Second set of review questions, and some additional notes

What was the name of the 19th century biologist who invented the once popular phrase "ontogeny recapitulates phylogeny"

What does this phrase mean?

Anatomical changes undergone by developing embryos of a given species often repeat changes in the evolution of that species. For example: we develop gill slits during embryonic government because we evolved from fish. (& hundreds of other examples). Barnacles evolved from swimming larvae that look like the earliest stages of shrimp development. This concept stimulated embryologists to make detailed descriptive studies of embryos from as many different taxonomic groups as possible, in order to figure out their evolutionary family tree.

If there were such a thing as a neotenic frog, describe its appearance, and what sexually mature adults of this species would look like.

If there were any neotenic echinoderms, what would they look like?

List at least 5 changes that occur in a tadpole as it undergoes metamorphosis into a frog.
Hint: Tail, eyes, skin, many others.


Why is it possible for an insect to have some of its cells be male (with all the normal properties of a male), although other cells of that same individual insect have all properties of a normal female of that species?

Explain how this can happen, in terms of the hormonal control of anatomical sex.

Mutation of the human gene for testosterone receptors can cause a genetic male to be indistinguishable from a woman, except for having testes rather than ovaries.

Explain how this can happen, in terms of the hormonal control of anatomical sex.

What are some consistent differences between cancer cells versus normal cells of the same differentiated cell type?

    a) The "Warburg Effect": Non-cancerous cells make most of their ATP by the series of oxidation reactions called Krebs Cycle, and do this in the mitochondria. This is in contrast to cancer cells, which make most of their ATP by glycolysis of glucose (in the cytoplasm) and accumulate high concentrations of lactic acid in their cytoplasm, tissue culture media, and surrounding tissues.

    b) "Anchorage Dependence" = Non-Cancerous cells die when cultured on agar, or other surfaces to which they do not adhere strongly enough to spread. Cancer cells survive and continue to grow when cultured on agar surfaces.

    c) "Contact Inhibition" (of locomotion) Non-cancerous cells (when cultured on glass suraces) slow their locomotion by about 50% when in contact with 5 or 6 neighboring, as compared with their average speed of crawling locomotion when not touching any other cells, or onlt 1 or 2. In comparison, some cancer cells continue to crawl at the same speeds when in contact with other cells. Actin polymerization is inhibited near sites of cell-cell contact, which is equivalent to "turning off" the exertion of traction.

    d) "Contact Inhibition of cell growth" has never been studied as carefully and quantitatively as "Contact Inhibition of cell locomotion".

    e) Shapes of nuclei become non-symmetrical, as compared with normal cells, whose nuclei are ellipsoidal or spherical. Spatial distribution of spots in chromatin also becomes less symmetrical as compared

    f) Disorganization of cytoplasmic actin and myosin (in cancer cells as compared with normal, non-cancerous cells).

    g) Weaker traction and weaker contractility exerted by cancer cells, as compared with non-cancerous cells.

    h) Although it a myth, or at best an over-simplification, to say that cancer cells grow faster than normal cells, growth rates can often be inhibited in crowded cultures, or when treated with certain growth-inhibiting chemotherapy drugs, or when cultured on non-adhesive surfaces

    Under these three conditions (that inhibit cell growth), mitosis and growth of non-cancer cells can often be inhibited more than normal cells, with the result that they really do grow faster (when something inhibits growth, the cancer cells are inhibited less than normal cells).

    In other words, growth of cancer cells can be less inhibitable. Low pH = high acidity also inhibits cancer cell growth less than it inhibits normal cells. Low concentration of serum in tissue culture media reduces growth rates in normal cells less than in cancer cells.

    A major abnormality of cancer cells is that their growth rate is less inhibited by crowding, low serum concentration, acidic pH, and probably other conditions yet to be discovered.

Thought Questions: Discuss whether cell cycle check points must not be working properly in cancer cells.

Considering that a major function of cell cycle check points is believed to be protection of cells from further damage to DNA or chromosome distribution (i.e. Until all chromosomes are properly lined up on the mitotic spindle, and/or all DNA cross-links and breaks have been repaired.

Possible new kinds of chemotherapy drugs: Please explain:

    A chemical that gets converted into a poison when many phosphates are bound to it.

    A chemical that gets converted into a poison when cytoplasm is highly acidic.

    A chemical that leaks into cancer cells (but less into normal cells) and which releases a particular 12 amino-acid long peptide into the cytoplasm, preceded by vaccination with this same peptide [so as to increase the number of T-lymphocytes that would induce apoptosis in cells containing this peptide.

    A chemical that selectively inhibits cell cycle check points, more in non-cancerous

What is meant by metastasis?
Answer: When cancer cells penetrate into lymph ducts or blood vessels, get carried to other parts of the body, stick there, penetrate out of a vein or lymph duct, and start a new tumor at one or many locations.

In what respect is the movement of primordial germ cells a special case of metastasis?

In bird embryos, and perhaps in embryos of other vertebrates, primordial germ cells colonize the gonads partly in flowing blood.

When salamanders regenerate legs, the new muscles are made entirely by splitting multinucleate myotubes into back into individual cells, which multiply, reaggregate, realign and reattach to the skeleton. Nuclei that had been part of the biceps become part hand muscles. It's entirely a rearrangement phenomenon, not at all like differentiation of multipotent stem cells (although most people tend to assume that anatomical patterns are created entirely by the special control of differentiation). Radioactive labeling of DNA has proven this again and again.

Maybe human myotubes can't split into individual cells! That might be why we can't regenerate arms and legs. If so, then researchers should be looking for methods to cause this splitting. Discovery of such a mechanism might help treat people with muscular dystrophy.

Nobody is studying this. Instead, billion$ are spent on stem cells, as if limbs regenerate by differentiation of multipotent cells.

Which, for many decades has been known not to be true. Why do we let medical progress be held back my disproven myths?

Another example is atherosclerosis. No researchers study reasons why macrophages crawl into the tunica media, or how to get them to crawl back out. Instead, treatments are designed as if the old myths were true about cholesterol sticking to the inside lining.

We should ban the words "plaque" and "build up". They hinder invention of cures.

Immunology has a comparable problem with the words "recognize" and "self". For a long time, scientists assumed embryology must work by lymphocytes detecting some special "self" molecules.

Cancer isn't caused by cells growing especially fast. But the search for treatments concentrates almost entirely on methods for damaging DNA and mitotic spindles. Chemotherapy drugs are sometimes amazingly effective, but nobody knows why.


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