https://cancerbiologyprogram.med.wayne.edu/pdfs/hallmarks_cancer_article.pdf

Hallmarks of cancer: the next generation.

抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

[신간의 별자리x] 우리/미술, 그리고 ‘슬픔의 박물관’

The process of programmed cell death, or apoptosis, is generally characterized by distinct morphological characteristics and energy-dependent biochemical mechanisms. Apoptosis is considered a vital component of various processes including normal cell turnover, proper development and functioning of the immune system, hormone-dependent atrophy, embryonic development and chemical-induced cell death. Inappropriate apoptosis (either too little or too much) is a factor in many human conditions including neurodegenerative diseases, ischemic damage, autoimmune disorders and many types of cancer. The ability to modulate the life or death of a cell is recognized for its immense therapeutic potential. Therefore, research continues to focus on the elucidation and analysis of the cell cycle machinery and signaling pathways that control cell cycle arrest and apoptosis. To that end, the field of apoptosis research has been moving forward at an alarmingly rapid rate. Although many of the key apoptotic proteins have been identified, the molecular mechanisms of action or inaction of these proteins remain to be elucidated. The goal of this review is to provide a general overview of current knowledge on the process of apoptosis including morphology, biochemistry, the role of apoptosis in health and disease, detection methods, as well as a discussion of potential alternative forms of apoptosis.

/pdf/apoptosis-a-review-of-programmed-cell-death-ly0ozrc0t6.pdf

Apoptosis: A Review of Programmed Cell Death

Immune checkpoints refer to the plethora of inhibitory pathways that are crucial to maintaining self-tolerance. Tumour cells induce immune checkpoints to evade immunosurveillance. This Review discusses the progress in targeting immune checkpoints, the considerations for combinatorial therapy and the potential for additional immune-checkpoint targets.

/pdf/the-blockade-of-immune-checkpoints-in-cancer-immunotherapy-j2cp4ba5s9.pdf

The blockade of immune checkpoints in cancer immunotherapy

Meta-hallmarks of aging and cancer.

HIV-1 protease inhibitors and cytomegalovirus vMIA induce mitochondrial fragmentation without triggering apoptosis

/pdf/hiv-1-protease-inhibitors-and-cytomegalovirus-vmia-induce-4exn749r1a.pdf

Detection of apoptosis and apoptosis-associated alterations

A major challenge in biomedical research is elucidating connections between stress responses within the cell and the extracellular microenvironment. This dialogue can transcend cellular life, and as such, premortem stress responses condition the mechanism through which corpses are cleared postmortem ( 1 , 2 ). This implies that the reason why, and the means by which, cells die determine whether their demise ultimately triggers immune responses against dead-cell antigens ( 3 ). On page 499 of this issue, Yoon et al. ( 4 ) explore the role of p53, a major stress-elicited transcription factor and tumor suppressor protein ( 5 , 6 ), in the clearance of dying cells by macrophages. The authors determine that p53 operates in a signaling pathway that protects against a systemic, life-threatening autoimmune disease encompassing ulcerative dermatitis, seizures, otitis, eye lesions, and glomerulonephritis ( 4 , 7 ).

https://science.sciencemag.org/content/sci/349/6247/476.full.pdf

A p53-regulated immune checkpoint relevant to cancer

Ageing is the most important risk factor for the majority of human pathologies. We propose the concept that the advancement of the hallmarks of ageing is dictated by several distinct biological clocks that can be decelerated by the induction of autophagy. This ‘time dilation’ delays the time-dependent manifestation of multiple diseases. Kroemer and Lopez-Otin discuss how the induction of autophagy could slow down human ageing and thus also delay the onset of ageing-associated diseases, by decelerating biological clocks.

/pdf/decelerating-ageing-and-biological-clocks-by-autophagy-20iu64dpus.pdf

Guido Kroemer

Papers

Meta-hallmarks of aging and cancer.

HIV-1 protease inhibitors and cytomegalovirus vMIA induce mitochondrial fragmentation without triggering apoptosis

Detection of apoptosis and apoptosis-associated alterations

A p53-regulated immune checkpoint relevant to cancer

Decelerating ageing and biological clocks by autophagy