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INTRINSIC FACTORS in the ETIOLOGY of NEOPLASMS' It Is

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INTRINSIC FACTORS in the ETIOLOGY of NEOPLASMS' It Is INTRINSIC FACTORS IN THE ETIOLOGY OF NEOPLASMS' CARL V. WELLER, MS., M.D. (From the Department of Pathology, University of Michigan) It is as true as it is trite that the cause of disease is never a single factor. Two elements always enter into etiology. One of these is inherent in the germ plasm of the individual; the other brought to bear upon the organism from beyond the confines of the germinal elements from which it has devel- oped. Better than internal and external, endogenous and exogenous, or con- stitutional and environmental, to designate these two groups of factors, are the terms intrinsic and extrinsic. Practical experience directs us to seek the relative importance of intrinsic and extrinsic factors whenever the causation of disease is studied, and we find that the two ingredients may be combined in every possible proportion. At one end of the series are diseases such as deaf mutism, transmitted as a simple recessive, in which the intrinsic element almost crowds out all other considerations. In the recessively sex-linked hemophilia, again the intrinsic element is so prominent that we see at once the mendelian significance of the process, although the bleeder may not be made known until the extrinsic factor, trauma, opens his blood vessels. The asthenic, dolichomorphic bodily configuration, which marks the phthisical habitus, is a familial character and therefore intrinsic, but it conditions infection by the tubercle bacillus in such a way as to give it serious or even lethal possibilities. When we consider syphilis, we find that the Treponema is no respecter of genetic constitution, yet sex and race may modify the character of the disease. These four com- monplace illustrations are chosen advisedly to invite attention to a serial arrangement of diseases between those predominantly intrinsic and those predominantly extrinsic. Where in this series does neoplasia belong? There are several destructively critical attitudes which seem to be incom- patible with an open-minded scientific approach to the question of intrinsic factors in the etiology of neoplasms. (1) The first of these is the assumption that intrinsic factors are not concerned in the causation of neoplasms, because, if they were, it would make popular education about cancer difficult. What other inference can be drawn from the statement, in a deservedly popular monograph on Neoplastic Dis- eases ( l), that the author subscribes to the conclusion : " Nothing authorizes us to affirm that cancer is hereditary; in the interests of the public this doctrine ought to be combated "? (2) The second conception which I believe to be largely fallacious is that information obtained from lower animals is of no value in the oncology of 1 Read in a Symposium on the Genesis of Tumors, American Association of Pathologists and Bacteriologists, Chicago, March 26, 1937. 39 40 CARL V. WELLER man, The problems of neoplasia are biological problems, and the processes of life are so fundamentally similar throughout the Vertebrata, and particu- larly in the Mammalia, that we cannot afford to disregard knowledge which comes from animal experimentation. That neoplasms of the lower animals and of man are as similar as they are should be occasion for rentark, and not otherwise. This similarity extends through gross and microscopic pathology, comparative age incidence, benignancy and malignancy, power of metastasis and mode of termination. (3) Again, the criticism is sometimes raised that familial incidence of benign neoplasms is of no significance in respect to the etiology of cancer. There are two reasons why this is not true. The first is that no sharp line of demarcation between benign and malignant new growths can be drawn; the second, that benign new growths, sometimes presenting a familial incidence, may furnish the essential preblastomatoid somatic alteration upon which cancer may appear. This seems to be the case with carcinoma developing upon intestinal polyposis, as may be illustrated by the family described by Barker (2). (4) It should be obvious that intrinsic factors are operating whether there be direct transmission of a predisposition to neoplasia or whether the inherit- able condition is a somatic structural or functional variation which makes the affected individual more vulnerable to the cancerigenic effect of extrinsic factors. Neither a gene for " cancer " nor a " cancer-resisting " gene is es- sential for exemplification of intrinsic factors in the etiology of neoplasms. (5) Finally, a necessary change in the point of view of many must come with the realization that both proponents and opponents of intrinsic factors in the etiology of cancer have, in years gone by, limited their discussions too rigidly to questions of genes and of mendelism. Achievements with Droso- phila and Oenethera may have provided alluring vistas, but there is accumu- lating evidence that very broad conceptions of the transmission of certain qualities must be entertained. The specialists in the field of genetics are fully aware of this trend. I quote from Baur (3) : "We have likewise reason to expect that hereditary transmission in accordance with other laws than the mendelian will occur in the case of all social differences which are based, not upon peculiarities of the chromosomes, but on those of some other part of the idioplasm. Differences in the structure of the remainder of the thread equipment of the cell nucleus, in the structure of chromosomes, etc., must certainly produce differences in the finished or- ganism. Very numerous observations on plants combine to show that hereditary dif- ferences in their vitality are transmitted in accordance with other laws than the mendelian. The mendefian laws of separation do not prevail universally, and . in the case of man no less than in that of other organisms, we are likely to encounter phenomena of hereditary transmission which do not occur in accordance with these laws." Marsh (4) recognized the importance of this broad view when he wrote in 1929: " One might infer from the discussions of cancer heredity in which dominance and re- cessiveness are set off against each other that cancer must belong to one or the other in in- heritance. This would be to forget that dominance is no essential of the mendelian system and that both members of an allelomorphic pair may appear in F,." And MacDowell (5) has recently made a vigorous statement of this view: INTRINSIC FACTORS IN THE ETIOLOGY OF NEOPLASMS 41 " It is highly regrettable that, outside the immediate circle of geneticists, there seems to be an impression that the gene is self-sufficient and is either dominant or recessive. Espe- cially as applied to neoplasia this misunderstanding has led to erroneous conclusions both on the part of hostile critics and ardent believers. Dominance is only a special case at the end of a continuous series of interrelations between pairs of genes. No gene can produce its effect without cooperation of many other genes. And genes and extrinsic conditions co- operate in all cases." CLINICALEVIDENCE FOR AND AGAINSTINTRINSIC FACTORS IN THE ETIOLOGYOF NEOPLASMS From the clinical side there are several classes of evidence for and against the significance of intrinsic factors. From each of these only illustrative samples can receive specific reference. (1) Cancer Families: The occurrence of several cancers in the same family attracts both lay and medical attention. Since approximately one-tenth of the population dies of cancer, the operation of the laws of chance should give some families with no cancer at all and others with an excess of cancer. It is doubtful if the basic data are as yet available by which to determine through statistical methods the degree of familial concentration which is mathematically significant of transmitted predisposition. Yet, practical experience gives at least a temporary answer, and the general opinion is that there are families in which the mass incidence of cancer is significantly in excess of the normal expectation. More than a hundred such families can be collected from the world's literature, but many such reports lose part of their value in that often only affected individuals are indicated. Perhaps the most thoroughly studied cancer family is that twice reported by Dr. Warthin and recently brought up to date by Hauser and myself (6). Of 174 members of this family attaining an age of twenty-five years, 41 developed 43 malignant neoplasms. Of even greater importance than the total number of malignant neoplasms are the facts (1) that in some branches of this family cancer has never occurred, and (2) that with two exceptions all cancers in the family have been of the gastro- intestinal tract and uterus. Twenty males have shown cancer, all of the gastro-intestinal tract. It is expecting too much of chance distribution that 20 men with gastro-intestinal cancer should be found in one family without a single example of cancer of the lips, tongue, mouth, esophagus, bronchus, or penis. The only example of a squamous-cell carcinoma in this large family was a small lesion of a woman's nose, treated successfully by local eradication. (2) Family History of Cancer Patients: The family histories of large groups of cancer patients should be of value in determining whether effects of intrinsic factors are revealed through heredity. Evidence from this source is somewhat contradictory. Hunter (7) reviewed family histories from the insurance application blanks of those who subsequently died of cancer, in comparison with those of insured persons dying from other conditions. He found that there was no significant difference between the two groups. If anything, those dying of non-cancerous conditions were somewhat more apt to have given cancer as a cause of death of parents or siblings than were those who had died of cancer. Lack of accurate knowledge of causes of death of ancestors, reluctance to admit deaths from cancer, and preponderance of males among the insured, are obvious difficulties in a study conducted in this manner.
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