Essential Cell Biology 5th edition

732 CHAPTER 20 Cell Communities: Tissues, Stem Cells, and Cancer
• During development, the actin bundles at the adherens junctions that
connect cells in an epithelial sheet can contract, helping the epithelium
to bend and pinch off, forming an epithelial tube or vesicle.
• Hemidesmosomes attach the basal face of an epithelial cell to the
basal lamina, a specialized sheet of extracellular matrix; the attachment
is mediated by transmembrane integrin proteins, which are
linked to intracellular keratin filaments.
• Tight junctions seal one epithelial cell to the next, barring the diffusion
of water-soluble molecules across the epithelium.
• Gap junctions form channels that allow the direct passage of inorganic
ions and small, hydrophilic molecules from cell to cell; in plants,
plasmodesmata form a different type of channel, which traverses the
cell walls, is lined by plasma membrane, and allows both small and
large molecules to pass from cell to cell.
• Most tissues in vertebrates are complex mixtures of cell types that
are subject to continual turnover.
• Most tissues of an adult animal are maintained and renewed by
the same basic cell processes that generated them in the embryo:
cell proliferation, movement, differentiation, and death. As in the
embryo, these processes are controlled by intercellular communication,
selective cell–cell adhesion, and cell memory.
• In many tissues, nondividing, terminally differentiated cells are generated
from stem cells, usually via proliferating precursor cells.
• Embryonic stem cells (ES cells) can proliferate indefinitely in culture
and remain capable of differentiating into any cell type in the body—
that is, they are pluripotent.
• Induced pluripotent stem cells (iPS cells), which resemble ES cells,
can be generated from the cells of adult mammalian tissues, including
those of human, through the artificial expression of a small set of
transcription regulators.
• Pluripotent stem cells can be induced to form specific cell types and
even small organs (organoids) in suitable culture conditions, providing
powerful models for studying human development and genetic
diseases.
• Cancer cells fail to obey the social constraints that normally ensure
that cells survive and proliferate only when and where they should,
and do not invade regions where they do not belong.
• Cancers arise from the accumulation of many mutations in a single
somatic cell lineage; they are genetically unstable, having increased
mutation rates and, often, major chromosomal abnormalities.
• Unlike most normal human cells, cancer cells typically express telomerase,
enabling them to proliferate indefinitely without losing DNA
at their chromosome ends.
• Most human cancer cells harbor mutations in the p53 gene, allowing
them to survive and divide even when their DNA is damaged.
• The mutations that promote cancer can do so either by converting
one copy of a proto-oncogene into a hyperactive (or overexpressed)
oncogene or by inactivating both copies of a tumor suppressor gene.
• Sequencing of cancer genomes reveals that most cancers have
mutations that subvert the same key pathways controlling cell proliferation,
cell growth, cell survival, and the response to DNA damage.
In different cases of cancer, these pathways are subverted in different
ways.
• Knowing the molecular abnormalities that underlie a particular cancer,
one can begin to design treatments targeted specifically to those
abnormalities.