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An Introduction to Human Cancers

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Molecular Biology of Human Cancers
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Abstract

This introductory chapter delineates first the scope of the cancer problem, providing an overview on the incidence and mortality caused by cancers worldwide. Cancers are caused by many types of exogenous carcinogens, comprising physical, chemical, and biological agents (including viruses, bacteria, and parasites), and by endogenous processes that cause damage to the genome or facilitate the expansion of cell clones with altered genomes. Usually, several factors interact. Cancers display characteristic properties, prominently uncontrolled cell proliferation that is not balanced by cell death, suppression of replicative senescence, disturbed differentiation, genomic instability, as well as various metabolic changes, which are detailed in a special section. The defining properties of cancers—as opposed to benign tumors—are invasion and metastasis. Rational treatment of cancer requires classification by staging, grading, and histology and is increasingly supported by molecular diagnostics. Current cancer treatment relies primarily on surgery, radiotherapy, and chemotherapy. Cytotoxic chemotherapy is more and more supplemented and—in some cases—replaced by molecularly targeted chemotherapies employing small molecule drugs or antibodies. Their development—in particular—is based on insights from molecular cancer research. Immunotherapies have become more efficient and more widely used. New “genetic therapies” employing nucleic acids or therapeutic viruses add to the options for efficient cancer treatment.

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Notes

  1. 1.

    GLOBOCAN by the IARC reports these data on a regular basis.

  2. 2.

    Given the high costs of many novel cancer therapies, minimizing expenses has become another consideration.

  3. 3.

    The IARC regularly publishes monographs on individual (or classes of) carcinogens that can be freely downloaded.

  4. 4.

    ‘While enrichment of “osteotropic” radioactive isotopes from elements with properties similar to calcium (like strontium) in bone tissue may cause damage it can be exploited for treatment of bone metastases.

  5. 5.

    What follows is a highly simplified crude model of tissue homeostasis. It neglects among others that stem cells may also undergo symmetric divisions to maintain their overall number and that early precursor cells may reverse to stem cells following damage.

  6. 6.

    Epigenetic changes may similarly serve as a means for adaptation during tumor expansion as well as under therapy.

  7. 7.

    These include lactylation of histones, e.g., which could be highly relevant in hypoxic cancers.

  8. 8.

    e.g., as stage I–IV, where stage I corresponds to T1N0M0 and stage IV to T3/4N1M1.

  9. 9.

    With increasing numbers and varieties of therapeutic options, third line, etc., treatments have become possible.

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Correspondence to Wolfgang A. Schulz .

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© 2023 The Author(s), under exclusive license to Springer Nature Switzerland AG

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Schulz, W.A. (2023). An Introduction to Human Cancers. In: Molecular Biology of Human Cancers. Springer, Cham. https://doi.org/10.1007/978-3-031-16286-2_1

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