How stress helps cancer flourish
Researchers at Monash University have found that stress increases the number and diameter of lymphatic vessels associated with tumours, increasing the flow of cancerous cells around the body. In a study published in Nature Communications last week, the researchers, using special microscopy, demonstrated that stress hormones can increase the flow of fluorescently labelled nanoparticles through the lymphatic system. By blocking the activity of proteins that detect stress or those that enhance formation of the lymphatic vessels, they could reduce the spread of cancer cells in the mice. “These findings reveal unanticipated communication between stress-induced neural signalling (SNS) and inflammation, which regulates tumour lymphatic architecture and lymphogenous tumour cell dissemination. These findings suggest that limiting the effects of SNS signalling to prevent tumour cell dissemination through lymphatic routes may provide a strategy to improve cancer outcomes.”
Type 1 diabetes associated with increased risk of some cancer types
New research published in Diabetologia reveals that type 1 diabetes is associated with an increased risk of various cancer types including cancers of the stomach, liver, pancreas, endometrium, ovary and kidney, but a reduced risk of other cancer types, including prostate and breast cancer. The study analysed more than 9000 cancer cases in type 1 diabetes patients diagnosed across five countries, using data from five nationwide diabetes registers: Australia (2000-2008), Denmark (1995-2014), Finland (1972-2012), Scotland (1995-2012) and Sweden (1987-2012). Using the data of those in national cancer registries, the authors were able to compare the cancer incidence among people with type 1 diabetes to that of the general population. “The analyses across all cancers combined revealed no increased overall cancer risk among men with type 1 diabetes, whereas women with type 1 diabetes experienced a 7% increased overall cancer risk. The neutral overall cancer risk among men with type 1 diabetes was largely due to a 44% decreased incidence of prostate cancer – the most common non-skin cancer among men. When the authors excluded data for sex-specific cancer types (prostate, testis, breast, cervix, endometrium and ovary), excess cancer risk appeared in both men and women with type 1 diabetes (15% for men and 17% for women). For specific cancer sites among people with type 1 diabetes, the study revealed increased risks of cancers of the stomach (23% for men, 78% for women); liver (two-fold among men, 55% for women); pancreas (53% for men, 25% for women), endometrium (42%) and kidney (30% for men, 47% for women). Conversely, women with type 1 diabetes were 10% less likely to have a diagnosis of breast cancer, although the reasons for this are unclear.”
Zika linked with Guillain-Barré syndrome in French Polynesia
Analysis of blood samples from 42 patients diagnosed with Guillain-Barré syndrome (GBS) during the Zika virus outbreak in French Polynesia provides the first evidence that Zika virus might cause GBS, a severe neurological disorder, according to new research published in The Lancet. Based on the analysis of data from French Polynesia, if 100 000 people were infected with Zika virus, 24 would develop GBS. Between October 2013 and April 2014, French Polynesia experienced the largest Zika outbreak to be reported at the time. An estimated 32 000 patients consulted a doctor about a suspected Zika virus infection, and 42 patients were diagnosed with GBS between November 2013 and February 2014. All 42 patients with GBS diagnosed at the Centre Hospitalier de Polynésie Française in Papeete, Tahiti were included in the study. Most (88%) of the patients with GBS reported symptoms of Zika virus infection approximately 6 days before the onset of neurological symptoms. While none tested positive for a Zika virus infection once in hospital, blood tests showed that 41 (98%) were carrying Zika virus antibodies, and all (100%) had neutralising antibodies against Zika virus. By comparison, only 54 (56%) of the patients without a fever were carrying Zika virus neutralising antibodies. All 42 patients were diagnosed with a type of GBS called acute-motor axonal neuropathy (AMAN), but few carried the biological markers typically associated with AMAN, suggesting a previously unknown disease mechanism.
Spread of chikungunya masked by misdiagnosis as dengue
Chikungunya, a viral disease transmitted by infected mosquitoes, could have been misdiagnosed as dengue because both have similar symptoms, according to a study published in the open-access journal BMC Infectious Diseases. The study, a systematic review led by researchers from the London School of Hygiene and Tropical Medicine, created global maps that represent the geographical spread of both viruses, identifying their current geographical limits, as well as countries at risk of future infection. Chikungunya and the acute phase of dengue share symptoms such as fever, rash, muscle and joint pain. “As there is no specific antiviral drug treatment or vaccine, treatment is directed primarily at alleviating symptoms. Misdiagnosis could have an effect on how the symptoms of each disease are relieved – potentially with serious consequences.” The authors wrote: “Diagnoses are typically only symptom-based. During dengue outbreaks, or in countries that historically suffer dengue epidemics, clinicians tend not to confirm their diagnosis in the laboratory; dengue infection is assumed. Co-infection is typically only detected during recognized chikungunya outbreaks and this reflects a widespread bias in how these diseases are reported. The vector species that spread these pathogens – and also the Zika virus – are the same, yet the number of countries that have reported dengue cases is considerably higher than countries that have reported chikungunya. Our study highlights that this may be an aberration caused by continuing and pervasive misdiagnosis of chikungunya as dengue.”
A new approach to treating Alzheimer’s, perhaps
UK scientists have described a new model for the mechanism of neurodegeneration leading to Alzheimer’s disease and its potential for new treatments in a pair of papers published last week in Neuropharmacology. The researchers say they’ve found a novel peptide (a short protein) found at raised levels in Alzheimer’s diseased brains which is the primary driver of neurodegeneration, and have developed a drug prototype that blocks its damaging activity in human cell lines, offering a promising strategy for future therapeutics. They report raised levels of the novel peptide in Alzheimer’s midbrain and cerebrospinal fluid compared with controls, and demonstrate that, in vitro, the peptide drives production of both amyloid and hyperphosphorylated tau. In the first paper, the damaging effects of either the AChE peptide or amyloid are shown to be blocked by a novel prototype drug (NBP-14), a cyclised form of the AChE peptide. In the second paper, the effects of the AChE peptide and their blockade by NBP14 are demonstrated in ex vivo rat basal forebrain, using real-time optical imaging of large-scale, transient “neuronal assemblies”.
Does radiotherapy for prostate cancer make it spread?
Canadian researchers, published in The BMJ last week, found a possible association between radiotherapy for prostate cancer and a risk of secondary cancers of the bladder (0.1-3.8%), colorectal tract (0.3-4.2%) and rectum (0.3-1.2%), although they warned that the absolute rates of these secondary cancers remain low, “particularly compared with other rates of complications associated with treatment for prostate cancer”. They analysed the results of 21 studies assessing the risk of secondary malignancies in patients exposed or unexposed to radiotherapy in the course of treatment for prostate cancer. They found an increased risk of cancers of the bladder, colorectum, and rectum, but not cancers of the lung or hematologic (blood) system, after radiotherapy compared with no radiotherapy or surgery. These results were consistent when the researchers restricted analyses to studies using 5- or 10-year lag periods between treatment and the development of a secondary cancer.