oncologywatch

Waters EA, Sullivan HW, Nelson W, Hesse BW. What is my cancer risk? How internet-based cancer risk assessment tools communicate individualized risk estimates to the public: content analysis. J Med Internet Res. 2009 Jul 31;11(3):e33. 

We have all seen – and most of us have probably used – interactive Web-based tools designed to predict cancer risks. How good are these sites? Not very, if education is the goal, according to a recent survey by staff at the National Cancer Institute.

Risky Business
“Internet-based cancer risk assessment tools can provide cancer risk and prevention information to millions of people worldwide,” writes Erika Waters, a postdoctoral fellow in the NCI’s Cancer Prevention Fellowship Program, and her co-authors in their report, which was published recently in the Journal of Medical Internet Research. “However, poorly communicated risk information could mislead people or frighten them unduly, resulting in maladaptive health behaviors.”

The team of researchers, from the NCI’s Health Communication and Informatics Research and Basic and Biobehavioral Research groups, used popular search engines to locate more than a thousand websites dealing with cancer risk. They identified 44 unique interactive sites providing individualized cancer risk estimates. Nearly half of the sites were run by cancer centers and the health care industry (e.g., Blue Cross/Blue Shield, Merck); others were run by public health agencies (including the NCI) and a variety of private nonprofit groups.

Although they don’t report findings for individual websites, Waters and her co-authors find much room for improvement overall. Of particular concern, they observe that few of the sites communicate basic concepts of probability that are critical for an understanding of risk estimates. Few sites provide risk estimates in both numbers and words, or describe how a user’s cancer risk compares to other hazards.

They offer several recommendations to improve online risk-assessment tools, including the following:

• Describe the risk using both words and numbers. Words can be ambiguous; numbers can lack context.
• Communicate numeric risk as N in 1000 or as a percentage.
• Provide absolute and comparative (i.e., below or above average) risk information.
• Compare cancer risk to the risk of other hazards (e.g., being struck by lightening, being in a car accident) to place the risk in context.
• Frame the risk in positive and negative terms (eg, “Your risk of cancer is 5%”/ “This means you have a 95% chance of not getting cancer)
• Specifying whether the risk estimate is applicable to the next 5 years, 10 years, or over the user’s lifetime.
• Provide safety messages and risk reduction strategies.
• Include a visual display of risk, while avoiding biasing perceptions of risk.
• Acknowledge that the risk estimate contains an element of uncertainty, as it is based on statistical modeling of population-level data.

The study also references several review articles with additional recommendations on communicating risk in ways that help end users become better critical users of health information.

[OncologyWatch directory of open-access oncology journals.]

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Tonelli M, Hemmelgarn B, Reiman T, et al. Benefits and harms of erythropoiesis-stimulating agents for anemia related to cancer: a meta-analysis. CMAJ. 2009 May 26;180(11):E62-71. PMCID: PMC2683210.

Noting "a striking lack of data to support Health Canada’s labels and the American Society of Clinical Oncology’s guidelines for the use of erythropoiesis-stimulating agents in people with cancer-related anemia," researchers from the University of Alberta and other Canadian centers undertook a systematic review of the benefits and risks of these controversial agents in adult patients with anemia related to cancer or chemotherapy.

The researchers analyzed 52 clinical trials including more than 12,000 patients receiving treatment for various solid tumors and hematologic malignancies. Measures of benefit included health-related quality of life and use of blood transfusions; measures of risk included all-cause mortality, cardiovascular events and hypertension, and other adverse events.

Their conclusion:

"Use of erythropoiesis-stimulating agents in patients with cancer-related anemia improved some disease-specific measures of quality of life and decreased the use of blood transfusions. However, it increased the risk of death and serious adverse events. Our findings suggest that such therapy not be used routinely as an alternative to blood transfusion in patients with anemia related to cancer."

The authors found no evidence that use of erythropoiesis-stimulating agents affected the risk of cardiovascular events, but did find a borderline increase in the risk of hypertension.

[OncologyWatch directory of open-access oncology journals.]

OncologyWatch: Posts about free-access articles on aspects of oncology theory, practice and policy (about the blogger). This blog is not a source for medical advice.

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Idowu OE, Idowu MA. Environmental causes of childhood brain tumours. Afr Health Sci. 2008 Mar;8(1):1-4. PubMed PMID: 19357723

Something new in the world, and not welcome.

From the summary:

"Brain tumours hitherto said to be rare in Africans are now known to be common. They cause considerable concern due to their relatively high morbidity, mortality and enormous cost of care, especially in the developing world."

No likely causes are verified. Investigation most warranted.

 

[OncologyWatch directory of open-access oncology journals.]

OncologyWatch: Posts about free-access articles on aspects of oncology theory, practice and policy (about the blogger). This blog is not a source for medical advice.

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This year I’m focusing on Tumor Biology and Human Genetics, with close attention to molecular diagnostics.

Lots of abstracts look promising, including these:

CANCER GENETICS
Comen EA, Lautenberger J, McGee K et al. (Memorial Sloan-Kettering Cancer Center, National Cancer Institute.)
Use of genome-wide scan in women with breast cancer to identify common germline variants that may be associated with recurrence.
J Clin Oncol 27:15s, 2009 (suppl; abstr 11049).
Conclusions: "Genome-wide SNP genotyping of women with breast cancer identified two novel loci that may be associated with disease recurrence. Further studies in larger cohorts will be performed to replicate these findings."
Read the ASCO abstract.

Geier LJ, Sheehan M, Elia M et al. (Kansas City Cancer Center.)
The oncologist as genetic consultant: Two-year results in a large community-based practice.
J Clin Oncol 27, 2009 (suppl; abstr e22140)
Conclusions: "This oncologist-centered model proved to be very effective in identifying mutation carriers, particularly among cancer survivors in whom the hereditary syndrome had been previously overlooked. Acceptance of this approach by pts, physicians, and payers has been extremely high. This model should be considered by oncology practices wanting to add GCRA to their service lines."
Read the ASCO abstract.

EPIDEMIOLOGY/MOLECULAR EPIDEMIOLOGY
Cheung WY, Zhai R, Kulke M et al. (University of Toronto, Harvard School of Public Health, Dana-Farber Cancer Institute, Massachusetts General Hospital, Princess Margaret Hospital.)
Epidermal growth factor (EGF) gene polymorphism, gastroesophageal reflux disease (GERD), and esophageal adenocarcinoma (EAC) risk.
J Clin Oncol 27:15s, 2009 (suppl; abstr 11029)
Conclusions: "EGF A61G polymorphism exerts its effect on EAC susceptibility through an interaction with GERD. Performing EGF genotyping for patients with severe or longstanding GERD can help to identify individuals at the greatest risk of EAC."
Read the ASCO abstract.

IMMUNOBIOLOGY
Busse A, Asemissen A, Schmittel A et al. (Charité-CBF, Charité-CBF/CCM.)
Immune self-tuning in renal cell carcinoma patients.
J Clin Oncol 27, 2009 (suppl; abstr e22069)
Conclusions: "RCC caused an immune-suppressive phenotype in PBMC characterized by increased mRNA expression levels of IL10 and TGFβ. Surprisingly, in contrast to IL10, a high TGFβ mRNA expression level was an independent good prognostic factor. Whether this observation can be attributed to recently described immune promoting functions of TGFβ needs to be determined."
Read the ASCO abstract.

MOLECULAR DIAGNOSTICS & STAGING
Tobin D, Bårdsen K, Kauczynska M et al. (Bhagawan Mahavir Jain Hospital; Shrey Hospital Private Ltd; SP Medical College; Dr. Kamakshi Memorial Hospital; Department of Genetics, Radium-Riskhospitalet; Mercy Health Center.
Performance of a blood-based gene-expression test, BCtect, for early breast cancer detection.
J Clin Oncol 27:15s, 2009 (suppl; abstr 11012)
Conclusions: "The blood based gene expression test showed similar diagnostic performance between women with early and late stage BC, and the test was independent of the subject’s BMI and menopausal status suggesting broad applicability of the test and indicating its clinical potential in younger women where mammography is of less value due to dense breast tissue. No correlation with lesion size was seen suggesting the lower limit of detection is below 8mm."
Read the ASCO abstract.

Müller BM, Kronenwett R, Hennig G et al. (Charité Hospital; Siemens Healthcare Diagnostics; University Hospital.)
Quantitative determination of predictive cancer biomarkers in formalin-fixed, paraffin-embedded tissue using a new, fully automated method for RNA isolation.
J Clin Oncol 27:15s, 2009 (suppl; abstr 11032)
Conclusions: "This novel RNA extraction method is a major technical improvement for implementation of reproducible, high-throughput and cost-efficient testing of cancer biomarkers in the clinical routine and in gene-expression research studies using archived FFPE material in molecular labs."
Read the ASCO abstract.

Rosenwald S, Gibori H, Gilad S et al. (Rosetta Genomics; Sheba Medical Center; NYU School of Medicine; Rabin Medical Center.)
Identification of tumor tissue origin by a microRNA-based molecular assay.
J Clin Oncol 27:15s, 2009 (suppl; abstr 11036)
Conclusions: "Previous studies highlighted the tissue-specificity of microRNA expression. We developed this potential into a diagnostic assay that identifies tumor origins with high accuracy. This assay provides an important new tool for diagnosing tumor tissue origin."
Read the ASCO abstract.

Lebanony D, Benjamin H, Gilad S et al. (Rosetta Genomics; NYU School of Medicine; Rabin Medical Center.)
MicroRNA-based assay for differential diagnosis of squamous from non-squamous non-small cell lung carcinoma.
J Clin Oncol 27:15s, 2009 (suppl; abstr 11069)
Conclusions: "MicroRNAs are becoming an important tool for classification of cancers. A diagnostic assay based on the specificity of a single microRNA accurately identifies squamous from non-squamous NSCLC. This assay provides an important new tool for the classification of NSCLC."
Read the ASCO abstract.

Greco FA, Spigel DR, Yardley DA et al. (Sarah Cannon Research Institute; bioTheranostics.)
Unknown primary cancer (UPC): Accuracy of tissue of origin prediction by molecular profiling.
J Clin Oncol 27:15s, 2009 (suppl; abstr 11070)
Conclusions: "RT-PCR performed on FFPE initial diagnostic tissue was accurate in predicting the primary site of origin in 11 of 16 pts with UPC who eventually had their primary site identified clinically. These data provide a direct validation of the reliability of this RT-PCR assay in predicting the primary site in pts with UPC. When used in concert with clinical features and IHC stains, molecular profiling may provide the basis for more successful site-directed therapy for many of these pts. Prospective studies of RT-PCR in UPC are ongoing."
Read the ASCO abstract.

PROGNOSTIC FACTORS
Pachmann K, Camara O, Runnebaum IB et al. (Clinic for Internal Medicine II; University Hospital Friedrich Schiller University.)
Gauging the response of circulating epithelial tumor cells (CETC) and tumor stem cell subpopulations to therapy of early-stage cancer in the individual patient.
J Clin Oncol 27:15s, 2009 (suppl; abstr 11026).
Conclusions: "CETC and subpopulation monitoring provides an invaluable tool for prompt gauging of systemic therapy in early stage solid tumors as a tool for therapy guidance and optimal personalized therapies to improve therapy results and spare unnecessary treatments."
Read the ASCO abstract.

Mook S, Schmidt MK, van de Velde AO et al. (Netherlands Cancer Institute; Comprehensive Cancer Center Amsterdam (IKA); University of Texas.)
Validation of the web-based tool Adjuvant! in 5,381 Dutch breast cancer patients.
J Clin Oncol 27:15s, 2009 (suppl; abstr 11090)
Conclusions: "Adjuvant! accurately predicts 10-year OS for common tumor types in this first large scale European validation study and is of use for adjuvant treatment-decision making."
Read the ASCO abstract.

TUMOR & CELL BIOLOGY
Kalinsky K, Jacks LM, Hedvat C et al. (Memorial Sloan-Kettering Cancer Center).
Use of multiplex mutation genotyping to identify novel and protective mutations in breast cancer.
J Clin Oncol 27:15s, 2009 (suppl; abstr 11004)
Conclusions: "We have recently defined the positive prognostic significance of PIK3CA mutations in breast cancer. RAS mutations are confirmed to occur rarely in breast cancer. The finding of RET mutations in breast cancer is novel. Future tumor biomarker identification directed towards predictive measurement will assist in tailoring therapy to appropriate patient populations."
Read the ASCO abstract.

Tsai C, Chen T, Chang K, Hsiao S. (Taipei Veterans General Hospital; Taipei-Veterans General Hospital.)
Combination effects of gefitinib plus cisplatin in non-small cell lung cancer (NSCLC): Why have phase III trials failed?
J Clin Oncol 27:15s, 2009 (suppl; abstr 11022)
Conclusions: "In NSCLC cells, combination of GC showed antagonistic interaction likely because gefitinib interfered with cisplatin cell entry. Three-drug combination PCG was not better than two-drug combination PC or PG in either EGFR wild type or mutant cells. Clinically, simultaneously combined EGFR TKI with platinum in NSCLC should be avoided regardless of EGFR mutation status."
Read the ASCO abstract.

Kaiser T, Klein G, Solomayer E et al. (Department of Obstetrics and Gynecology; Center for Medical Research.)
Interactions of breast cancer cells with the microenvironment of the human bone marrow.
J Clin Oncol 27, 2009 (suppl; abstr e22097)
Conclusions: "These data indicate that the crosstalk with osteoblasts affects both the adhesive and the migratory ability of BrCa cells favoring the bone colonization process. Furthermore, the presented experimental conditions may provide useful tools to study effects of antiresorptive drugs like bisphosphonates to improve therapeutic strategies for treatment metastatic bone disease."
Read the ASCO abstract.

[OncologyWatch directory of open-access oncology journals.]

OncologyWatch: Posts about free-access articles on aspects of oncology theory, practice and policy (about the blogger). This blog is not a source for medical advice.

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Pietropaolo V. In the face of cancer. CMAJ. 2009 Mar 17;180(6):645-6. PMID: 19289813

Photosensitive, a collective of photographers using photography as a vehicle for social change, and the Canadian Cancer Society cosponsored this online gallery and traveling exhibition of more than 400 photographs (and growing) of people with cancer.

From the review by Vincenzo Pietropaolo:

“The photographs are mostly portraits of people who look just like you and me, except that that they have physical and/or psychological scars from the experience of having lived with, through and in spite of myriad forms of cancer. The people portrayed are patients, survivors, health care workers, friends — in short, what can be loosely called the “cancer community.” A short and often poignant descriptive caption, usually identifying the subjects, accompanies each picture."

View the online gallery.

[OncologyWatch directory of open-access oncology journals.]

OncologyWatch: Posts about free-access articles on aspects of oncology theory, practice and policy (about the blogger). This blog is not a source for medical advice.

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Wodarz D. Use of oncolytic viruses for the eradication of drug-resistant cancer cells. J R Soc Interface. 2009 Feb 6;6(31):179-86. PMID: 18664430

Dominik Wodarz, professor of Ecology and Evolutionary Biology at UC-Irvine, writes on the theoretical possibility of some day using oncolytic viruses to eradicate drug-resistant cancer cells prior to treatment with targeted therapies such as imatinib. Although critical conditions necessary for experimental investigation have yet to be reached, Wodarz hopes the study will stimulate new avenues of research and thinking.

Wodarz developed his mathematical model working from a concept in population dynamics, apparent competition: 

“Even if two populations or two species do not directly compete with each other, the fitter species can drive the less fit species extinct if they are infected by the same pathogen. For example, if the growth rate of the drug-sensitive cancer cells is higher than that of the resistant cancer cells, then the resistant cells will be driven extinct if a virus can infect both cell populations. In the context of CML [chronic myeloid leukemia] therapy with the targeted drug imatinib, it has been reported that certain drug-resistant mutants have a reduced growth rate and are less fit than the drug-sensitive cells."

According to the model, when drug-resistance mutations are demonstrated to have a "fitness cost" compared with drug-sensitive cells in a cancer, a virus can be used to drive resistant cell clones toward extinction prior to drug therapy. Because both drug-resistant and drug-sensitive cancer cells share the virus, competition with the fitter drug-sensitive cells would drive the resistant cells extinct. Then drugs could be used to treat the cancer without the emergence of resistance. 

Currently no cancers meet the three conditions that must exist before the model can be tested: the existence of an efficient targeted drug therapy, a detailed knowledge of drug resistance mutations, and a feasible oncolytic virus.

[OncologyWatch directory of open-access oncology journals.]

OncologyWatch: Posts about free-access articles on aspects of oncology theory, practice and policy (about the blogger). This blog is not a source for medical advice.

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Lleonart ME, Artero-Castro A, Kondoh H. Senescence induction; a possible cancer therapy. Mol Cancer. 2009 Jan 8;8(1):3. PMID: 19133111

In normal cells, the ends of chromosomes (telomeres) tend to become shortened with each cell division. When telomeres shorten to a certain length, the cell can no longer replicate and enters senescence. In many cancer cells, a protein normally present in fetal development but not in adults (telomerase) maintains the length of telomeres, effectively conferring immortality. [See CancerQuest for a full explanation, with visuals.]

In Molecular Biology, authors from Fundació Institut de Recerca Hospital Vall d´Hebron in Barcelona and the Graduate School of Medicine, Kyoto University, describe telomerase inhibition and senescence induction as potential strategies for the development of novel cancer therapies. From the paper:

“Cellular senescence has become an attractive therapeutic concept because [it] mimics programmed cell death by excluding cells from active progression through the cell cycle. As an intact apoptotic machinery is unavailable in most established malignancies, a senescence-induced mechanism emerges as a back-up program to substitute for or to reinforce an insufficient apoptotic response. Importantly, the therapeutic potential of senescence induction strongly relies on the irreversibility of this process. Although, it has not been formally tested whether drug-inducible senescence is a complete[ly] reversible process, the acquisition of spontaneous mutations that disable p53 or pRB in a resting cell without DNA replication seems rather unlikely. Thereby it would be very interesting for preclinical investigations to explore future therapies which directly prompt a clear senescence response as those observed in vitro. It would be tempting to speculate that the combination of a senescence induced therapy and a conventional therapy might cooperate to entirely abolish cancer."

[OncologyWatch directory of open-access oncology journals.]

OncologyWatch: Posts about free-access articles on aspects of oncology theory, practice and policy (about the blogger). This blog is not a source for medical advice.

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McConnell P, Dash RC, Chilukuri R, et al. The Cancer Translational Research Informatics Platform. BMC Med Inform Decis Mak. 2008 Dec 24;8(1):60. PMID: 19108734

Researchers at Duke University Medical Center and SemanticBits (Herndon, Virginia) describe a new outcomes analysis tool that allows oncologists to query clinical data from geographically dispersed patients with similar characteristics to find treatments that were administered with success. The Cancer Translational Research Informatics Platform (caTRIP, https://cabig.nci.nih.gov/tools/caTRIP) facilitates the aggregation of clinical and molecular cancer data which can then be exchanged across institutions.

The authors detail the objectives, overall software architecture, security, implementation, usability, and future development plans for caTRIP. From the paper:

“A motivating use case for the development of caTRIP is one of outcomes analysis, whereby a clinician can query data from a cohort of preexisting patients to help guide treatment of another patient. An oncologist can ask "What are the treatments and outcomes of other patients that have similar characteristics to my patient?" caTRIP makes this possible on multiple levels: local, institutional, regional, national, and beyond by leveraging grid infrastructure to scale beyond traditional query systems."

The tool has the potential to effectively broaden institutional experience with highly atypical cancers:

"The fact of the matter is that even a large tertiary care facility will rarely come across such tumors. caTRIP provides a mechanism to examine all those patients who have been seen at any institution where caTRIP has been deployed and identify the cohort of patients that matches the specified criteria. It is a matter of a few minutes, at most, to construct a query that narrows the cohort to patients that have lobular tumors of the breast, are ER negative, PR negative, and Her-2/neu overexpressed. Furthermore, the type of treatment employed and the time to recurrence or death are easily captured as part of the result set by drawing upon the Tumor Registry as an additional data source. This permits a level of decision in the clinic - heretofore impossible with prior technologies."

caTRIP is available on the U.S. National Cancer Institute’s caBIG™ Community Website.

OncologyWatch: Posts about free-access articles on aspects of oncology theory, practice and policy (about the blogger). This blog is not a source for medical advice.

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Lewis MT. Faith, heresy and the cancer stem cell hypothesis. Future Oncol. 2008 Oct;4(5):585-9. PMID: 18922113

Baylor professor Michael Lewis reviews current theory about cancer stem cells, starting from arguments for their existence:

“Arguments for the existence of tumor-initiating ‘cancer stem cells’ are rooted ultimately in cell theory. A central tenet of cell theory states that, other than the first cell, all cells arise from pre-existing cells. Since all cancers are composed of cells, and have, in most cases, been demonstrated to be clonally derived, most cancers must arise from a single, pre-existing cell – a ‘tumor-initiating cell’. The cancer stem cell hypothesis proposes that tumor-initiating ‘cancer stem cells’ arise from cells that either innately possess or acquire the ability to self-renew (reproduce a new tumor-initiating cell) and serve as a precursor cell able to generate all other cell types characteristic of a given tumor. Thus, the term ‘stem cell’ in the ‘cancer stem cell hypothesis’ refers to a defining set of cellular behaviors responsible for tumor formation, and not necessarily to the identity of the cell of origin."

 

OncologyWatch: Posts about free-access articles on aspects of oncology theory, practice and policy (about the blogger). This blog is not a source for medical advice.

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Mead MN. Strong signal for cell phone effects. Environ Health Perspect. 2008 Oct;116(10):A422. PMID: 18941554.

Drawing upon a meta-analysis published in the May 2008 issue of the International Journal of Oncology, finding significant associations between long-term cell phone use and brain tumor risk, this review encourages limiting children’s use of cell phones and using speaker phones to minimize direct exposure to the head.

“We found that cell phone use is linked to gliomas [malignant brain tumors] and acoustic neuromas [benign tumors of the brain’s auditory nerve] and are showing up after only ten years,” says lead author Lennart Hardell, an oncologist and cancer epidemiologist at University Hospital in Örebro, Sweden. Specifically, for studies that included at least 10 years of exposure, there was a doubling in the risk of gliomas for ipsilateral (same-side) but not contralateral (opposite-side) exposures to the head (as reflected by which hand the subject typically used to hold his/her cell phone). A 2.4-fold increase in risk was seen for acoustic neuromas due to ipsilateral exposures, whereas no increased risk occurred for meningiomas (tumors that occur in the membranes covering the brain and spinal cord).

 

OncologyWatch: Posts about free-access articles on aspects of oncology theory, practice and policy (about the blogger). This blog is not a source for medical advice.

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