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Concerned that erythropoiesis-stimulating agents may actually undo what chemotherapy has done, promoting tumor progression or recurrence and shortening overall survival, the FDA is clamping down on these products, marketed by Amgen as Aranesp (darbepoetin alfa) and Epogen (epoetin alfa), and by Centocor Ortho Biotech Products as Procrit (epoetin alfa).

The epigenetic control of gene expression has been shown to play an important role in cancer initiation, progression, and resistance. Thus, agents that modify the epigenetic environment of tumors will likely be an important addition to the anticancer arsenal. Specifically, there is much interest in modulating histone acetylation using a new class of drugs, histone deacetylase (HDAC) inhibitors. Preclinical data have demonstrated the efficacy of various HDAC inhibitors as anticancer agents, with the greatest effects shown when HDAC inhibitors are used in combination with other therapies. As a result of encouraging preclinical data, numerous HDAC inhibitors are being investigated in clinical trials either as monotherapies or in conjunction with other treatments such as chemotherapy, biologic therapy, or radiation therapy. In fact, vorinostat and depsipeptide, two actively studied HDAC inhibitors, were recently approved for the treatment of refractory cutaneous T-cell lymphoma. Although the use of HDAC inhibitors has generated great enthusiasm, a significant amount of work still needs to be done in order to understand their mechanisms of action, as well as to determine the appropriate patient characteristics and subsets of cancer for which HDAC inhibitors hold the most potential for effective treatment.

Shabason and colleagues’ review of the development of histone deacetylase (HDAC) inhibitors as treatment for cancers is timely, with an emphasis on therapeutic strategies combining HDAC inhibitors and radiation therapy. As the authors indicate, vorinostat (Zolinza)-originally known as suberoylanilide hydroxamic acid, or SAHA-was the first of the HDAC inhibitors approved by the US Food and Drug Administration (FDA) for clinical use in the treatment of cutaneous T-cell lymphoma (CTCL).[1] In November 2009, a second HDAC inhibitor-romidepsin (Istodax)-received FDA approval for the treatment of CTCL. Currently there is a great deal of competition in the HDAC inhibitor field, as several new and, hopefully, more effective compounds are being developed and entering clinical trials.[2]

Shabason et al have written a thoughtful review of an exciting new class of agents, histone deacetylase (HDAC) inhibitors. While the authors focus primarily on the role of HDAC inhibitors in combination with radiation therapy, we would like to highlight some potential strategies combining these agents with systemic therapies for the treatment of cancer.

Who's News

ASCO and RSNA elect new presidents while the Children's Oncology Group selects a new leader. Read more about the latest awards and appointments in oncology and cancer care.

In the largest survey to date of US oncologists’ attitudes about the cost of cancer treatments, researchers at Tufts Medical Center and the University of Michigan found that 84% of oncologists consider their patients’ out-of-pocket costs when recommending cancer treatment. However, fewer than half of the respondents surveyed frequently discuss cost issues with patients.

Cancer patients sometimes develop neurologic complications directly caused by their cancers. Sometimes, however, these disorders are due not to the growth of a cancer tumor but to cancer-fighting antibodies that mistakenly attack cells in the nervous system. PET/CT may help physicians tell the difference.

Practitioners of Gerson therapy believe that cancer is caused by an accumulation of toxic substances in the body. They recommend a special diet including high carbohydrate and potassium intake, no sodium or fat, low animal protein, supplementation with exogenous digestive enzymes, and coffee enemas aimed at detoxifying the body and stimulating metabolism. However, available scientific evidence does not support use of Gerson therapy.

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colon cancer 2010

In this January 2010 supplement to Oncology, guest editor Axel Grothey from the Mayo Clinic, explores adjuvant therapy considerations in stage II colon cancer.

      Taking place in London this year, SMi’s Imaging in Oncology will focus on a wide range of imaging techniques in a wide range of settings - from the preclinical, to the clinical, to the future of oncological imaging. 

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In this January 2010 supplement to Oncology, guest editor Axel Grothey from the Mayo Clinic, explores adjuvant therapy considerations in stage II colon cancer.

Introduction

Two decades since the first demonstration that fluorouracil (5-FU)-based adjuvant chemotherapy improves outcomes in resected colon cancer,[1] clinicians are still struggling with the question of which patients with stage II colon cancer should receive postoperative therapy. It is well-accepted that the absolute survival benefit associated with 5-FU–based therapy for unselected patients with stage II colon cancer is in the range of 3% at 5 years. But it is also obvious that some patients with stage II cancers have excellent outcomes and do not require additional therapy, whereas other patients have cancers that biologically behave more like stage III tumors.

Some believed the unraveling of the human genome would lead overnight to the genetic tweaking of errant cells and the tailoring of treatments to patients. That dream’s time has not yet come, even a decade after the human genome was first sequenced. But the scientific community has made enormous progress in developing tools to examine the genome and their application. And those efforts may soon lead to practical results for mainstream oncology.