About Cancer Biology &Therapy
| Mission Statement (March 22, 2001) |
| First Call for Papers (July 24, 2001) |
| Reviewed in the journal Nature (November 7, 2002) |
| Special Issue: Anti-Cancer Therapy (July 1, 2003) |
| Most highly cited papers (July 9, 2003) |
| Reviewed in JAMA (April 7, 2004) |
| Most highly cited papers (July 10, 2004) |
| Download CB&T Masthead |
| CB&T Celebrates 5 Years of Publication (January 1, 2007) |
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Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource. |
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Excerpted from Nature, Vol 420, 7 Nov 2002, Page 26, "From Bench to Bedside and Back", Michelle D. Garrett "Cancer Biology and Therapy provides a comprehensive look at this [cell cycle misregulation] and other molecular and cellular aspects of cancer biology, along with current and future cancer treatments. The readership for this journal will be broad, encompassing all who wish to learn more about cancer and current thinking on both its diagnosis and treatment. This journal will be of interest to the clinician on the front line of cancer treatment and also to the bench scientist at the forefront of biological research into this diseaseÑit brings together basic cancer biology and the clinical aspects of this disease. ...The layout of the journal...has several delightful nuances. The first of these, the 'Bedside to Bench' report, in many ways, epitomizes the journal, as it has a very translational feel, highlighting a specific clinical area and then discussing the basic aspects of molecular and cellular biology that it may involve. Each of these articles opens with case reports on particular patients, an excellent reminder to all of us why we are involved in cancer research and treatment in the first place. The Bedside to Bench concept is, in many ways, the opposite of other journals, which often provide reports that go from the bench to the bedside, and I found it refreshing. ...The original research papers presented in this journal are at the forefront of both basic biological research and the treatment of cancer. The added nuance here is that many are accompanied by a commentary that provides both a critique of the research paper and valuable background information that the reader may not be aware of. ..Cancer Biology and Therapy provides an excellent forum for the presentation of new information on the basic biology, diagnosis and treatment of cancer, the second most common cause of death worldwide. ...Another unique feature is the ÔResearch PhilosophyÕ section, which covers ethics and thinking on science, along with its practice. Cancer Biology and Therapy deserves a round of applause for highlighting an extremely important aspect of scientific research that should be read by both newcomers to the field and the old hands. ...To conclude, Cancer Biology and Therapy provides an excellent forum for the presentation of new information on the basic biology, diagnosis and treatment of cancer, the second most common cause of death worldwide." |
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1— BRCA1 Transcriptionally
Regulates Damaged DNA Binding Protein (DDB2) In the DNA Repair
Response Following UV-Irradiation 2—A Nucleotide Excision Repair Master-Switch:
p53 Regulated Coordinate Introduction of Global Genomic Repair
Genes 3—Apoptosis Inhibitor as a Suppressor
of Tumor Progression: Expression of Bcl-2 Eliminates Selective
Advantages for p53-Deficient Cells in the Tumor 4—Differential Inactivation of Caspase-8
in Lung Cancers 4—Retinoid-Induced Growth Arrest of
Breast Carcinoma Cells Involves Co-Activation of Multiple Growth-Inhibitory
Genes 4—The Mutant p53-Conformation Modifying
Drug, CP-31398, Can Induce Apoptosis of Human Cancer Cells and
Can Stabilize Wild-Type p53 Protein 5—Inhibitors of MEK1/2 Interact with
UCN-01 to Induce Apoptosis and Reduce Colony Formation in Mammary
and Prostate Carcinoma Cells 5—Loss of the BCL-2 Phosphorylation
Loop Domain Is Required to Protect Human Myeloid Leukemia Cells
from Flavopiridol-Mediated Mitochondrial Damage and Apoptosis
5—A Recombinant Adenovirus Expressing
Wild-Type Bax Induces Apoptosis in Prostate Cancer Cells Independently
of Their Bcl-2 Status and Androgen Sensitivity 5—Cellular and Molecular Biology of
Human Melanoma 6—SU5416 Delays Wound Healing Through
Inhibition of TGF-b1 Activation 6—Notch Signaling in Cancer |
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1—Differential
Inactivation of Caspase-8 in Lung Cancers 2—BRCA1 Transcriptionally Regulates
Damaged DNA Binding Protein (DDB2) In the DNA Repair Response
Following UV-Irradiation 3—A Nucleotide Excision Repair Master-Switch:
p53 Regulated Coordinate Introduction of Global Genomic Repair
Genes 4—Ras Family Signaling 5—Notch Signaling in Cancer 6—DF3/MUC1 Signaling In Multiple Myeloma
Cells Is Regulated by Interleukin-7 6—Cellular and Molecular Biology of
Human Melanoma 6—The Mutant p53-Conformation Modifying
Drug, CP-31398, Can Induce Apoptosis 7— SU5416 Delays Wound Healing Through
Inhibition of TGF-beta 1 Activation 7— DNA Repair and Tumorigenesis: Lessons
from Hereditary Cancer Syndromes |
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