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

Oxidative Stress, Inflammation, and Cancer: How Are They Linked?

ALDH1 is a marker of normal and malignant human mammary stem cells and a predictor of poor clinical outcome.

Tumours grow within an intricate network of epithelial cells, vascular and lymphatic vessels, cytokines and chemokines, and infiltrating immune cells. Different types of infiltrating immune cells have different effects on tumour progression, which can vary according to cancer type. In this Opinion article we discuss how the context-specific nature of infiltrating immune cells can affect the prognosis of patients.

The immune contexture in human tumours: impact on clinical outcome

Irrespective of the morphological features of end-stage cell death (that may be apoptotic, necrotic, autophagic, or mitotic), mitochondrial membrane permeabilization (MMP) is frequently the decisive event that delimits the frontier between survival and death. Thus mitochondrial membranes constitute the battleground on which opposing signals combat to seal the cell's fate. Local players that determine the propensity to MMP include the pro- and antiapoptotic members of the Bcl-2 family, proteins from the mitochondrialpermeability transition pore complex, as well as a plethora of interacting partners including mitochondrial lipids. Intermediate metabolites, redox processes, sphingolipids, ion gradients, transcription factors, as well as kinases and phosphatases link lethal and vital signals emanating from distinct subcellular compartments to mitochondria. Thus mitochondria integrate a variety of proapoptotic signals. Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria. These catabolic enzymes as well as the cessation of the bioenergetic and redox functions of mitochondria finally lead to cell death, meaning that mitochondria coordinate the late stage of cellular demise. Pathological cell death induced by ischemia/reperfusion, intoxication with xenobiotics, neurodegenerative diseases, or viral infection also relies on MMP as a critical event. The inhibition of MMP constitutes an important strategy for the pharmaceutical prevention of unwarranted cell death. Conversely, induction of MMP in tumor cells constitutes the goal of anticancer chemotherapy.

Mitochondrial Membrane Permeabilization in Cell Death

Su1267: ENDOSONOGRAPHIC CHANGES IN HIGH-RISK INDIVIDUALS UNDERGOING SCREENING FOR PANCREATIC ADENOCARCINOMA

639 Figure 1 Abstract 639 Figure 2639 Figure 2 http://dx.doi.org/10.1136/jitc-2022-SITC2022.0639 Abstracts J Immunother Cancer 2022;10(Suppl 2):A1–A1595 A669 RE P I T Journal for ImmunoTherapy of Cancer (JITC) preprint. The copyright holder for this preprint are the authors/funders, who have granted JITC permission to display the preprint. All rights reserved. No reuse allowed without permission.

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639 BASECAMP-1: Leveraging HLA loss of heterozygosity in solid tumors by NGS to identify patients with relapsed solid tumors for future CEA and MSLN logic-gated Tmod™ CAR T-cell therapy

Diane M. Simeone

Papers

Su1267: ENDOSONOGRAPHIC CHANGES IN HIGH-RISK INDIVIDUALS UNDERGOING SCREENING FOR PANCREATIC ADENOCARCINOMA

639 BASECAMP-1: Leveraging HLA loss of heterozygosity in solid tumors by NGS to identify patients with relapsed solid tumors for future CEA and MSLN logic-gated Tmod™ CAR T-cell therapy