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Thursday, 25 April 2019


Anti-tumor activity of curcumin on stomach cancer


Image result for golden latteYou may have seen it popping up on cafe menus recently — the "golden latte". It's hot milk mixed with turmeric, coconut oil, maybe a bit of honey. Curcumin has been proclaimed a superfood; a health booster — the yellow powder used as a central component in Asian cooking for thousands of years. turmeric was known as a healing food in the ancient Indian system of medicine Ayurveda — where it was used for many medical uses. Recently a new research indicates the curcumin also help prevent or combat stomach cancer.

A recent study by researchers at the Federal University of São Paulo (UNIFESP) and the Federal University of Pará (UFPA) in Brazil identified possible therapeutic effects of this pigment and of other bioactive compounds found in food on stomach cancer, the third and fifth most frequent type of cancer among Brazilian men and women, respectively. They undertook a vast review of the scientific literature on all nutrients and bioactive compounds with the potential to prevent or treat stomach cancer and found that curcumin is one of them. Curcumin is a natural regulator of histone activity.

Histones are proteins in cell nuclei that organize the DNA double helix into structural units called nucleosomes. Each nucleosome is made of DNA coiled like a spool around eight histone proteins (a histone octamer) to compact the DNA so that it fits in the cell, where it is packaged into chromatin. The activity of the histones is regulated by some enzymes like histone acetyltransferases (HATs) and histone deacetylases (HDACs). These alterations are epigenetic and affect the structure and integrity of the genome in many tumors, including stomach cancer.

The researchers have found that curcumin influences histone modifications primarily by inhibiting HATs and HDACs to suppress cancer cell proliferation and induce apoptosis (programmed cell death) on the tumoral cells.

Journal Reference:

Danielle Q Calcagno, Fernanda Wisnieski, Elizangela R da Silva Mota, Stefanie B Maia de Sousa, Jéssica M Costa da Silva, Mariana F Leal, Carolina O Gigek, Leonardo C Santos, Lucas T Rasmussen, Paulo P Assumpção, Rommel R Burbano, Marília AC Smith. Role of histone acetylation in gastric cancer: implications of dietetic compounds and clinical perspectives. Epigenomics, 2019; 11 (3): 349 DOI: 10.2217/epi-2018-0081

Wednesday, 24 April 2019


Why does exercise protect against cancer? Inflammation may play a role


One of the most important benefits of exercise is in how it reduces our risk of developing a number of types of cancer — especially colorectal cancer, which according to some estimates is the malignancy most influenced by physical activity. But how workouts guard against colon cancer remains largely unknown. The new done at the University of Queensland in Brisbane, Australia, and other institutions recruiting 20 men who had survived colon cancer. (Women were excluded because menstruation might have affected results.).

The scientists asked 10 of the men to start working out strenuously three times a week: pedaling a stationary bicycle hard for four minutes, resting for three, and repeating that sequence three more times. They trained for a month and then, a few days after completing the program, rested quietly while researchers drew blood. The other 10 men completed the same 4 x 4 interval session, but only once. The researchers drew their blood before, immediately following and an additional two hours after that lone workout.

The scientists then carefully added a tiny amount of fluid from the men’s blood to petri dishes containing human colon-cancer tumor cells often used to study cancer growth. At several points during the subsequent 72 hours, the researchers counted the numbers of cells in each dish. They soon saw substantial differences.

Image result for physical exercise
In the dishes containing fluid taken from the men immediately after a single workout, the scientists counted far fewer cancer cells than in those awash in fluid drawn two hours after exercise. There was no similar decline in the dishes from the men who had trained for a month. In effect, something about the blood drawn immediately after the workout was slowing the growth of cancer cells.

The researchers think they may have identified that something in subsequent analyses of the men’s blood. They found a large increase in molecules involved in inflammation immediately after exercise. Inflammation can slow cell growth and reproduction. So a transitory increase in inflammatory markers after exercise might be helping to jam the proliferation of tumor cells.
 

Tuesday, 23 April 2019

Cancer rates in young children are increasing worldwide                                                                                                    

Rates of pediatric cancer have been rising since the 1980s; however, this increase varies by age group and cancer type. University of Minnesota researchers studied children under 5 years of age to understand cancer trends that occur in this age group around the world. Their findings were recently published in the journal JNCI Cancer Spectrum.

Researchers analyzed data from individual countries in 15 subregional categories to compare trends in cancer rates for 11 different types of pediatric cancer from 1988 to 2012.
The study found:
  • in children under 5 years, cancer rates increased for both common types of childhood leukemia, one brain tumor subtype, neuroblastoma and hepatoblastoma;
  • hepatoblastoma, a rare liver tumor, had the largest increase in incidence in 11 out of 15 regions (the increases ranged from 1.9-6.5 percent per year);
  • hepatoblastoma incidence increased in all regions except southern Asia;
  • astrocytic tumors in the brain were the only cancer that decreased over the time period.
The study reported small but significant increases in the rates of several types of childhood cancer in developer countries. The fastest rising cancer in children under five, this is still a very rare cancer. 

Monday, 22 April 2019


The amazing HeLa cells of Henrietta Lacks


In early 1951, Ms. Lacks, a 31-year old mother of five children, was found to have a malignant tumor of the cervix. During her examination at Johns Hopkins Hospital in Baltimore, MD, a sample of the tumor was removed and provided to Dr. George Gey. He was head of tissue culture research at Hopkins who for years had been attempting to produce a line of immortal human cells.  When Ms. Lacks died in October 1951, Dr. Gey announced on national television that he had produced from Ms. Lacks’ tumor a line of cells that propagated as no other cells ever had before. He called them ‘HeLa’ cells in her honor, and showed a vial of the cells to the television audience.
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HeLa cells have since been used in many laboratories all over the world to make countless research discoveries. For example, shortly after Dr. Gey announced the HeLa cell line, it was used to propagate poliovirus, an event that played an important role in the development of poliovirus vaccines. But Ms. Lacks’ family never learned about the important cells that were derived from her until 24 years after her death. The history of this event, described in the Johns Hopkins Magazine, is a commentary on the lack of informed consent common in medical research at the time.


Heart Attack May Be Early Sign of Cancer

The risk of a heart attack or stroke rose in patients who would later be diagnosed with cancer.

Image result for heart attack Researchers studied records of 374,331 Medicare beneficiaries, mean age 76, who were given cancer diagnoses from 2005 to 2013. They matched them with an equal number of controls without cancer. Then they retrospectively tracked heart attacks and strokes in the two groups in the year before the cancer diagnosis. At one month before diagnosis, those with a cancer diagnosis had more than five times the risk of heart attack or stroke compared with those without a cancer diagnosis.
The researchers found that the highest risks were in those with diagnoses of lung and colorectal cancers. It may be that cancer disrupts the body’s blood system well before the disease is detectable, causing clots that lead to cardiovascular events.
The study, in the journal Blood, had no data on the severity of the heart attacks and strokes, and the authors acknowledge that the results may not apply to younger patients.
 

 

FDA Approves First FGFR Kinase Inhibitor for Advanced Bladder Cancer


The FDA granted accelerated approval to erdafitinib (Balversa, Janssen) for the treatment of adults with locally advanced or metastatic urothelial cancer with susceptible fibroblast growth factor receptor (FGFR) alterations that has progressed during or after platinum-containing chemotherapy. Patients should be selected for therapy using an FDA-approved companion diagnostic device.
Image result for bladder cancer
FGFR alterations are present in approximately one in five patients with recurrent and refractory urothelial cancer. The approval was based on the phase 2, multicenter, open-label, single-arm BLC2001trial (ClinicalTrials.gov Identifier: NCT02365597) evaluating 87 patients who had locally advanced or metastatic urothelial cancer that had progressed during or after at least one prior chemotherapy and had at least one FGFR3 gene mutation or FGFR2 gene fusions, as determined by a clinical trial assay performed at a central laboratory.

The investigators found that erdafitinib yielded an objective response rate of 32.2% (95% CI, 22.4%-42.0%), with a complete response of 2.3% and a partial response of 29.9%.

The FDA simultaneously approved a companion diagnostic for use with erdafitinib, the therascreen FGFR RGQ Reverse-transcription (RT)-polymerase chain reaction (PCR) Kit (Qiagen), the first PCR-based companion diagnostic approved to detect FGFR alterations.