218 Index Birthmarks (nevi), 128 Bishop, J. Michael, 137, 139–41, 162. See also Oncogene model <strong>of</strong> cancer Bissell, Mina, 172–73 Black bile, 118, 119 Blau, Helen, 97 Blebbing <strong>of</strong> membranes, 90 Blood, 118, 119 Blumenbach, Johann Friedrich, xvi, 125 influence <strong>of</strong>, 12, 120 on organizational urge, 10–11, 199n.6 on reflective judgment, 9 on water polyps, regeneration in, 10–11 Boerhaave, Hermann, 124 Bohr, Niels, 54, 55 Boll, Franz, 127 Bonnet, Charles, 199–200n.7 Book <strong>of</strong> Life, 110 Boveri, Theodore on chromosomes as site <strong>of</strong> Mendelian factors, 33–34, 35 on cytoplasm, 42 merogony experiments <strong>of</strong>, 33–34 on somatic mutation, xx, 118, 130, 156 Brandon, R., 5, 199n.2 Breast cancer, 145, 172–73, 182 Brockes, J. P., 163 Burdach, Karl Friedrich, 202n.1 Burdette, W. J., 132 Bureau <strong>of</strong> Ordinance (U.S. Navy), 64 Cadherins, 177 CAG trinucleotides, 193–94, 203n.7 Cancer, xix–xx, xx, 117–82 and activated proto-oncogenes, 145–49, 150, 160, 162 and age, 165–67 and amplification <strong>of</strong> genes, 160–61 aneuploidy in, 146, 148, 202n.2 and the APC gene, 145, 154, 155, 175–78 and autonomous cells as cancer cells, 129–30, 140, 156–58 <strong>of</strong> the breast, 145, 172–73, 182 carcinogenesis vs. mutagenesis, 131–33 and cell-adhesion molecules, 161, 177, 181 cell culture model <strong>of</strong>, 170–72, 181 and cell division, 151 and cell fusion, 142–44, 146–48 chemical carcinogens, 164–65 class 1 vs. class 2 types <strong>of</strong>, 166 <strong>of</strong> the colon, 145, 153–54, 160 colorectal, 174–81, 182 and the DCC gene, 145, 154, 155, 176, 178 by decree vs. default, 142–45 dominant vs. recessive genes for, 145–55, 202nn.3–5 and dynamic reciprocity, 172–73 and ECM, 172–73 environmental carcinogens, 127 experimental carcinogenesis, 128–31 and the fibronectin anti-sense gene, 152–53, 202nn.4–5 genetic predisposition for, 173–82 and heterozygosity loss, 145 history <strong>of</strong> biology <strong>of</strong>, 118–28, 157 initiation/promotion <strong>of</strong>, 132, 168–69 and intracellular vs. extracellular fields, 160–61 irritant-induced, 129, 180, 181 and the Keime und Anlagen, 155–56 <strong>of</strong> the liver, 167–68, 170 monoclonal view <strong>of</strong>, 165, 170, 172 multi-hit theory <strong>of</strong>, 131 and normality vs. pathology, 156 oncogene model <strong>of</strong>, 133–42, 145–52, 156, 157–58 oncology after the phylogenetic turn, 128–33 organizational view <strong>of</strong>, 158–65, 167, 170, 181 progress on, 173–82 reductionist view <strong>of</strong>, 156–57
and regeneration, 162–63 and resistant hepatocytes, 167–70 retinoblastoma, 144–45 somatic mutation hypothesis, 117–18, 130–33, 135–36, 144–45, 156, 159–60 SOS system <strong>of</strong>, 193 and transgenic mouse experiments, 148 tumor suppressor genes, 142–46, 149–52, 154–55, 157–58 virally induced, 133–37 Cartesian vs. Newtonian matter, 8 Celera, 201n.3 Cell, 174 Cell-adhesion molecules, 161, 177, 181 Cell culture model <strong>of</strong> cancer, 170–72, 181 Cell fusion, 142–44, 146–48 Cell theory and cancer theory, 124 and the genesis <strong>of</strong> genes, 18–19 modern, 124–26 Omnis cellula a cellula (cells come only from cells), 126 Center vs. periphery, 31 Chargaff, Erwin, 65 Cherry, R. J., 94 Child, C. M., 36 Chromatin/chromosome marking, xix, 76, 77, 111–14, 200n.8 Chromosomes, 19–21, 30–31, 33, 113, 202n.4. See also DNA; Genes, genesis <strong>of</strong> Chunk-<strong>of</strong>-anlagen, xvi Circular causality, 9–10 Cirrhosis <strong>of</strong> the liver, and cancer, 167 Classical medicine, 118 Clockworks, as dynamical processes, 60–61 Cloning, 42, 136, 200–201n.14 Code-script. See Hereditary code-script Coding problem, 65–66 Cohnheim, Julius, 127–28, 129 Index 219 Colon cancer, 145, 153–54, 160 Colorectal cancer, 174–81, 182 Compartmentalization <strong>of</strong> cells, membrane-based, 77–98 amphipathic substances/boundaries, 78–79, 87 archaea, 78 Band 3 molecules, 93–94 blebbing <strong>of</strong> membranes, 90 cellular membranes, composition <strong>of</strong>, 78 cytoskeletal interaction with membrane proteins, 90, 93 endoplasmic reticulum, 82–83 and equilibrium thermodynamics, 76, 84–85, 91, 94–95, 98–99 eubacteria, 78 eukaryotes, 78, 80 fluid-mosaic model, 87 FRAP, 88–90 glycocalyx, 85–86 Golgi complex, 81 guanosine triphosphate molecules, 84 membrane/genome organization as mutually dependent, 79–80, 95–98 metazoan ontogeny, 96–98 nuclear envelope, 80–81 nuclear pores, 80–81 Paramecium, 96 phospholipid membranes, 79, 87 protein differentiation, 79, 81–83, 85–86, 104 protein movement, 79, 83–84, 86–94 red blood cells, 92–93 SNAPs, 84 SNARES, 83–84 Tetrahymena, 96 Teutophrys, 96 vector relationship between membranous stacks, 80–81 water molecules on a hydrophobic surface, 79 Complexity. See Modularity and complexity
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What Genes Can’t Do
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What Genes Can’t Do Lenny Moss A
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To my daughters, Julie and Rachel
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Series Foreword We are pleased to p
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Introduction There can be little do
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Introduction xv argument was mistak
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Introduction xvii The empirical fru
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Introduction xix Schrödinger, rely
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What Genes Can’t Do
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2 Chapter 1 ubiquitous types of mol
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4 Chapter 1 The Phylogenetic Turn a
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6 Chapter 1 achievement of an ontog
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10 Chapter 1 3. The parts of the tr
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12 Chapter 1 Judgment). Kant famous
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14 Chapter 1 Figure 1.1 Von Baer’
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16 Chapter 1 “embryological metho
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22 Chapter 1 Charles Otis Whitman w
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24 Chapter 1 hybrids, Mendel’s in
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28 Chapter 1 simplify further the e
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30 Chapter 1 compromising ante-act,
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32 Chapter 1 hypothesis, cellular d
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34 Chapter 1 “merogony” experim
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40 Chapter 1 remainder of DNA is go
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42 Chapter 1 Johannsen reproduces i
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54 Chapter 2 (Gene-D) in a renewed
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56 Chapter 2 i.e., the acquisition,
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58 Chapter 2 Atomic configurations,
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60 Chapter 2 “aperiodic solids,
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64 Chapter 2 Gamow’s Translation
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70 Chapter 2 Melding Heidegger’s
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80 Chapter 3 dictated by “genetic
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84 Chapter 3 protein that ultimatel
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88 Chapter 3 little by way of expla
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90 Chapter 3 of retinal rod cells,
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92 Chapter 3 The cell’s system of
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96 Chapter 3 stamp on them, then th
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100 Chapter 3 that homeostatic, aut
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106 Chapter 3 artificially simplifi
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108 Chapter 3 lactose concentration
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110 Chapter 3 context. The ability
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112 Chapter 3 sex-specific patterns
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116 Chapter 3 primacy then any expl
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118 Chapter 4 a probability approac
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120 Chapter 4 suit, suggested that
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122 Chapter 4 Von Baer accepted Cuv
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126 Chapter 4 size. The cell walls
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128 Chapter 4 residual embryonic ce
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130 Chapter 4 distinctively aberran
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132 Chapter 4 Proponents of the som
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134 Chapter 4 radiation sensitivity
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136 Chapter 4 different place. In e
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138 Chapter 4 A DNA probe must sati
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140 Chapter 4 been led well beyond
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142 Chapter 4 if this correlation h
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144 Chapter 4 chromosomes provided
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148 Chapter 4 malignant, continued
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150 Chapter 4 molecular oncology, b
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152 Chapter 4 associated with the o
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154 Chapter 4 then sequential loss
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158 Chapter 4 divide. Smithers’s
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162 Chapter 4 example, the followin
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166 Chapter 4 capsule of an adult m
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- Page 228 and 229: 210 References Keller, E. F. (2001)
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