Incidence patterns indicated the prominent role of genetic factors in this type of cancer. A histocompatibility leukocyte antigen (HLA) profile of A2 and B-locus antigen, Singapore 2 (Sin 2), was identified. An association between these genes and increased risk for nasopharyngeal carcinoma (NPC), was confirmed. The risk was restricted to the "co-occurrence" of A2, B-Sin 2, suggesting that the genotype predisposing to the development of NPC was the A, B-Sin 2 haplotype. Similar associations were found to exist in Malaysian and Hong Kong Chinese so the A2, B-Sin 2 phenotype is a feature common to Asian Chinese in at least three locations. Preliminary HLA studies of medium NPC incidence in Tunisians and Malays indicated that patients with NPC of both ethnic types have altered HLA antigen profiles. If the findings of a locus-B antigen deficit in Tunisians and the role of A9 with B-locus antigens in Malays can be confirmed and clarified, the histocompatibility genetic hypothesis of NPC predisposition would be substantially strengthened.
Serum samples from Sinhalese subjects, from Punjab and from Singapore have been studied. The Gm phenotypes found are very numerous and we can observe some similarities concerning the Gm gene frequencies between the Singapore Indians with the Indians of North India, and with the Sinhalese. In contrast, Gm gene frequencies found among Chinese and Malays from Singapore are quite different from those found among Indians of Singapore. Our results here are very similar to those obtained in Malaya studies.
Samples from 378 Chinese and 259 Malay blood donors in Singapore have been studied for electrophoretic variants in 13 red cell enzyme systems and for abnormal haemoglobins. Variants were detected in 8 of the enzyme systems, and the frequencies were polymorphic for acid phosphatase, 6 phosphogluconate dehydrogenase phosphoglucomutase (locus 1) among both Chinese and Malays, and for adenylate kinase also among Malays. Rare variants were detected in the phosphohexose, NADH diaphorase and lactate dehydrogenase systems. A new GPGD phenotype and three new LDH phenotypes have been described. Electrophoretic variants of haemoglobin were more frequent among Malays than among Chinese.
Histocompatibility locus A typing of 43 Malaysian Chinese and 51 Hong Kong Chinese patients with nasopharyngeal carcinoma (NPC) confirmed the association between the occurrence of A2-Sin 2 and the increased risk for NPC that was previously demonstrated in Singapore Chinese. The results support the previous interpretation that the histocompatibility locus A genotype of importance in NPC predisposition is the A2-Sin 2 haplotype. The histocompatibility locus A-linked, genetically determined NPC risk is common to Asian Chinese from at least three geographic locations.
New data are presented concerning the relationship between NPC and HLA antigens among Chinese. When attention is confined to newly diagnosed cases, it can be shown that, apart from the increased risk associated with the joint occurrence of A2 and B-Sin 2, there is also an increased risk associated with BW17 and a decrease in risk associated with A11. Among long-term survivors, however, BW17 is appreciably decreased, whereas A2 in the absence of B-Sin 2 or BW17 is increased. Among Malays, a non-Chinese group, there is an excess among NPC patients of a locus A blank, a blank which is probably associated with the AW19 complex.
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.