Armin C. Braun

A non-auxinic growth-promoting factor present in crown gall tumor tissue.

Summary A biologically active factor is present in crown gall tumor tissue extracts which when used in association with an auxin is capable of encouraging the very active proliferation of normal tobacco pith tissue. Neither the factor present in the tumor extract nor the auxin is by itself effective in stimulating the active division of the pith cells.

The Plant Tumor Problem

Publisher Summary This chapter focuses on the plant tumor problem. The tumor problem is a cellular problem and, at that level, no real fundamental differences exist between members of the two kingdoms. In comparing plant and animal tumors, it must be remembered that there are certain developmental and functional differences commonly used in the differentiation of animal cancers that are more or less restricted to animals and cannot be carried over and applied to plants. The first of the nonself-limiting neoplastic diseases of plants is known as Blacks wound tumor disease. The second nonself-limiting tumorous disease of plants, known as the Kostoff genetic tumors, is one in which the genetic constitution of the host and, more particularly, all of the cells comprising the host play a primary role. The third nonself-limiting tumor disease is the crown-gall disease. Tumor formation takes place in essentially two distinct phases. In the first phase, normal cells are altered to tumor cells which do not, as yet, develop into a neoplastic growth. The second phase, according to this concept, is concerned with the continued abnormal and autonomous proliferation of the tumor cells once the cellular alteration has been accomplished. The rapid and consistent response of susceptible plant cells to transformation by a tumor-inducing principle in the crown-gall disease makes possible a very accurate seriation of events that occur during tumor inception. Studies dealing specifically with the biochemistry of the inception phase of tumor formation in the crown-gall disease are very limited in number and of recent origin. The abnormal histological and cytological picture observed in the plant tumor cells can be accounted for in terms of the abnormal growth hormone physiology, which is characteristic of the tumor tissue. Findings indicate that the crown-gall tumor cell contains both genetic and nongenetic factors that are present in a normal cell.

The Cell Cycle and Tumorigenesis in Plants

The experimental oncologist is interested in persistently dividing cells and in discovering the reason why tumor cells divide continuously in their hosts while the growth of all normal cells is precisely regulated. The development by tumor cells of a capacity for essentially unrestrained or autonomous growth is the essential feature that characterizes the tumorous state for without it there would be no tumors. It is therefore clear that an understanding of those substances and mechanisms that regulate normal cell growth and division is important if insight is to be gained into how those regulatory mechanisms are affected when a cell is transformed to the neoplastic state. Other clinically important characteristics, such as, for example, the ability of certain tumor cells to invade and metastasize, may be acquired, sometimes relatively late, and can therefore be dismissed in a search for the earliest events that lead to the establishment and maintenance of the tumorous state.

The Multipotential Cell and the Tumor Problem

One of the most firmly held beliefs in the field of oncology is that once a cell has been converted into a true tumor cell the resulting heritable change is of a permanent and irreversible type. This concept of irreversibility has for about a century now so completely dominated the thinking of cancer biologists that until quite recently few attempts were made to determine whether it might, in fact, be possible to cause a true tumor cell to revert to a benign or normal state under appropriate experimental conditions. There are now a number of well documented examples ranging from tumors of higher plant species to those of man in which a reversal of the neoplastic state has been achieved experimentally. Several examples of this type will be described and the possible significance of these findings as they relate to the nature of the heritable change will be discussed.

Genetic and biochemical studies on the suppression of and a recovery from the tumorous state in higher plants.

SummaryFour neoplastic diseases of plants: crown gall, which is caused by Ti plasmid DNA; Blacks wound tumor disease by an RNA virus; the Kostoff genetic tumors by chromosomal imbalance; and habituation, which results from a spontaneous activation of select biosynthetic systems, have been analyzed and compared. It has been found that both the development of a capacity for autonomous growth and the nature of the heritable cellular change that underlies tumorigenesis are similar in the four instances. All develop a capacity for autonomous growth as a result of the persistent activation of select biosynthetic systems, the products of which are concerned with cell growth and division. That the persistent activation of these biosynthetic systems does not involve heritable changes of an irreversible type is indicated by the finding that a reversal of the neoplastic state occurred in three of the test systems. Since the tumor cells in these instances were found to remain totipotent the results suggest that whether the normal or tumor phenotype is expressed is determined by how the genetic information is regulated in a cell. Regulation appears to be accomplished in part through positive feedback control mechanisms. Foreign genetic information could act either in a regulatory manner to persistently activate normal biosynthetic systems or it could code for one or more essential but normally limiting substance(s) and thus replace a substance(s) that in the case of the Kostoff tumors or habituation is specified by host cell genes, or it could do both. In either case, the foreign genetic information can be regulated in much the same manner as are the host cell genes to give rise to either the normal or tumor phenotype.