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Biomedical subjects

W W Chang

Publications and source records attributed to W W Chang.

At least 37 records · Page 2Linked to original sources
PubMed1989

Histogenesis of tubular adenomas in hereditary colonic adenomatous polyposis.

Tubular adenomas were studied morphometrically and histopathologically in colectomy specimens from seven children and five young adults with hereditary colonic adenomatous polyposis. In each age group and in each patient, the diameter and height of adenomas showed a log normal distribution. Both variables differed significantly among patients in each age group and also between the two age groups. In the young adults, there was a selective growth of certain adenomas. Scatter diagrams of the diameter vs height of adenomas showed that adenomas grew preferentially in the horizontal plane in early development, giving adenomas a discoid shape. Adenomas greater than 8 mm in diameter grew both horizontally and vertically. The horizontal growth was due to division of adenomatous crypts, and adenomas greater than 8 mm in diameter also exhibited elongation of crypts.

Adenoma↗
PubMed1986

The mode of growth and compartmentalization of neoplastic glands during experimental colon carcinogenesis.

During the growth of 1,2-dimethylhydrazine (DMH)-induced colon neoplasms in mice from microscopic ones at 9 weeks to macroscopic, invasive ones at 25-26 weeks after the initiation of DMH treatments, the neoplastic glands became increasingly but variably elongated and tortuous, with epithelial evaginations and/or invaginations. For assessment of the mode of growth and genesis of heterogeneity of neoplasms, colon neoplasms induced by two different cumulative doses of DMH were compared at 25-26 weeks after the initial DMH injection. At this time they invaded the colonic wall similarly in depth. However, neoplasms that developed in mice given a higher cumulative dose of DMH had a more homogeneous cell population, a higher proliferative activity, and more apoptotic bodies than those with a lower dose. By 73 hours after multiple tritiated thymidine injections, most neoplastic cells became labeled. There were numerous foci of unlabeled cells seen among, or alternating with, areas of labeled cells. Epithelial evaginations into the glandular lumen consisted of proliferating cells and/or differentiated cells; whereas invaginations into the lamina propria contained only proliferating cells. These findings suggest a compartmentalization of neoplastic glands into multiple neoplastic clonogenic units during growth, from which cellular heterogeneity and architectural complexities of neoplastic glands develop.

1,2-Dimethylhydrazine↗
PubMed1985

Modulation of symmetrical 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis by isoproterenol (IPR).

The modulatory effect of IPR on the initiation and promotion of DMH-induced colon carcinogenesis was investigated using CF-1 young adult female mice. IPR given soon after each of weekly DMH injections inhibited the initiation phase of colon carcinogenesis when the cumulative dose of DMH was small. However, such inhibition was not observed when the cumulative dose of DMH was doubled. Colon neoplasms that developed in spite of IPR treatments seemed to infiltrate the colon wall earlier as compared to those without IPR. On the other hand, IPR did not appear to affect the promotion phase of colon carcinogenesis.

1,2-Dimethylhydrazine↗
PubMed1984

Histogenesis of colon cancer in experimental animals.

Following the introduction of colon-specific carcinogens, the mode of formation and evolution of colon cancer has been investigated in experimental animals. These carcinogens are cytotoxic to epithelial cells in colonic crypts and induce a series of non-specific acute and chronic changes including cryptal hyperplasia when administered repeatedly. During such processes, a number of neoplastically transformed cells may appear in many crypts. Only when they occur at the base of or form an outpocketing pouch in a crypt, do they appear to succeed in repopulating the given crypt to form a dysplastic crypt, from which an early neoplastic lesion develops usually in the upper part of the mucosa. The neoplastic lesion thus formed grows by various mechanisms, depending on its intrinsic properties of unceasing proliferative activity of neoplastic cells and interaction with the microenvironment: (a) by elongation and tortuosity of neoplastic glands, (b) by evagination of the glandular epithelial lining, with the formation of septa to dichotomise the glands to increase the number of neoplastic glands or with formation of incomplete septa or villi to expand the surface area of the neoplasm, and (c) by invagination and outpocketing pouch formation of neoplastic glands when accompanied with the changes in the basement membrane. In doing so, it may progress in various directions to form a polypoid or discoid lesion. Concomitant with growth, the neoplastic cells may undergo a series of cytological alterations and penetrate through their basement membrane in some areas to manifest early malignant behaviour. With downward progression, the neoplasm penetrates the muscularis mucosae and invades the submucosa, muscularis externa and serosa. Such an invasive process is often associated with the rearrangement of fibroblasts, marked changes in the production of collagen and proteoglycans of the extracellular matrix and lysis of the existing structures of the colonic wall. On morphological grounds, colonic carcinogenesis is a multiple process and is associated with successive breakdown of the host defence barriers. From the studies on experimental colonic tumourigenesis, adenomas and adenocarcinomas appear to share a common aetiological factor, or factors, and they are different end-stages in the evolution of neoplastically transformed cells. At any stage of evolution, however, benign neoplasms may develop dysplastic foci within neoplasms and evolve into a malignant form.

Adenocarcinoma↗
PubMed1983

Primary sarcoma of the liver in the adult.

Primary undifferentiated sarcoma of the liver is a rare tumor, being documented primarily in the pediatric age group. This report describes the occurrence of such a tumor in a 55-year-old white woman with Meyenburg's complexes of the liver and the CRST syndrome. The clinicopathologic features of the tumor in the adult are characterized and the literature is reviewed.

Bile Duct Neoplasms↗
PubMed1982

Morphological basis of multistep process in experimental colonic carcinogenesis.

Carcinogenesis has been shown to be a multistep process. However, the morphological basis of the multistep process in colonic carcinogenesis has not been adequately investigated. In the distal colon of adult female CF-1 mice given weekly injections of DMH, we are able to demonstrate that colonic adenocarcinomas develop and evolve in four distinct but continuous steps on morphological grounds. (1) A colonic neoplasm develops in a single crypt. A given crypt is first repopulated by atypical epithelial cells which have either originated at the cryptal base or occurred as an outpocketing pouch in the proliferative zone of the crypt. (2) In the atypical crypt thus repopulated by atypical cells, the epithelial lining becomes invaginated and/or evaginated in the upper half to form an earliest identifiable neoplastic glandular lesion there. (3) The neoplastic lesion thus formed keeps invaginating, evaginating and expanding in various directions by unceasing proliferation of neoplastic cells, giving rise to a polypoid or a discoid lesion. (4) As the neoplasm grows, its leading downward edge would eventually penetrate the muscularis mucosae, and the malignant behavior of the neoplasm becomes apparent with further invasion into the submucosa, muscularis externa and serosa. In the due process, we have also explored the mode of villous formation in some neoplasms and analyzed the possible regulatory mechanisms in the various steps of colonic carcinogenesis.

Animals↗
PubMed1982

Hepatotoxicity associated with ticrynafen--a uricosuric diuretic.

Herein, we describe a patient who had ticrynafen-associated acute hepatitis. This complication has been reported in 57 patients (52 to the manufacturer, four to the Food and Drug Administration, and the current patient) in this country. The mechanism of hepatocellular injury is not known, but from the data to date it seems most likely to result from a hypersensitivity reaction rather than a direct hepatotoxic effect. The histopathological findings are difficult to differentiate from acute viral hepatitis. Removal of this drug from the market resulted from the prompt action of physicians in reporting the complications to the manufacturer and the rapid response of the pharmaceutical firm once the risks became known.

Adult↗
PubMed1981

Effect of estrogen on cell proliferation in colonic mucosa of the mouse.

The effect of estrogen on cell proliferation in the descending colon of the mouse as an example of a non-target organ was investigated. Ovariectomized mice were given single or multiple injections of 10 ng/g body weight of 17 beta-estradiol and were killed 1 h after 3H-thymidine injection. Estrogen treatments decreased incorporation of 3H-thymidine into the DNA of colonic mucosa most markedly at 4 h after the single or the last of multiple injections. The inhibitory effect of estrogen on 3H-thymidine incorporation was greater and lasted longer after a single injection than after multiple ones. A similar inhibitory effect was observed in the colonic mucosa of male mice as well as in the mucosa of mice in which colonic epithelial cell proliferation was enhanced by refeeding after 48 h of fasting. However, the colonic mucosa of mice treated with estrogen implants for up to 4 days was not affected. Estrogen treatments caused no significant change in the DNA, RNA and protein contents of the colonic mucosa. The efficacy of estrogen treatments was verified by an increase in both the wet and dry weights of the uterine horns of ovariectomized mice.

Animals↗
PubMed1981

Degenerative behavior of epithelial cells in the colonic crypt of the mouse following administration of colonic carcinogen, 1,2-dimethylhydrazine.

The degenerative behavior of cells following administration of 1,2-dimethylhydrazine was analyzed in its target organ, the distal colon of the mouse. Within 3-6 h after carcinogen treatment, an increasing number of epithelial cells in the proliferative compartment of the crypt degenerated. Degenerating cells were present most frequently as phagosomes in the neighboring epithelial cells, and infrequently as pyknotic nuclei being extruded from the epithelial lining in the crypt. Epithelial cells prelabeled with [3H]thymidine degenerated first, followed by those not prelabeled, indicating that the carcinogen-induced degeneration of cells occurred after passage of cells through the DNA synthesis phase.

1,2-Dimethylhydrazine↗
PubMed1980

An evolution of malignant mixed müllerian tumor.

In an unusual example of malignant mixed müllerian tumor, a tumor originated in the uterine corpus as an endometrial carcinoma consisting of ordinary endometrial adenocarcinoma, papillary adenocarcinoma, mucinous adenocarcinoma, and squamous cell carcinoma. Following hysterectomy, the tumor recurred at the vaginal vault as poorly differentiated papillary adenocarcinoma. During the second recurrence as a pelvic tumor about 3 years after hysterectomy, the tumor evolved into a malignant mixed müllerian tumor with predominance of sarcomatous element. The latter included undifferentiated sarcoma, endometrial stromal sarcoma, fibromyxosarcoma, leiomyosarcoma and rhabdomyosarcoma. These findings support the contention of Sternberg et al. that a malignant mixed müllerian tumor may exceptionally originate in an endometrial carcinoma.

Adenocarcinoma↗
PubMed1979

Cell population kinetics of 1,2-dimethylhydrazine-induced colonic neoplasms and their adjacent colonic mucosa in the mouse.

The parameters of cell population kinetics of symmetrical 1,2-dimethylhydrazine-induced colonic neoplasms and their adjacent colonic mucosa in the mouse were analyzed using the fraction labeled-mitoses curve method and compared with those of three groups of epithelial cells in the crypt of the descending colon of normal mouse. The analysis of three groups of epithelial cells in the crypt of normal mouse indicates that differentiation of epithelial cells was associated not only with a smaller proliferative pool of cells but also with a shortening of the duration of G2 phase and a prolongation of mitotic time. Other parameters of cell cycle did not change significantly. The mean cell cycle time of neoplastic cells in chemically induced colonic neoplasms was similar to that of epithelial cells in normal colon, but the variance was much greater in neoplastic cells. In neoplastic cells, the proliferative pool was greater, the G1 phase prlonged, and the S phase and the mitotic time became shorter as compared to epithelial cells in normal colon. The duration of G2 phase of neoplastic cells fell between the values of presumptive stem cells and differentiating cells in normal colon, compatible with the hypothesis that neoplastic cells are transformed stem cells defective in cellular differentiation. In the colonic mucosa immediately adjacent to neoplasms, the fraction-labeled-mitoses curve showed a flat second wave, indicating that the group of cells initially labeled by the pulse became a mixture of cells, some continuing the proliferative cycle normally, some going out of cycle, some slowing down in their passage from S through G2 to M, and some being arrested in mitotic phase. Such heterogeneous behavior of cells may be closely related to expansion of neoplasms. With some assumptions, however, cell cycle parameters of those normally cycling cells were estimated: the cell cycle time and the duration of G1 phase and mitotic phase were prolonged as compared to neoplastic cells and epithelial cells of normal colon.

Adenocarcinoma↗
PubMed1979

The effect of estrogen on epithelial cell proliferation and differentiation in the crypts of the descending colon of the mouse: a radioautographic study.

The regulatory role of estrogen on cell population kinetics in the descending colon was studied in intact female and ovariectomized mice. In the colonic crypts from intact mice, the crypt size (the number of epithelial cells per crypt column) and the proliferative activity of epithelial cells fluctuated slightly during the estrous cycle. Peak cellularity per crypt column was exhibted during estrus and early diestrus, whereas peaks in labeling index were seen during estrus and late metestrus. While the population size of mucous cells showed a minimal variation, the number of proliferative vacuolated cells per crypt column varied inversely with that of differentiated columnar cells during estrous cycle. The vacuolated cells were increased in number in the preovulatory phase and the columnar cells in the postovulatory phase. Three weeks after bilateral ovariectomy, the colonic crypt appeared to reach a new steady state, which was characterized by a small crypt size, a decrease in the number of differentiated cells, an increase in the relative number of proliferative cells and a relative increase in the proliferative activity of the crypt as compared to intact mice. When ovariectomized mice were treated with estrogen, the number of 3H-thymidine-labeled cells in the crypt was decreased as compared to untreated ovariectomized mice, the decrease being greater after a single injection than after multiple injections of estrogen, and the vacuolated-columnar cell line being affected more than mucous cell line. Meanwhile, the crypt size as well as the population size of differentiated cells in the crypt failed to return to normal after estrogen treatments. Thus, estrogen did not promote differentiation of epithelial cells in the crypt.

Animals↗