A group of researchers from Hiroshima recently discovered the origin of a normal-looking stomach lining that covers sites of gastric cancer and makes it difficult to spot after the eradication of an H. pylori infection. H. pylori infection is a major cause of stomach cancer and causes inflammation by releasing substances that can destroy cells that line the stomach. This destruction and regeneration of tissue can lead to stomach cancer. This study found that even after treatment of the infection, H. pylori leaves behind layers of cells that seem normal but actually originate from stomach cancer tissue. Thus, clinicians should be aware of these layers as to not miss potential stomach cancer sites when treating patients who have been treated for H. pylori infection.
Stomach cancer should no longer be considered a disease only of older people, and patients under 40 with chronic digestive symptoms should be more actively investigated – especially if they are of Latin American ethnicity. This advice follows new data from a retrospective, observational study in Mexico which showed that one in seven of over 2,000 patients diagnosed with gastric cancer between 2004 and 2016 were under 40.
Helicobacter pylori, a specific strain of bacteria found more often in East Asian patients may be a risk factor for stomach cancer. Doctors want to identify who is most at risk for cancer carrying out a pilot study that would shape treatment and screening strategies for patients infected with this bacterium. Dr. Nina Salama considers that the global differences in stomach cancer risk can be partly attributed to differences in H. pylori itself. One way that H. pylori varies is in the CogA gene which encodes a toxin that helps the bacterium better attach to cells lining the stomach.
Understanding the mutation in the MUC16 gene may be vital to help predict the outcome of the disease as well as possible treatments available for gastric cancer patients. The MUC16 mutation is thought to increase cancer cell’s susceptibility to immunotherapies. Although the genetics of gastric cancer varies greatly from person to person, mutations in the MUC16 gene are very common in gastric cancer as well as other types of cancer. Researchers at Wake Forest University analyzed this mutation and found that MUC16 mutations affects 38.4% of stomach cancer. Moreover, samples containing MUC16 were 1.87 times more likely to have additional mutations. However, patients with the MUC16 mutation lived longer than those with the unaltered gene with a 39% increase in survival. The researchers believe that the use of therapeutic regimens to abrogate immune inhibition may be beneficial for patients with gastric cancer who have MUC16 mutations.
Researchers at Spain’s Universitat Politecnica de Valenicia studied the effects of lycopene in the body. Lycopene is an antioxidant found in several fruits and tomatoes, hence it is also found in ketchup. Researchers found that lycopene is more potent in the sauce rather than the fruits because it has been cooked down thus facilitation absorption in the body. This is relevant because previous studies have shown that the consumption of tomatoes inhibit cell growth which can help to guard off gastric cancer. Furthermore, increasing levels of healthy bacteria in the gut can decrease the risk of gastric cancer. Another recommendation is to eliminate the use of cigarettes as it can double the risk of gastric cancer. Lastly, lowering the consumption of salt is recommended as it can have negative effects to diets.
The RAINBOW study pre-treated patients with the doublet of fluoropyrimidine plus a platinum, and later gave paclitaxel plus or minus ramucirumab. Survival rates for this study increased to more than 2 months. Another second line study, REGARD lead by Charlie Fuchs, consisted of best supportive care plus a placebo or best supportive care plus ramucirumab. Looking at both studies together we can say that ramucirumab plus paclitaxel is fit for patients in the second line treatment given as the mean survival of the RAINBOW study was around 9 months for the combination.
Current research of esophagogastric cancer is heading toward building on the signals of activity seen for immunotherapy. Though phase I and phase II trials have given a mixed results, scientists are looking forward to the results of first line immunotherapy trials some of which involve the claudin protein in the body. This protein is overexpressed in most gastric cancers and it is a gap junction protein. Claudin protein combined with chemotherapy has shown great data for its phase II trials and will soon be undergoing phase III trials given improved overall survival of esophagogastric patients. We now know that VEGF-targeted drugs, HER-2 targeted agents, neoadjuvant chemotherapy and radiation added to surgery all improve outcomes in patients with esophagus and gastroesophageal cancers.
In a recent study, researchers found that MUC16 gene mutations in gastric cancer patients lead to higher mutational loads than patients who do not have these mutations. Furthermore, the researchers also found that MUC16 gene mutations affect the immune system and could in also be used to identify patients who could respond to immunotherapies. Of the samples tested in the study, MUC16 gene mutation samples show to have the highest mutation rates compared to those without MUC16. This phenomenon was attributed to tumor instability which is prevalent in gastric cancer. According to The Cancer Genome Atlas (TCGA) patients with MUC16 mutations survived a median 46.9 months, as compared to 26.7 months for those without. In addition, researchers reported MUC16 mutations appeared to influence expressions of other genes such as cell cycle checkpoints, DNA replication and repair, antiaging processing, and signaling pathways involved in the immune system. Lastly, MUC16 is known to modulate immune response to cancer thus patients with MUC16 mutations could benefit from treatments that boost the immune system.