hall markers of cancer

Sustaining Proliferative Signaling

Cancer cells acquire the ability to continuously signal themselves and others to divide. They may produce their own growth factors (autocrine signaling), overexpress growth factor receptors (e.g., EGFR), or activate downstream signaling pathways (e.g., RAS-MAPK) independently of external signals.
Significance:
Promotes uncontrolled cell division and tumor growth.

Evading Growth Suppressors

Normal cells are restrained by tumor suppressor genes such as TP53 and RB1. Cancer cells bypass these controls by mutating or inactivating these genes, thereby avoiding cell cycle arrest and apoptosis.
Significance:
Leads to unchecked progression through the cell cycle and accumulation of mutations.

Resisting Cell Death

Cancer cells develop resistance to programmed cell death (apoptosis) through mechanisms like overexpression of BCL-2, downregulation of pro-apoptotic proteins (e.g., BAX), or mutations in p53.
Significance:
Allows cells with DNA damage or oncogenic mutations to survive, promoting tumor persistence.

Enabling Replicative Immortality

Normal cells have a limit to how many times they can divide due to telomere shortening. Cancer cells upregulate telomerase, which extends telomeres, allowing endless division.
Significance:
Contributes to immortalization of cancer cells and tumor maintenance.

Inducing Angiogenesis

Tumors require oxygen and nutrients to grow beyond a few millimeters. Cancer cells secrete angiogenic factors like VEGF to stimulate new blood vessel formation.
Significance:
Supports sustained tumor growth and provides routes for metastasis.

Activating Invasion and Metastasis

Cancer cells gain the ability to invade surrounding tissues, enter blood/lymph vessels, and colonize distant organs. This involves changes in adhesion molecules (e.g., loss of E-cadherin), degradation of extracellular matrix (e.g., via MMPs), and motility.
Significance:
Leads to spread of cancer, making treatment more difficult and prognosis poorer.

Genome Instability and Mutation

Cancer cells often have defective DNA repair mechanisms, leading to accumulation of mutations. This instability accelerates evolution of cancer, enabling acquisition of other hallmarks.
Significance:
Drives tumor heterogeneity and resistance to therapy.

Tumor-Promoting Inflammation

Chronic inflammation can promote cancer through release of cytokines, growth factors, and ROS that damage DNA and promote proliferation. Inflammatory cells in the tumor microenvironment support progression.
Significance:
Creates a pro-tumorigenic environment and enhances metastasis.

Deregulating Cellular Energetics

Cancer cells shift to aerobic glycolysis (Warburg effect), favoring rapid ATP production and biosynthesis even in oxygen-rich conditions. This supports growth and survival.
Significance:
Supports anabolic demands of fast-dividing cancer cells.

Avoiding Immune Destruction

Explanation:
Cancer cells evade immune surveillance by downregulating MHC I, expressing PD-L1, or secreting immunosuppressive cytokines (e.g., TGF-β).
Significance:
Enables immune evasion and long-term survival of tumor cells.