Produced Tumor Growth Research Articles

Response of a Pregnancy-Dependent Mouse Mammary Tumor to Hormones<xref ref-type="fn" rid="fn2">2</xref>

A transplantable, pregnancy-dependent, mouse mammary tumor line (TPDMT-4) showed a pregnancy-dependent growth in DDD breeders. The tumors grew during pregnancy, regressed rapidly after parturition, and reached ascending peaks in subsequent pregnancies. Growth without regression occurred in animals with pituitary isografts (PI), but not after the hosts were ovariectomized. The effects of ovariectomy was negated by sc injections of both 17beta-estradiol (E) and progesterone (P), but single injections of E or P did not abolish the effect of the ovariectomy. The tumors also grew in virgins given sc implants of E and P or deoxycorticosterone acetate (DCA) pellets. Adrenalectomy had no influence on the tumor growth in PI-bearing animals, but DCA injections stimulated secretion production by both tumor cells and normal mammary cells. The hormonal conditions that produced tumor growth caused in the host mammary glands the full lobulo-alveolar development seen in mid- to late-pregnant animals. In the hosts without tumor growth, the mammary glands had small clusters of acini at most. The tumors were classified as type A morphologically. Our results suggest that the growth of TPDMT-4, like that of normal mammary glands, is controlled by prolactin, E, and P.

Urine Extractives in Cancer

The study of the experimental production of malignant tumors by tar has led in recent years to the isolation and synthesis of numerous aromatic polycyclic compounds, for the most part hydrocarbons, whose specific ability to produce tumor growth has earned them the designation “carcinogens” (1). The structure of some of them bears a formal relationship to the sterids or cyclopentenophenanthrene derivatives, and potent carcinogens, such as methylcholanthrene, have been derived experimentally from bile acids. This structural resemblance of several potent carcinogenic hydrocarbons to cyclopentenophenanthrene, which forms the cyclic portion of cholesterol, bile acids, and steroid hormones, has given rise in recent years to speculations which center in the following ideas: ( a ) the cell proliferation which characterizes the estrous state is in some respects reminiscent of the early stages of malignant growth; ( b ) the series cholesterol—bile acids—progesterone—adrenal cortex hormones—male sex hormones constitutes the stages of oxidative degradation of the sterol molecule, leading to numerous physiologically important substances. After complete degradation of the side chain the same trend for dehydrogenation is manifested, yielding aromatic rings in estrin and equilenin. It is argued that this hypothetical trend may exceed the bounds of physiological usefulness and that exaggerated dehydrogenation may lead to the formation of such powerful aromatic carcinogens as methylcholanthrene, which may play a part in the etiology of spontaneous tumors. These assumptions are further made plausible by observations of definite estrogenic action of some carcinogens and noticeable carcinogenic action of sex hormones, at least in large amounts under special conditions. On the other hand, Reichstein (2) has proposed the hypothesis that the first step in the synthesis of steroid compounds may be a condensation of three-carbon sugars. He considers the various active and inactive steroid substances with high oxygen content, isolated from adrenal cortex, as possible intermediates, and the more reduced sterids he regards as secondary products of bio-reduction. This assumption makes a genetic connection between sterids and carcinogens appear improbable.

Action of Enzymes on Causative Agent of the Chicken Sarcoma

SummaryI. The causative agent of the Kous chicken sarcoma in the tumor fragments or in the cell-free tumor filtrate was inactivated by trypsin and pepsin, but was unaffected by the lipase, urease, or amylase preparations which were used as regards its capacity to produce tumor growth. 2. The causative agent was not destroyed if the proteolytic energy of trypsin and pepsin was abolished by heat inactivation. 3. Specificity of the proteolytic enzymes upon the causative agent of the chicken sarcoma suggests that the active agent is a protein or associated in sowe way with protein material.