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Cancers, Volume 1, Issue 1 (December 2009), Pages 1-38

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Editorial

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Open AccessEditorial Why Another Cancer Journal?
Cancers 2009, 1(1), 1-2; doi:10.3390/cancers1010001
Received: 23 July 2009 / Published: 24 July 2009
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Abstract
Why do we need yet another cancer journal? An excellent question, of course, in light of the profusion of general as well as specialized cancer journals in recent times. An easy answer would simply be to say that this journal will be [...] Read more.
Why do we need yet another cancer journal? An excellent question, of course, in light of the profusion of general as well as specialized cancer journals in recent times. An easy answer would simply be to say that this journal will be better than the rest; however a less glib (and probably more accurate) response is simply that there is currently an explosion of new techniques and approaches in the field of cancer biology, and that the new, and sometimes unusual and unorthodox, data so generated demands an open-access and unrestricted forum for its dissemination. This was the impetus for starting the journal which you are now reading. [...] Full article

Research

Jump to: Editorial, Other

Open AccessArticle BAGE Hypomethylation Is an Early Event in Colon Transformation and Is Frequent in Histologically Advanced Adenomas
Cancers 2009, 1(1), 3-11; doi:10.3390/cancers1010003
Received: 27 September 2009 / Revised: 28 October 2009 / Accepted: 13 November 2009 / Published: 18 November 2009
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Abstract
We showed earlier that BAGE (B melanoma antigen) loci are hypermethylated in normal tissues and hypomethylated in 98% of human cancers. More recently, we provided evidence that hypomethylation of BAGE loci represents an informative marker for colon cancer detection. In [...] Read more.
We showed earlier that BAGE (B melanoma antigen) loci are hypermethylated in normal tissues and hypomethylated in 98% of human cancers. More recently, we provided evidence that hypomethylation of BAGE loci represents an informative marker for colon cancer detection. In this study, we show that hypomethylation of BAGE loci was an early event that occurred in 43% of colorectal adenomas. Interestingly, hypomethylation of BAGE loci was frequent (50%) in tubulo-villous and villous adenomas, these adenomas having a high probability of being transformed into colorectal cancers. Full article
(This article belongs to the Special Issue Biomarkers: Oncology Studies)
Open AccessArticle Comparison of Locoregional Recurrence with Mastectomy vs. Breast Conserving Surgery in Pregnancy Associated Breast Cancer (PABC)
Cancers 2009, 1(1), 12-20; doi:10.3390/cancers1010012
Received: 13 October 2009 / Revised: 23 November 2009 / Accepted: 25 November 2009 / Published: 4 December 2009
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Abstract
We have compared outcomes, including the locoregional recurrence, between mastectomy and breast conserving therapy in PABC. Patients were divided into those who were treated with mastectomies (group 1) and those with breast conserving surgery (group 2). The groups were comparable except for [...] Read more.
We have compared outcomes, including the locoregional recurrence, between mastectomy and breast conserving therapy in PABC. Patients were divided into those who were treated with mastectomies (group 1) and those with breast conserving surgery (group 2). The groups were comparable except for lower mean age in group 2 and more patients with stage III disease and higher number of nodes positive in the group 1. Five-year actuarial LRR, distant metastases free survival and overall survival in group 1 vs. 2 were 10% vs. 37%, 73% vs. 81% and 57% vs. 59% respectively. The patients with PABC treated with breast conserving therapy, despite having lower stage disease, have a higher risk of local regional recurrence in comparison with those treated with mastectomy. Full article
(This article belongs to the Special Issue Breast Cancer)
Open AccessArticle N′1,N′3-Dimethyl-N′1,N′3-bis(phenylcarbonothioyl) Propanedihydrazide (Elesclomol) Selectively Kills Cisplatin Resistant Lung Cancer Cells through Reactive Oxygen Species (ROS)
Cancers 2009, 1(1), 23-38; doi:10.3390/cancers1010023
Received: 11 November 2009 / Revised: 25 November 2009 / Accepted: 8 December 2009 / Published: 16 December 2009
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Abstract
Cisplatin is an important chemotherapeutic agent in lung cancer treatment. The mechanism of drug resistance to cisplatin is complex and historically has been difficult to overcome. We report here that cisplatin resistant lung cancer cell lines possess high basal levels of reactive [...] Read more.
Cisplatin is an important chemotherapeutic agent in lung cancer treatment. The mechanism of drug resistance to cisplatin is complex and historically has been difficult to overcome. We report here that cisplatin resistant lung cancer cell lines possess high basal levels of reactive oxygen species (ROS) when compared to normal cells and their parental cell counterparts. These resistant cells also have low thioredoxin (TRX) levels which may be one of the contributory factors to high ROS. N′1,N′3-dimethyl-N′1,N'3-bis(phenylcarbonothioyl) propanedihydrazide (elesclomol), an agent known to increase ROS is selectively toxic to cisplatin-resistant cells, while sparing normal cells and the parental counterpart. The cytotoxic effect of elesclomol in resistant cells is accompanied by further decreases in TRX and glutathione (GSH) antioxidant systems, while opposite results were found in parental cells. The ID50 of elesclomol in cisplatin-resistant cells ranged from 5–10 nM, which is well within clinically achievable ranges. N-Acetylcysteine (NAC), which is known to neutralize ROS, can abolish the cytotoxic effect of elesclomol, suggesting that the cytotoxic effect results from increased ROS. Overall, our data suggest that elesclomol selectively kills cisplatin-resistant tumor cells through increased ROS. This agent may hold potential to overcome cisplatin resistance and should be further explored to treat patients who have failed cisplatin therapy. Full article
(This article belongs to the Special Issue Oxidative Stress and Cancer)

Other

Jump to: Editorial, Research

Open AccessBook Review Precancer: The Beginning and the End of Cancer. Edited by Jules J. Berman, MD, PhD (E-Mail: jjberman1@comcast.net) with G. William Moore, MD, PhD. Jones & Bartlett Publishers: Sudbury, MA, USA, 2009; 186 pp; 42.95$; ISBN: 9780763777845
Cancers 2009, 1(1), 21-22; doi:10.3390/cancers1010021
Received: 3 December 2009 / Revised: 7 December 2009 / Accepted: 8 December 2009 / Published: 11 December 2009
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Abstract
This concisely written book makes a powerful argument that the focus of research in the cancer field should be shifted from full-stage cancer to the more promising area of precancer. The entire book encompasses less than 200 pages, including an extensive glossary [...] Read more.
This concisely written book makes a powerful argument that the focus of research in the cancer field should be shifted from full-stage cancer to the more promising area of precancer. The entire book encompasses less than 200 pages, including an extensive glossary aimed at clarifying terminology with which a person lacking a research background may be unfamiliar. Because explanations of scientific terminology are located in the glossary, Berman and Moore have prevented the book from being too elementary for an advanced scientist. The logical organization of the chapters results in this becoming quite an easy book to read. [...] Full article

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