Lung cancer is the most common cancer worldwide, accounting for 1.8 million new cases and 1.6 million deaths in 2012. Non-small cell lung cancer (NSCLC), which is one of two types of lung cancer, accounts for 85–90% of all lung cancers. Despite advances in therapy, lung cancer still remains a leading cause of death. Cancer relapse and dissemination after treatment indicates the existence of a niche of cancer cells that are not fully eradicated by current therapies. These chemoresistant populations of cancer cells are called cancer stem cells (CSCs) because they possess the self-renewal and differentiation capabilities similar to those of normal stem cells. Targeting the niche of CSCs in combination with chemotherapy might provide a promising strategy to eradicate these cells. Thus, understanding the characteristics of CSCs has become a focus of studies of NSCLC therapies.

Cancer is a major health problem worldwide. The failure of current treatments to completely eradicate cancer cells often leads to cancer recurrence and dissemination. Studies have suggested that tumor growth and spread are driven by a minority of cancer cells that exhibit characteristics similar to those of normal stem cells, thus these cells are called cancer stem cells (CSCs). CSCs are believed to play an important role in initiating and promoting cancer. CSCs are resistant to currently available cancer therapies, and understanding the mechanisms that control the growth of CSCs might have great implications for cancer therapy. Cancer cells are consist of heterogeneous population of cells, thus methods of identification, isolation, and characterisation of CSCs are fundamental to obtain a pure CSC populations. Therefore, this chapter describes in detail a method for isolating and characterizing a pure population of CSCs from heterogeneous population of cancer cells and CSCs based on specific cell surface markers.

Background: The XRCC1 protein facilitates various DNA repair pathways; single-nucleotide polymorphisms (SNPs) in this gene are associated with a risk of gastrointestinal cancer (GIC) with inconsistent results, but no data have been previously reported for the Sabah, North Borneo, population. We accordingly investigated the XRCC1 Arg194Trp and Arg399Gln SNPs in terms of GIC risk in Sabah. Materials and Methods: We performed genotyping for both SNPs for 250 GIC patients and 572 healthy volunteers using a polymerase chain reactionrestriction fragment length polymorphism approach. We validated heterozygosity and homozygosity for both SNPs using direct sequencing. Results: The presence of a variant 194Trp allele in the Arg194Trp SNP was significantly associated with a higher risk of GIC, especially with gastric and colorectal cancers. We additionally found that the variant 399Gln allele in Arg399Gln SNP was associated with a greater risk of developing gastric cancer. Our combined analysis revealed that inheritance of variant alleles in both SNPs increased the GIC risk in Sabah population. Based on our etiological analysis, we found that subjects ≥50 years and males who carrying the variant 194Trp allele, and Bajau subjects carrying the 399Gln allele had a significantly increased risk of GIC. Conclusions: Our findings suggest that inheritance of variant alleles in XRCC1 Arg194Trp and Arg399Gln SNPs may act as biomarkers for the early detection of GIC, especially for gastric and colorectal cancers in the Sabah population.

Highlight ResearchThe Set Net was identified and recorded.Length and weight of the catch of set net was analyzed. AbstractSet net fisheries are made according to traditional fishing gears method in the coastal waters of Sungai Sembilang, Selangor, Peninsular Malaysia. These fisheries system are the passive structure of gear used to catch fish that swim in shallow water with muddy substrate. This study focused on determining the species variety and the possible future of set net fisheries in Sungai Sembilang. Catch composition of set net was investigated based on the catch data during July to December 2020 and continued from January to February 2021. The catch data was recorded by a research assistant on site during fishing season. The data consist of species, length and weight of all catches recorded. Total catch of 60 fish species belonging to 23 families were captured during this study period. Ariidae (31.73%), Clupeidae (11.56%), and Scatophagidae (7.96%) were determined as dominant families caught this set net. The total dominant catch amount of species Plicofollis argyropleuron (18.71%), Nemapteryx caelata (9.96%), and Anodontostoma chacunda (8.92%) compromised 37.6% of the total catch. This type of fishing gear can be used by local fisherman to catch fishes and can prevent trawl net from come closer to the shore. This study would provide some general useful information about the status of set net fisheries as well as the species abundance caught from the set net.

Purpose: This study was aimed to isolate the putative cancer stem cell (CSC) populations from A549 lung cancer cell line and to evaluate the difference of carcinogenesis-related genes expression within parental population (A549) and isolated CSC populations (A549 CD166+ /EpCAM+ and CD166+ /CD44+). Methods: We performed flow cytometry analysis to sort out cell positive for these markers; CD166+ /EpCAM + and CD166+ /CD44+ from A549 cancer cell line. The isolated cells were tested for multipotent capacities by clonogenic and differentiation assays. Quantitative real time PCR was performed for both isolated CSC population and parental population to test expression of ALDH1A1 and 6 other genes that known to contribute to carcinogenesis; RARβ CYP24A1, BIRC5, EDN1, IL1β and PTGS2. Result(s): Both CD166+ /EpCAM+ and CD166+ /CD44+ have ability to form colonies and able to differentiate into adipocytes and osteocyte. Expression of ALDH1A1 was downregulated in all three cell populations (parental A549, A549 CD166+ /EpCAM+ and A549 CD166+ /CD44+) whereas the other 6 carcinogenesis-related genes were upregulated in all three cancer cell populations. There are no significant differences of gene expressions were detected among all three populations (p > 0.05). Conclusion(s): Downregulation of ALDH1A1 in all three cancer populations up-regulate the expression of other 6 carcinogenesis-related genes. Gene regulations between parental cancer cell (A549) and both putative CSC populations show no significant difference suggesting the existence of various CSC subpopulations reside within parental A549 population