Do preserved foods increase prostate cancer risk?

Preserved foods have been found in some studies to be associated with increased cancer risks. The possible relationship between preserved foods and prostate cancer was investigated in a case-control study in southeast China during 2001-2002 covering 130 histologically confirmed cases and 274 inpatient controls without malignant disease. The total amount of preserved food consumed was positively associated with cancer risk, the adjusted odds ratio being 7.05 (95% CI: 3.12-15.90) for the highest relative to the lowest quartile of intake. In particular, the consumption of pickled vegetables, fermented soy products, salted fish and preserved meats was associated with a significant increase in prostate cancer risk, all with a significant dose-response relationship.     

Do prostate cancer patients want to choose their own radiation treatment?

PURPOSE: The aims of this study were to investigate whether prostate cancer patients want to be involved in the choice of the radiation dose, and which patients want to be involved. METHODS AND MATERIALS: This prospective study involved 150 patients with localized prostate cancer treated with three-dimensional conformal radiotherapy. A decision aid was used to explain the effects of two alternative radiation doses (70 and 74 Gy) in terms of cure and side effects. Patients were then asked whether they wanted to choose their treatment (accept choice), or leave the decision to the physician (decline choice). The treatment preference was carried out. RESULTS: Even in this older population (mean age, 70 years), most patients (79%) accepted the option to choose. A lower score on the designations Pre-existent bowel morbidity, Anxiety, Depression, Hopelessness and a higher score on Autonomy and Numeracy were associated with an increase in choice acceptance, of which only Hopelessness held up in multiple regression (p < 0.03). The uninformed participation preference at baseline was not significantly related to choice acceptance (p = 0.10). CONCLUSION: Uninformed participation preference does not predict choice behavior. However, once the decision aid is provided, most patients want to choose their treatment. It should, therefore, be considered to inform patients first and ask participation preferences afterwards.     

Do regular ovulatory cycles increase breast cancer risk?

The "estrogen window hypothesis" of the etiology of breast cancer proposes that unopposed estrogen stimulation is the most favorable state for tumor induction and that normal postovulation progesterone secretion reduces susceptibility. The authors believe that epidemiologic and experimental studies suggest rather that the opposite is true, i.e., that breast cancer risk is directly related to the cumulative number of regular ovulatory cycles. Unlike the endometrium, breast tissue mitotic activity is enhanced in the luteal phase of the menstrual cycle. Regular vigorous physical activity is one method of reducing the frequency of ovulatory cycles, and such exercise could markedly reduce a woman's lifetime risk of developing breast cancer.     

Do cancer cells die because of Nogo-B?

Nogo-A is a potent neurite outgrowth inhibitory protein in vitro and is suggested to play a role in the lack of regeneration in the central nervous system of adult higher vertebrates. A shorter splice isoform, ASY/Nogo-B, has recently been reported to act as a proapoptotic protein, the loss of which would be typical for cancer cells. Here, we show that the osteosarcoma cell line SaOS-2 and the cell line CHO do express high levels of endogenous Nogo-B and that stable transfectants overexpressing high levels of Nogo-B do not differ significantly from the respective parental wild-type or control cell lines both in respect to cell proliferation and to spontaneous apoptosis or cell death induced by staurosporine and tunicamycin. The deletion of the second transmembrane domain of Nogo-B, which has been claimed to abolish its proapoptotic activity, leads to a shift of the protein from the ER to a cytoplasmic localization, suggesting that ER stress of highly overexpressed Nogo-B may lead to aversive cellular reactions under particular conditions. Our data do not support a function of Nogo-B as a physiological pro-apoptotic protein in certain types of cancer.     

Do fatty breasts increase or decrease breast cancer risk?

Few studies have investigated the association of non-dense area or fatty breasts in conjunction with breast density and breast cancer risk. Two articles in a recent issue of Breast Cancer Research investigate the role of absolute non-dense breast area measured on mammograms and find conflicting results: one article finds that non-dense breast area has a modest positive association with breast cancer risk, whereas the other finds that non-dense breast area has a strong protective effect to reduce breast cancer risk. Understanding the interplay of body mass index, menopause status, and measurement of non-dense breast area would help to clarify the contribution of non-dense breast area to breast cancer risk.     

Do diagnostic and treatment delays for colorectal cancer increase risk of death?

Background

Using 1998–2005 SEER-Medicare data, we examined the effect of diagnostic and treatment delays on all-cause and colorectal cancer (CRC)-specific death among US adults aged ≥ 66 years with invasive colon or rectal cancer. We hypothesized that longer delays would be associated with a greater risk of death.

Methods

We defined diagnostic and treatment delays, respectively, as days between (1) initial medical consult for CRC symptoms and pathologically confirmed diagnosis (maximum: 365 days) and (2) pathologically confirmed diagnosis and treatment (maximum: 120 days). Cases (CRC deaths) and controls (deaths due to other causes or censored) were matched on survival time. Logistic regression analyses adjusted for sociodemographic, tumor, and treatment factors.

Results

Median diagnostic delays were 60 (colon) and 40 (rectal) days and treatment delays were 13 (colon) and 16 (rectal) days in 10,663 patients. Colon cancer patients with the longest diagnostic delays (8–12 months vs. 14–59 days) had higher odds of all-cause (aOR: 1.31 CI: 1.08–1.58), but not CRC-specific death. Colon cancer patients with the shortest treatment delays (<1 vs. 1–2 weeks) had higher odds of all-cause (aOR: 1.23 CI: 1.01–1.49), but not CRC-specific death. Among rectal cancer patients, delays were not associated with risk of all-cause or CRC-specific death.

Conclusions

Longer delays of up to 1 year after symptom onset and 120 days for treatment did not increase odds of CRC-specific death. There may be little clinical benefit in detecting and treating existing symptomatic disease earlier. Screening prior to symptom onset must remain the primary goal to reduce CRC incidence, morbidity, and mortality.     

IFN-γ selectively exerts pro-apoptotic effects on tumor-initiating label-retaining colon cancer cells

Label-retaining cancer cells (LRCCs) represent a novel population of stem-like cancer cells exhibiting slow cycling, chemoresistance and tumor-initiating capacities; however, their properties remain unclear, and approaches to eradicate LRCCs remain elusive. Here, we report that colon cancer cells with high fluorescent intensity, referred to as LRCCs, have the greatest cancer stem cell (CSC)-like capacities and that they preferentially express CSC markers and stemness-related genes. Moreover, we found that Lgr5, which has been reported to be a marker of rapid cycling CSCs, is almost negatively expressed in LRCCs but that its expression is gradually increased in the differentiation process of LRCCs. Interestingly, we found that LRCCs are especially sensitive to the pro-apoptotic effect of IFN-γ treatment both in vitro and in vivo because LRCCs possess higher IFN-γR levels compared with non-LRCCs, which results in the upregulation of the apoptosis pathway after IFN-γ treatment. Furthermore, we found that IFN-γ shows synergistic effects with the conventional anticancer drug Oxaliplatin to eliminate both LRCCs and non-LRCCs. In conclusion, this is the first study to suggest that LRCCs, as a distinct tumor-initiating population, can be selectively eradicated by IFN-γ, which may provide a novel therapeutic strategy for colon cancer treatment.     

Do cancer predictions work?

Two different types of simple extrapolation models were investigated as tools for cancer incidence prediction. The number of incident cancer cases by sex and site in Finland was predicted using a prediction interval for each year from 1967 to 2003 on the basis of historical cancer incidence data obtained 5 to 15 years earlier. Cancer sites where major human-made changes in aetiology and diagnostics had occurred were analysed separately. Assuming that such changes had not occurred, the 95% prediction intervals based on normal errors of the age-standardised rate and on Poisson models included the observed number in 65-100% of the years. The Poisson models produced, on average, shorter intervals and were more capable of indicating a site where the model assumptions did not hold true. Simple extrapolation models may be used with some caution on coverage when there are no known factors that might make abrupt changes in the temporal development of cancer incidence. On the other hand, they may be used for detecting the effects of such factors.     

Do founder mutations characteristic of some cancer sites also predispose to pancreatic cancer?

Understanding of the etiology and risk of pancreatic cancer (PaCa) is still poorly understood. This study evaluated the prevalence of 10 Polish founder mutations in four genes among PaCa patients and assessed their possible association with the risk of disease in Poland. In the study 383 PaCa patients and 4,000 control subjects were genotyped for founder mutations in: BRCA1 (5382insC, 4153delA, C61G), CHEK2 (1100delC, IVS2 + 1G > A, del5395, I157T), NBS1 (657del5) and PALB2 (509_510delGA, 172_175delTTGT). A statistically significant association between the 657del5 mutation and an increased risk of pancreatic cancer was observed for NBS1 gene. The Slavic NBS1 gene mutation (657delACAAA) was detected in 8 of 383 (2.09%) unselected cases compared with 22 of 4,000 (0.55%) controls (OR: 3.80, p = 0.002). The PALB2 509_510delGA and 172_175delTTGT mutations combined were seen in 2 (0.52%) unselected cases of PaCa and in 8 (0.20%) of 4,000 controls (OR: 2.61, p = 0.49). For BRCA1, the three mutations combined were detected in 4 of 383 (1.04%) PaCa patients and in 17 of 4,000 (0.42%) controls (OR: 2.46, p = 0.20). CHEK2 mutations were not associated with the risk of pancreatic cancer (OR: 1.11, p = 0.72). The founder mutation in NBS1 (657del5) was associated with an increased risk of PaCa in heterozygous carriers, indicating that this mutation appears to predispose to cancer of the pancreas. By identifying pancreatic cancer risk groups, founder mutation testing in Poland should be considered for people at risk for PaCa.     

Do newly diagnosed lung cancer patients feel their concerns are being met?

Lung cancer is the leading cause of cancer death worldwide. It has a poor prognosis and the majority of those affected are elderly. Evidence suggests that providing clear, relevant information and addressing patients' concerns can make a worthwhile difference to patients. This study aimed to: explore the concerns of lung cancer patients shortly after diagnosis; and enquire whether these concerns had been discussed by their care teams. Eighty patients with a new diagnosis of primary lung cancer were interviewed 14–28 days after the date on which they were told the diagnosis. Interviews were conducted either in the hospital ward, outpatient clinic or at home. Participants were asked to rate 17 specific items of concern from 1 = 'not a worry' to 5 = 'extremely worried', plus one non-specific item. Patients rated at least two items as worrying them to some degree with a median of nine concerns being reported. Major concerns for patients were the illness itself; the future relating to the illness and concerns about the family. Overall, patients in the study felt that less than half of their concerns (43%) had been discussed by the care team. Although levels of concern about physical symptoms were relatively low, these had been more frequently addressed than the psychosocial issues, which were rated higher by patients. There were some differences in the number of concerns reported between males/females and younger/older age groups, but the pattern of concerns was similar. There were no differences in the level of concerns between treatment groups; the location of the interview nor in the interval between diagnosis and delivery of the checklist. This study supports previous findings that there is a need for health professionals to provide emotional support and respond to the psychosocial needs of patients by eliciting their concerns and attempting to address them in the early stages of the disease process.     

Synergistic effects of genetically engineered stem cells expressing cytosine deaminase and interferon-β via their tumor tropism to selectively target human hepatocarcinoma cells

Stem cells have received a great deal of attention for their clinical and therapeutic potential for treating human diseases and disorders. Recent studies have shown that it is possible to genetically engineered stem cells (GESTECs) to produce suicide enzymes that convert non-toxic prodrugs to toxic metabolites, selectively migrate toward tumor sites and reduce tumor growth. In this study, we evaluated whether these GESTECs are capable of migrating to hepatocarcinoma cells and examined the potential therapeutic efficacy of gene-directed enzyme prodrug therapy against liver cancer cells in cellular and animal models. A modified transwell migration assay was performed to determine the migratory capacity of GESTECs to Hep3B hepatocarcinoma cells. GESTECs, that is, HB1.F3.CD or HB1.F3.CD.interferon-β (IFN-β) cells, engineered to express a suicide gene, cytosine deaminase (CD), selectively migrated toward liver cancer cells. Treatment of Hep3B, human liver cancer cells, with the prodrug 5-fluorocytosine (5-FC) in the presence of HB1.F3.CD or HB1.F3.CD.IFN-β cells resulted in the inhibition of Hep3B cell growth. In a xenografted mouse model injected with hepatocarcinoma, we investigated the therapeutic effect of these stem cells. For 9 weeks, the xenografted mice were treated with HB1.F3.CD or HB1.F3.CD.IFN-β in the presence of 5-FC. A growth of tumor mass was inhibited about 40-50% in the mice treated with GESTECs and a prodrug. In addition, we further confirmed the cytotoxic effect on tumor cells by histological analysis and migratory effect of therapeutic stem cells. Taken together, GESTECs expressing a fusion gene encoding CD and IFN-β may exert a synergistic antitumor effect on this type of tumor.     

Do people with cancer postpone death to celebrate special occasions?

Several researchers have claimed that a connection exists between deathdays and birthdays or other special occasions. Some people, especially women, appear to postpone death until after their birthdays or other special occasions to celebrate these events one more time. The purpose of this retrospective study was to determine if a deathday-birthday or deathday-Christmas connection was evident in cancer-related deaths. Data were obtained from the Rochester (New York) Regional Tumor Registry (N = 2566), the New York State Cancer Registry (N = 50,562), and the Ohio State Department of Health (N = 73,907) for three samples of individuals who died from cancer. Only a few deathday-birthday connections were evident. However, these connections were not replicated across states and years.     

Do early premalignant changes in normal breast epithelial cells predict cancer development?

A recent report suggests that, in an in vitro model of premalignant breast cells (vHMECs), silencing of INK4A gene is accompanied by over-expression of cyclo-oxygenase (COX)-2. This suggests that COX-2 over-expression may be an early event in breast cancer aetiology permitting clones within the normal epithelium to evade apoptosis, to increase their numbers and perhaps acquire further changes that promote the formation of hyperplasias, and eventually carcinomas. While COX-2 expression in normal breast epithelium in vivo has not been proven to be linked to an increased risk of breast cancer, its over-expression in the premalignant model in vitro does provide preliminary evidence that COX-2 inhibition may be a useful chemoprevention strategy.     

Do stress-related psychosocial factors contribute to cancer incidence and survival?

A substantial body of research has investigated the associations between stress-related psychosocial factors and cancer outcomes. Previous narrative reviews have been inconclusive. In this Review, we evaluated longitudinal associations between stress and cancer using meta-analytic methods. The results of 165 studies indicate that stress-related psychosocial factors are associated with higher cancer incidence in initially healthy populations (P = 0.005); in addition, poorer survival in patients with diagnosed cancer was noted in 330 studies (P <0.001), and higher cancer mortality was seen in 53 studies (P <0.001). Subgroup meta-analyses demonstrate that stressful life experiences are related to poorer cancer survival and higher mortality but not to an increased incidence. Stress-prone personality or unfavorable coping styles and negative emotional responses or poor quality of life were related to higher cancer incidence, poorer cancer survival and higher cancer mortality. Site-specific analyses indicate that psychosocial factors are associated with a higher incidence of lung cancer and poorer survival in patients with breast, lung, head and neck, hepatobiliary, and lymphoid or hematopoietic cancers. These analyses suggest that stress-related psychosocial factors have an adverse effect on cancer incidence and survival, although there is evidence of publication bias and results should be interpreted with caution.     

Do early premalignant changes in normal breast epithelial cells predict cancer development?

A recent report suggests that, in an in vitro model of premalignant breast cells (vHMECs), silencing of INK4A gene is accompanied by over-expression of cyclo-oxygenase (COX)-2. This suggests that COX-2 over-expression may be an early event in breast cancer aetiology permitting clones within the normal epithelium to evade apoptosis, to increase their numbers and perhaps acquire further changes that promote the formation of hyperplasias, and eventually carcinomas. While COX-2 expression in normal breast epithelium in vivo has not been proven to be linked to an increased risk of breast cancer, its over-expression in the premalignant model in vitro does provide preliminary evidence that COX-2 inhibition may be a useful chemoprevention strategy.