Cancer, various tissues

Cancer, Classification of cell types
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Xeroxed then later scanned from 2000 medical textbook (which unfortunately I didn’t copy publication information therefrom--jk)

 

For these reasons any classification of the cell types in the body must be somewhat arbitrary with respect to the fineness of its subdivisions. Here, we list only the adult human cell types that a histology text would recognize to be different, grouped into families roughly according to function. We have not at­tempted to subdivide the class of neurons of the central nervous system. Also, where a single cell type such as the keratinocyte is conventionally given a suc­cession of different names as it matures, we give only two entries—one for the differentiating cell and one for the stem cell. With these serious provisos, the 210 varieties of cells in the catalogue represent a more or less exhaustive list of the distinctive ways in which a given mammalian genome can be expressed in the phenotype of a normal cell of the adult body.

 

Keratinizing Epithelial Cells

keratinocyte of epidermis (= differentiating epidermal cell) basal cell of epidermis (stem cell) keratinocyte  of fingernails and toenails basal cell of nail bed  (stem cell) hair shaft cells medullary cortical cuticular hair-root sheath cells cuticular of Huxley's layer of Henle's layer external hair matrix cell (stem cell)

Cells of Wet Stratified Barrier Epithelia

surface epithelial cell of stratified squamous  epithelium of comea, tongue, oral cavity,  esophagus, anal canal, distal urethra, vagina basal cell of these epithelia (stem cell) cell of urinary epithelium (lining bladder and urinary ducts)

Epithelial Cells Specialized for Exocrine Secretion

cells of salivary gland mucous cell (secretion rich in

polysaccharide) serous cell (secretion rich in

 glycoprotein enzymes) cell of von Ebner's  gland in tongue (secretion to wash over taste buds) cell of mammary

gland, secreting milk cell of lacrimal gland,  secreting tears cell of ceruminous gland of  ear, secreting wax cell of eccrine sweat gland, secreting glycoproteins (dark cell)

cell of eccrine sweat gland, secreting small molecules (clear cell) cell of apocrine sweat gland (odoriferous secretion, sex-hormone sensitive) cell of gland of Moll in

eyelid (specialized

sweat gland) cell of sebaceous gland, secreting lipid-rich

sebum cell of Bowman's gland in nose (secretion to

wash over olfactory epithelium) cell of Brunner's gland

in duodenum,

secreting alkaline solution of mucus

and enzymes cell of seminal vesicle, secreting components

of seminal fluid, including fructose ias

fuel for swimming sperm)


cell of prostate gland, secreting other

components of seminal fluid cell of bulbourethral gland, secreting mucus cell of Bartholin's gland, secreting vaginal

lubricant

cell of gland of Littre, secreting mucus cell of endometrium of uterus, secreting

mainly carbohydrates isolated goblet cell of respiratory and

digestive tracts, secreting mucus mucous cell of lining of stomach

zymogenic cell of gastric gland, secreting

pepsinogen

oxyntic cell of gastric gland, secreting HC1 acinar cell of pancreas, secreting digestive

enzymes and bicarbonate Paneth cell of small intestine, secreting

lysozyme type II pneumocyte of lung, secreting

surfactant Clara cell of lung (function unknown)

Cells Specialized for Secretion of Hormones

cells of anterior pituitary, secreting

growth hormone

follicle-stimulating hormone

luteinizing hormone

prolactin

adrenocorticotropic hormone

thyroid-stimulating hormone cell of intermediate pituitary, secreting

melanocyte-stimulating hormone cells of posterior pitutiary, secreting

oxytocin

vasopressin cells of gut and respiratory tract, secreting

serotonin

endorphin

somatostatin

gastrin

secretin

cholecystokinin

insulin

glucagon

bombesin cells of thyroid gland, secreting

thyroid hormone

calcitonin cells of parathyroid gland, secreting

parathyroid hormone

oxyphil cell (function unknown) cells of adrenal gland, secreting

epinephrine

norepinephrine

 

Keratinizing Epithelial

 

Cells

keratinocyte of epidermis (= differentiating epidermal cell) basal cell of epidermis (stem cell) keratinocyte of fingernails and toenails basal cell of nail bed (stem cell) hair shaft cells medullary cortical cuticular hair-root sheath cells cuticular of Huxley's layer of Henle's layer external hair matrix cell (stem cell)

 

Cells of Wet Stratified Barrier Epithelia

surface epithelial cell of stratified squamous epithelium of comea, tongue, oral cavity, esophagus, anal canal, distal urethra, vagina basal cell of these epithelia (stem cell) cell of urinary epithelium (lining bladder and urinary ducts)

 

Epithelial Cells Specialized for Exocrine Secretion

cells of salivary gland mucous cell (secretion rich in polysaccharide) serous cell (secretion rich in glycoprotein

enzymes) cell of von Ebner's gland in tongue (secretion to wash over taste buds) cell of mammary gland, secreting milk cell of lacrimal gland, secreting tears cell of ceruminous gland of ear, secreting wax cell of eccrine sweat gland, secreting glycoproteins (dark cell) cell of eccrine sweat gland, secreting small molecules (clear cell) cell of apocrine sweat gland (odoriferous secretion, sex-hormone sensitive) cell of gland of Moll in eyelid (specialized sweat gland) cell of sebaceous gland, secreting lipid-rich sebum cell of Bowman's gland in nose (secretion to wash over olfactory epithelium) cell of Brunner's gland in duodenum, secreting alkaline solution of mucus and enzymes cell of seminal vesicle, secreting components of seminal fluid, including fructose ias fuel for swimming sperm) cell of prostate gland, secreting other components of seminal fluid cell of bulbourethral gland, secreting mucus cell of Bartholin's gland, secreting vaginal lubricant cell of gland of Littre, secreting mucus cell of endometrium of uterus, secreting mainly carbohydrates isolated goblet cell of respiratory and digestive tracts, secreting mucus mucous cell of lining of stomach zymogenic cell of gastric gland, secreting pepsinogen oxyntic cell of gastric gland, secreting HC1 acinar cell of pancreas, secreting digestive enzymes and bicarbonate Paneth cell of small intestine, secreting lysozyme type II pneumocyte of lung, secreting surfactant Clara cell of lung (function unknown)

 

Cells Specialized for Secretion of Hormones

cells of anterior pituitary, secreting growth hormone  follicle-stimulating hormone  luteinizing hormone prolactin

adrenocorticotropic hormone thyroid-stimulating hormone cell of intermediate pituitary, secreting melanocyte-stimulating hormone cells of posterior pitutiary, secreting oxytocin vasopressin cells of gut and respiratory tract, secreting serotonin endorphin somatostatin gastrin secretin cholecystokinin insulin glucagons  bombesin cells of thyroid gland, secreting thyroid hormone calcitonin cells of parathyroid gland, secreting parathyroid hormone oxyphil cell (function unknown) cells of adrenal gland, secreting epinephrine norepinephrine, steroid hormones mineralocorticoids glucocorticoids cells of gonads, secreting testosterone (Leydigc ell of testis) estrogen (theca interna cell of ovarian follicle) progesterone (corpus luteum cell of ruptured ovarian follicle) cells of juxtaglomerular apparatus of kidney juxtaglomerular cell (secreting renin) .   Uncertain but macula densa,   probably related cell in function; peripolar cell possibly involved mesangial cell  in secretion of      erythropoietin).

 

Epithelial Absorptive Cells in Gut, Exocrine Glands, and Urogenital Tract

brush border cell of intestine (with microvilli) striated duct cell of exocrine glands gall bladder epithelial cell brush border cell of proximal tubule of  kidney distal tubule cell of kidney nonciliated cell of ductulus efferens epididymal principal cell epididymal basal cell

 

Cells Specialized for Metabolism and Storage

hepatocyte (liver cell) fat cells white fat brown fat lipocyte of liver.

 

Epithelial Cells Serving Primarily a Barrier Function, Lining the Lung, Gut, Exocrine Glands, and Urogenital Tract

Type I pneumocyte (lining air space of lung) pancreatic duct cell (centroacinar cell) nonstriated duct cell of sweat gland, salivary gland, mammary gland, etc. (various) parietal cell of kidney glomerulus podocyte of kidney glomerulus cell of thin segment of loop of Henle (in kidney) collecting duct cell (in kidney) duct cell of seminal vesicle, prostate gland, etc. (various).

 

Epithelial Cells Lining Closed Internal Body Cavities

vascular endothelial cells of blood vessels and lymphatics.


1188  Chapter 22 : Differentiated Cells and the Maintenance of Tissues

 

 

Table 24-1 Cancer Incidence and Cancer Mortality in the United States, 1993

Type of Cancer                                         New Cases per Year

 

Deaths per Year

 

Total cancers

 

1,170,00

 

 

 

528,300

 

 

 

Cancers of epithelia: carcinomas

 

992,700

 

(85%)

 

417,175

 

(79%)

 

Oral cavity and pharynx

 

29,800

 

(3%)

 

7,700

 

(1%)

 

Digestive organs (total)

 

236,900

 

(20%)

 

120,325

 

(23%)

 

Colon and rectum

 

152,000

 

(13%)

 

57,000

 

(11%)

 

Pancreas

 

27,700

 

(2%)

 

25,000

 

(5%)

 

Stomach

 

24,000

 

(2%)

 

13,600

 

(3%)

 

Liver and biliary system

 

15,800

 

(1%)

 

12,600

 

(2%)

 

Respiratory system (total)

 

187,100

 

(16%)

 

154,200

 

(29%)

 

Lung

 

170,000

 

(15%)

 

149,000

 

(28%)

 

Breast

 

183,000

 

(16%)

 

46,300

 

(9%)

 

Skin (total)

 

(>700,000)*

 

 

 

9,100

 

(2%)

 

Malignant melanoma

 

32,000

 

(3%)

 

6,800

 

(1%)

 

Reproductive tract (total)

 

244,400

 

(21%)

 

59,950

 

(11%)

 

Prostate gland

 

165,000

 

(14%)

 

35,000

 

(7%)

 

Ovary

 

22,000

 

(2%)

 

13,300

 

(3%)

 

" Uterine cervix

 

13,500

 

(1%)

 

4,400

 

(1%)

 

Uterus (endornetrium)

 

31,000

 

(3%)

 

5,700

 

(1%)

 

Urinary organs (total)

 

79,500

 

(7%)

 

20,800

 

(4%)

 

Bladder

 

52,300

 

(4%)

 

9,900

 

(2%)

 

Cancers of the hemopoietic and immune system: leukemias and lymphomas

 

93,000

 

(8%)

 

50,000

 

(9%)

 

Cancers of central nervous system and eye: gliomas, retinoblastoma, etc.

 

18,250

 

(2%)

 

12,350

 

(2%)

 

Cancers of connective tissues, muscles,

 

 

 

 

 

 

 

 

 

and vasculature: sarcomas

 

8,000

 

(1%)

 

4,150

 

(1%)

 

All other cancers + unspecified sites

 

57,050

 

(5%)

 

43,425

 

(8%)

 

'Nonmelanoma skin cancers are not included in total of all cancers, since almost all are cured easily and many go unrecorded.

 

In the world as a whole, the five most common cancers are those of the lung, stomach, breast, colon/rectum, and uterine cervix, and the total number of new cancer cases per year is just over 6 million. Note that only about half the number of people who develop cancer die of it. (Data for USA from American Cancer Society, Cancer Facts and Figures, 1993.)

the corresponding type of malignant tumor being an adenocarcinoma (Figure 24-2); a chondroma and a chondrosarcoma are, respectively, benign and malig­nant tumors of cartilage. About 90% of human cancers are carcinomas, perhaps because most of the cell proliferation in the body occurs in epithelia or perhaps because epithelial tissues are most frequently exposed to the various forms of physical and chemical damage that favor the development of cancer.

 

Each cancer has characteristics that reflect its origin. Thus, for example, the cells of an epidermal basal-cell carcinoma, derived from a keratinocyte stem cell in the skin, will generally continue to synthesize cytokeratin intermediate fila­ments, whereas the cells of a melanoma, derived from a pigment cell in the skin, will often (but not always) continue to make pigment granules. Cancers originat­ing from different cell types are, in general, very different diseases. The basal-cell carcinoma, for example, is only locally invasive and rarely forms metastases, whereas the melanoma is much more malignant and rapidly gives rise to many metastases (behavior that recalls the migratory tendencies of the normal pig­ment-cell precursors during development, discussed in Chapter 21). The basal-cell carcinoma is usually easy to remove by surgery, leading to complete cure; but the malignant melanoma, once it has metastasized, is often impossible to extir­pate and consequently fatal.

 

Cancer as a Microevolutionary Process

 

This hastens evolution of the complex set of properties required for neoplasia and malignancy and helps the cancer cells develop resistance to anticancer drugs. At the same time, however, defects ofDNA metabolism underlying such mutability may make the cancer cells uniquely vulnerable to a suitably designed therapeutic attack.

The Molecular Genetics of Cancer 15

 

Because cancer is the outcome of a series of random genetic accidents subject to natural selection, no two cases even of the same variety of the disease are likely to be genetically identical. Nevertheless, all cancers can be expected to involve a disruption of the normal restraints on cell proliferation, and for each cell type there is a finite number of ways in which such disruption can occur. In fact, changes in a relatively small set of genes appear to be responsible for much of the derangement of cell behavior in cancer. The identification and characteriza tion of many of these genes has been one of the great triumphs of molecular biology.

 

Cell proliferation can be regulated directly or indirectly — directly through the mechanism that determines whether a cell passes the restriction point, or "Start," of the cell-division cycle, as discussed in Chapter 17; or indirectly, for example, through regulation of the commitment to terminal differentiation or programmed cell death. In either case the normal regulatory genes can be loosely classified into those whose products help stimulate an increase in cell numbers and those whose products help inhibit it. Correspondingly, there are two mutational routes toward the uncontrolled cell proliferation and invasiveness that are characteristic of cancer.  'The first is to make a stimulatory gene hyperactive: this type of mutation has a dominant effect — only one of the cell's two gene copies need undergo the change — and the altered gene is called an oncogene (the normal allele being a proto-oncogene; from Greek onkos, a tumor). The second is to K make an inhibitory gene inactive: this type of mutation usually has a recessive effect — both the cell's gene copies must be inactivated or deleted to free the cell of the inhibition — and the lost gene is called, for want of a better term, a tumor suppressor gene.

 

The mutant genes with a dominant effect — that is, the oncogenes — can be identified directly by taking DNA from the tumor cells and searching for fragments of it that, when introduced into normal cells, will cause these cells to behave like tumor cells. Techniques for achieving this feat were first devised in the late 1970s; their development followed earlier studies of a very similar process that occurs naturally, when viruses move their genetic material from cell to cell. | This work paved the way for an explosion of discoveries of oncogenes and proto-4 oncogenes. More recently, progress has been made in the more difficult task of identifying and cloning tumor suppressor genes.

 

In this section we discuss oncogenes and tumor suppressor genes in turn. We conclude by presenting a case study of one common variety of cancer, where the steps of tumor progression can be related to a series of identified mutations.

 

Retroviruses Can Act as Vectors for Oncogenes That Transform Cell Behavior 16> 17> 18

Viruses have played a remarkable part in the search for the genetic causes of human cancer. Although viruses have no role in the majority of common human cancers, they are more prominent as causes of cancer in some animal species, and analysis of animal tumor viruses has provided a key to the mechanisms of cancer in general.

 

The first animal tumor virus was discovered more than 80 years ago in chick­ens, which are subject to infections that cause connective-tissue tumors, or sar­comas. The infectious agent was characterized as a virus — the Rons sarcoma virus,

The Molecular Genetics of Cancer 1273

1 Some Changes Commonly Observed When a Normal Tissue-Culture Cell Is transformed by a Tumor Virus

1.  Plasma-membrane-related abnormalities

A.    Enhanced transport of metabolites

B.    Excessive bleeding of plasma membrane

C.    Increased mobility of plasma membrane proteins

2.  Adherence abnormalities

A.    Diminished adhesion to surfaces: therefore able to maintain a rounded

morphology

B.    Failure of actin filaments to organize into stress fibers C.    Reduced external coat of fibronectin D.   High production of plasminogen activator, causing increased extracellular

proteoiysis

3.  Growth and division abnormalities

A. Growth to an unusually high cell density.  B. Lowered requirement for growth factors. C. Less anchorage dependence (can grow even without attachment to rigid surface).  D.   "Immortal" (can continue proliferating indefinitely).  E. Can cause tumors when injected into susceptible animals which we now know to be an RNA virus. Like all the other RNA tumor viruses discovered since, it is a retrovirus. When it infects a cell, its RNA is copied into DNA by reverse transcription and the DNA is inserted into the host genome, where it can persist and be inherited by subsequent generations of cells. Figure 6-82 outlines the life cycle of a retrovirus and shows how its genome undergoes reverse transcription, integration into host DNA, and exit from and entry into host cells.

 

"But how does the viral infection cause tumors? The solution to this problem, as to so many others in cell biology, depended on the development of a conve­nient assay by which different strains of virus could be rapidly tested for their tumor-causing capacity. The assay system, still widely used, consists simply of fibroblasl cells proliferating in a culture dish. If active tumor virus is added to the culture medium, small colonies of abnormally proliferating transformed cells appear within a few days. Each such colony is a clone derived from a single cell that has been infected with the virus and has stably incorporated the viral genetic material. Released from the social controls on cell division, the transformed cells outgrow normal ones in the culture dish just as in the body and are therefore usually easy to select. The transformed cells commonly show a complex syn­drome of abnormalities (summarized in Table 24-3). They tend not to be con­strained by density-dependent inhibition of cell division (see Figure 17-39), for example, but pile up in layer upon layer as they proliferate (Figure 24-21). In addition, they often do not depend on anchorage for growth and are capable of comaci-inhibited monolayer of normal cells

growth medium multilayer of uninhibited cancer cells.

 

 Loss of contact inhibition. Canter cells, unlike ™f» normal cells, usually continue 10 fi'»" and pile up on top of one another after they have formed a confluent monolayer.

plastic tissue-culture dish dividing even when held in suspension; they have an altered shape and adhere poorly to the substratum and to other cells, maintaining a rounded appearance reminiscent of a normal cell in mitosis; they may be able to proliferate even in the absence of growth factors; they are immortal and do not undergo senescence in culture; and when they are injected back into a suitable host animal, they can give rise to tumors.

The misbehavior of the transformed cells can be traced to an oncogene dial is carried by the virus but is not necessary for the virus's own survival or repro­duction. This was first demonstrated by the discovery of mutant Rous sarcoma viruses that multiply normally but no longer transform their host cells. The loss of transforming ability could be shown to correspond to loss or inactivation of a particular gene, which was given the name sir (Figure 24-22). This specific gene in the Rous sarcoma virus is responsible for cell transformation in vitro and for tumor formation in vivo, but it is unnecessary baggage from the point of view of the virus's own propagation.

 

Retroviruses Pick Up Oncogenes by AccidentI6'17> l9

If the viral src gene is bad for the animal and unnecessary to the virus, why is it present and where does it come from? When a radioactive DNA copy of the vi­ral src gene sequence was used as a probe to search for related sequences by DNA-DNA hybridization, it was found that the genomes of normal vertebrate cells contain a sequence that is closely similar, but not identical, to the src gene of the Rous sarcoma virus. This normal cellular counterpart of the viral src gene (v-src) is called c-src {or just src). It is the proto-oncogene corresponding to the oncogene v-src. Evidently, the gene has been picked up accidentally by the retrovirus from the genome of a previous host cell but has undergone mutation in the process (Figure 24-23). The result is a perturbed gene function that leads to cancer and so brings the gene, and the virus that carries it, to the scientist's attention. The retrovirus has, in effect, cloned the gene for us. A large number of other oncogenes have been identified in other retroviruses and analyzed in simi­lar ways (Table 24-4]. Each has led to the discovery of a corresponding proto-oncogene that is present in every normal cell.

 

A Retrovirus Can Transform a Host Cell by Inserting Its DNA Next to a Proto-oncogene of the Host20

There are two ways in which a proto-oncogene can be converted into an oncogene upon incorporation into a retrovirus: the gene sequence may be altered

figure 24-22 Cell transformation by the Rous sarcoma virus. The

scanning electron micrographs show cells in culture infected with a form of the Rous sarcoma virus that carries a temperature-sensitive mutation in the gene responsible Tor transformation (the v-src oncogene). (A) The cells are transformed and have an abnormal rounded shape at low temperature (34°C), where the oncogene product is functional. IB) The same cells adhere strongly to the culture dish and thereby regain their normal flattened appearance when the oncogene product is inactivated by a shift to higher temperature (39"C). (Courtesy of G. Steven Martin.)

The Molecular Genetics of Cancer

p. 1275

 

 

murine leukemia virus terminal repeats Cap-C 939pol Rous sarcoma virus

CapH__L 5'

 

(A) host cell DNA pol intron region encoding kinase domain chicken c-src proto-oncogene

 

(B)

Table 24-4 Some Oncogenes Originally Identified Through Their Presence in Transforming Retroviruses

 

Oncogene  Proto-oncogene Function      Source of Virus   Virus-induced Tumor

abl

 

protein kinase (tyrosine)

 

mouse cat

 

pre-B-cell leukemia sarcoma

 

erb-B

 

protein kinase (tyrosine):

 

chicken

 

erythroleukemia,

 

epidermal growth factor (EGF) receptor

fes         protein kinase (tyrosine) cat/chicken

fins        protein kinase (tyrosine): cat macrophage colony-stimulating factor (M-CSF) receptor

fps    \ products associate to form mouse jun   j     AP-1 gene regulatory protein       chicken

kit         protein kinase (tyrosine): cat Steel factor receptor

raf        protein kinase (serine/threonine) chicken/ activated by Ras mouse

myc       gene regulatory protein of chicken the HLH family

H-ras    GTP-binding protein rat K-ras     GTP-binding protein                      rat

rel         gene regulatory protein related      turkey to NFKB

sis         platelet-derived growth factor,       monkey B chain

src         protein kinase (tyrosine) chicken

 

fibrosarcoma, sarcoma sarcoma, osteosarcoma fibrosarcoma, sarcoma sarcoma

sarcoma; myelocytoma, carcinoma sarcoma; erythroleukemia sarcoma; erythroleukemia reticuloendotheliosis sarcoma sarcoma

 

 The structure of the Rous sarcoma virus. (A) The organization of the viral genome as compared with that of a more typical retrovirus (murine leukemia virus). Rous sarcoma virus is unusual among the retroviruses that carry oncogenes in that it has retained all the three viral genes required for the ordinary viral life cycle: gag (which produces a polyprotein that is cleaved to generate the capsid proteins), pol (which produces reverse transcriptase and an enzyme involved in integrating the viral chromosome into the host genome), and env (which produces the envelope glycoprotein). In other oncogenic retroviruses one or more of these viral genes are wholly or partly lost in exchange for the acquisition of the transforming oncogene, and therefore infectious particles of the transforming virus can be generated only in a cell that is simultaneously infected with a nondefective, nontransforming helper virus, which supplies the missing functions. (Often the transforming oncogene is fused to a residual fragment of gag, leading to production of a hybrid oncogenic protein that includes part of the Gag sequence.) (B) The relationship between the v-src oncogene and the cellular src proto-oncogene from which it has been derived. The introns present in cellular src have been spliced out of v-src; in addition, v-src contains mutations that alter the amino acid sequence of the protein, making it hyperactive and unregulated as a tyrosine-specific protein kinase. Rous sarcoma virus has been highly selected (by cancer research workers) for its ability to transform cells to neoplasia, and it does this with unusual speed and efficiency.

p. 1276

 

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Disclaimer:  The information, facts, and opinions provided here is not a substitute for professional advice.  It only indicates what JK believes, does, or would do.  Always consult your primary care physician for medical advice, diagnosis, and treatment. 

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