Cancer

A mature B-cell malignancy characterized by accumulation of a clonal population. Its initiation, indolent expansion and progression are distinct biological endpoints.

The interval between a defined starting event and detection of tumour development under a specified assay. Detection threshold and competing causes of death affect interpretation.

Continued survival or growth of established malignant disease. A gene required before initiation need not remain necessary after additional alterations accumulate.

A model in which tumours arise within the relevant host tissue rather than being introduced as an established graft. Defined engineered initiation still differs from a full human exposure history.

A mouse modified to contain selected human biological components, such as immune biological cells. Humanization is partial and does not automatically reproduce all human immune interactions.

A tumour-graft model using a genetically compatible host and donor, enabling investigation in an immune-competent setting. It generally uses mouse rather than human tumour biological cells.

A mouse model in which defined genetic changes are introduced to test disease mechanisms. Tissue, timing, expression level and genetic background constrain its relationship to human cancer.

Avoidance or suppression of immune-mediated elimination. Normal immune-regulatory mechanisms can be repurposed in a tumour context.

The organization of a tumour into related lineages sharing inherited changes. A clonal alteration need not be a causal driver because passengers can hitchhike during expansion.

The proportion of a sampled tumour preparation contributed by malignant biological cells. It affects interpretation of copy number, variant fractions and expression measurements.

A requirement for a particular activity in maintenance of a cancer under specified conditions. A dependency is not automatically an initiating driver or a selective therapeutic target.

Strong dependence of an established tumour on an oncogenic activity. Dependence can change as the tumour acquires cooperating or bypass alterations.

A myeloid malignancy classically associated with the BCR-ABL fusion. Dependence on a defined kinase driver provides a mechanistic basis for targeted inhibition.

Cancer invasion is penetration of cancer cells into surrounding tissue across the normal boundaries of their compartment. It is distinct from cell proliferation and from completion of distant metastatic colonization.

Invasion by connected or coordinated groups of cancer biological cells rather than only isolated migrants. Leader and follower biological cells can perform different tasks.^[ref]

An actin-rich cellular protrusion associated with localized extracellular matrix degradation during invasion. Formation, matrix digestion and whole-cell invasion are related but distinct experimental endpoints.