Cancer Stem Cells: Emerging Key Players in Immune Evasion of Cancers

Cancer stem cells (CSCs) are subpopulations of undifferentiated cancer cells within the tumor bulk that are responsible for tumor initiation, recurrence and therapeutic resistance. The enhanced ability of CSCs to give rise to new tumors suggests potential roles of these cells in the evasion of immune surveillance. A growing body of evidence has described the interplay between CSCs and immune cells within the tumor microenvironment (TME). Recent data have shown the pivotal role of some major immune cells in driving the expansion of CSCs, which concurrently elicit evasion of the detection and destruction of various immune cells through a number of distinct mechanisms. Here, we will discuss the role of immune cells in driving the stemness of cancer cells and provide evidence of how CSCs evade immune surveillance by exerting their effects on tumor-associated macrophages (TAMs), dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), T-regulatory (Treg) cells, natural killer (NK) cells, and tumor-infiltrating lymphocytes (TILs). The knowledge gained from the interaction between CSCs and various immune cells will provide insight into the mechanisms by which tumors evade immune surveillance. In conclusion, CSC-targeted immunotherapy emerges as a novel immunotherapy strategy against cancer by disrupting the interaction between immune cells and CSCs in the TME.

Undifferentiated cancer with unknown primary location infiltrating the rectum – a case report

Colorectal cancer (CRC) is the third leading malignancy in men after prostate and lung cancer. Adenocarcinomas account for about 90% of all colorectal cancer cases. Carcinomas of unknown primary site (CUPs) are usually found in patients > 60 years of age. They account for 3% of all malignancies in Poland. We describe a diagnostically challenging case of undifferentiated carcinoma of unknown primary site invading the rectum. Rectal specimens collected during endoscopy and open biopsy, as well as samples collected during laparotomy from the side of the peritoneal cavity did not confirm cancer despite progressing clinical symptoms of an ongoing neoplastic process. Histopathological diagnosis was obtained only with core-needle biopsy of the rectal infiltration and sphincter muscles. The histopathological confirmation of carcinoma invading the sigmoid colon, rectum, anus and the mesorectum described in PET-CT enabled patient qualification for further palliative treatment.

Eosinophil granuloma due to parasite treated by laparoscopic and endoscopic cooperative surgery: a case report

Background Gastric eosinophilic granuloma caused by parasitic infection is rare. It is often suspected to be a malignant disease and it is difficult to diagnose. We successfully diagnosed and removed a gastric eosinophilic granuloma using laparoscopic and endoscopic cooperative surgery (LECS). Case presentation A 35-year-old woman visited our hospital because of epigastric pain. Upper gastrointestinal endoscopy revealed a 15 mm submucosal tumor (SMT) with changes in the folds, such as enlargement and convergence, located in the greater curvature of the lower gastric body. Computed tomography (CT) showed a dense, nonenhanced area of 15 mm at the same site. SMT was suspected, but undifferentiated cancer could not be excluded. We performed laparoscopic partial gastrectomy using LECS for resection biopsy. Histopathological examination showed an SMT 8 × 8 × 5 mm in size with an unclear boundary and necrosed insects at the core of the tumor. There was marked eosinophilic infiltration around the area. The diagnosis was gastric granuloma caused by parasitic infection. Conclusions It is difficult to differentiate gastric eosinophilic granuloma caused by parasitic infection from malignant disease. In this case, LECS is considered a minimally invasive and useful procedure.

Study of microflora in stomach cancer and gastritis.

e15516 Background: The purpose of the study was to compare the rates of bacterial and fungal colonization of the mucosa in stomach cancer and gastritis. Methods: 59 tumor and healthy tissue samples in stomach cancer and 33 stomach mucosa bioptates in gastritis were studied. DNAs were extracted by the adsorption method. DNAs of Enterobacteriaceae, Staphylococcus spp., Streptococcus spp., Candida spp., Bacteroides spp. were determined by real-time PCR. Results: 40.0% of 30 patients with stomach cancer had adenocarcinoma, 13.3% – signet ring cell carcinoma, 6.7% – undifferentiated cancer, 6.7% – NHL, 3.3% – squamous cell carcinoma, 6.7% – combined signet ring cell carcinoma and neuroendocrine or undifferentiated cancer, 23.3% – combined adenocarcinoma and neuroendocrine, signet ring cell or undifferentiated cancer. The comparison group included 33 patients with morphologically verified superficial gastritis. DNA of Bacteroides spp. was found in tumor and healthy tissues of 80.0% of cancer patients; it was not found in gastritis. DNA of B. fragilis was found in all tumor tissue samples, BFT – in 8.3% of them. The mean amount of Enterobacteriaceae in tumor tissue was 6.7x105 copy/ml, in healthy tissue – 7.0x105 copy/ml, in bioptates in gastritis – 4.0х102 copy/ml; Staphylococcus spp. – 3.4х102 copy/ml, 2.6х102 copy/ml and 8.7х101 copy/ml, Streptococcus spp. – 9.1х105 copy/ml, 1.3х105 copy/ml and 5.1х103 copy/ml, respectively. Thus, the amount of Enterobacteriaceae in tumor tissue in stomach cancer exceeded the value in gastritis by 1675 times, Staphylococcus spp. – by 3.9 times, Streptococcus spp. – by 178 times. Genes of resistance to the penicillin class TEM were found in 50.0% of patients with stomach cancer and in 8.7% of patients with gastritis. DNAs of Candida spp. in stomach cancer were found in 40% of patients in tumor tissue and in 31.0% in healthy tissue, in gastritis – in 8.3% of patients. Conclusions: Enterobacteriaceae and Streptococcus spp., mostly combined, dominate among microflora colonizing gastric mucosa in stomach cancer. The established differences in microbiocenosis in stomach cancer in comparison with gastritis suggest the possible involvement of aerobic and anaerobic microflora in the process of malignant transformation.