, E., Lee, J., Lee, S.-Y., Farrand, L., Jung, S. K., Cho, Y.-Y., Um, S.-J., Sin, H.-S., Kwon, Y.-J., Zhang, C., Tsang, B. K., Bode, A. M., Lee, H. J., Lee, K. W., Dong, Z. Tags: Original Manuscript Source Type: research
Helicobacter pylori, cyclooxygenase-2 and evolution of gastric lesions: results from an intervention trial in China
To investigate the role of cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) in the process of Helicobacter pylori-induced gastric carcinogenesis, a prospective study based on an intervention trial was conducted in Linqu County, China. A total of 1401 subjects with histopathologic diagnosis were investigated at baseline, among those, 919 completed subsequent interventions (anti-H.pylori and/or celecoxib treatment). Expressions of COX-2 and Ki-67 were assessed by immunohistochemistry, and PGE2 levels were measured by enzyme immunoassay before and after interventions, respectively. We found a grade–response relationship b...
Source: Carcinogenesis - November 28, 2015 Category: Cancer & Oncology Authors: Zhang, Y., Pan, K.-f., Zhang, L., Ma, J.-l., Zhou, T., Li, J.-y., Shen, L., You, W.-c. Tags: Original Manuscript Source Type: research
Restoration of paclitaxel resistance by CDK1 intervention in drug-resistant ovarian cancer
Epithelial ovarian cancer (EOC) commonly acquires resistance to chemotherapy, and this is the major obstacle to the better prognosis. Elucidating the molecular targets altered by chemotherapy is critically required to understand and overcome drug resistance. As a drug combination including paclitaxel is a prevalent prescription for treatment of EOC, to uncover gene expression altered in paclitaxel-resistant EOC, we analyzed multidirectional microarray profiles in both EOC cell lines and patients with paclitaxel resistance. Cyclin-dependent kinase 1 (CDK1) was found to be a potential target of transcription factors to regul...
Source: Carcinogenesis - November 28, 2015 Category: Cancer & Oncology Authors: Bae, T., Weon, K.-Y., Lee, J.-W., Eum, K.-H., Kim, S., Choi, J. W. Tags: Original Manuscript Source Type: research
