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Biomedical subjects

W M Collins

Publications and source records attributed to W M Collins.

At least 37 records · Page 2Linked to original sources
PubMed1981

Host age and major histocompatibility genotype influence on Rous sarcoma regression in chickens.

The influence of host age and B (major histocompatibility complex) genotype on the fate of Rous sarcoma virus (RSV)-induced tumors was investigated. White Leghorn lines 61 and 151, developed at the Regional Poultry Research Laboratory (RPRL) at East Lansing, MI, and their crosses (F3 to F5) segregating for the B genotype were used. Preliminary experiments with noninbred White Leghorns showed that chickens RSV-inoculated at 4 weeks of age had a significantly lower incidence of tumor regression than chickens RSV-inoculated at 6, 8, 10, 12, and 14 weeks of age. The (61 X 151) F5B2/B2 and B5/B5 chickens inoculated at 6 weeks of age had a lower incidence of tumor regression than (61 X 151)F3 and F4, B2/B2 and B5/B5 chickens RSV-inoculated between 58 and 88 weeks of age, respectively. Some (61 X 151) B2/B2 chickens inoculated between 58 and 88 weeks of age regressed their tumors while all chickens of corresponding genotype inoculated at 6 weeks of age died with tumors. the (61 X 151) B2/B2 chickens had a higher incidence of tumor regression than B5/B5 chickens regardless of age. The genetic RSV-inoculation on the fate of RSV-induced tumors.

Age Factors↗
PubMed1980

Rous sarcoma regression in seven highly inbred lines of White Leghorns.

Response to Rous sarcoma virus (RSV)-induced tumors was studied in Regional Poultry Research Laboratory (RPRL) lines 61, 63, 72, 100, 151, and 15I5 and in Reaseheath line C, all highly inbred White Leghorn stocks. Virus inoculations were made in chickens at 6 weeks of age. Tumors were scored subjectively for size on a regular basis and in some instances a tumor profile index (TPI) was assigned which characterized tumor development over a 10 week period for each chicken (TPI 1 = complete regression in 28 days; TPI 5 = terminal tumor). The frequency of tumor regression, terminal tumors, and metastases and mean TPI was examined. The incidence of tumor regression ranged from 92% in line 61 to 0 % in lines 151 and 15I5. The frequency of terminal tumors varied from 100% in line 151 to 2% in line61, while metastasis in chickens with terminal tumors differed from 92% in line 15I5 to 0% in line 61. Mean TPI ranged from 2.0 in line 61 to 4.6 in line 15I5 and 4.7 in line C. The erythrocyte alloantigen genotype at the B blood group locus, (part of the B complex, MHC) and 11 additional blood group loci were known for each of the lines. The data indicate that genetic differences in tumor regression may be pronounced between inbred lines which share similar, if not identical, B locus erythrocyte alloantigens and that other unknown genes are also involved.

Animals↗
PubMed1979

Genetic nature of regression of Rous sarcoma virus-induced tumors in crosses of Regional Poultry Research Laboratory lines 6 and 7(2).

Regional Poultry Research Laboratory (RPRL) inbred lines 6(1), 6(3), and 7(2) and F1, F2, and reciprocal backcross progenies of these lines were used to investigate host-gene effects upon the regression of Rous sarcoma virus (RSV)-induced tumors. Lines 6(1) and 6(3) were susceptible to subgroup A and C lymphoid leukosis (LL) viruses and line 7(2) was resistant to subgroup A but was segregating for susceptibility to subgroup C LL virus. Viruses of RSV subgroups A and C were used. Lines 6(1), 6(3), and 7(2) were homozygous for shared blood group alleles B2, C5, L1 and r. The incidence of tumor regression was higher in line 6(3) than in 7(2), and in reciprocal F1 crosses of these lines was of the same order of magnitude as in line 6(3). Progeny from F1 generation parents mated to line 6(3) had a higher frequency of regression than offspring from F1 generation parents mated to line 7(2). The frequency of regression in F2 generation offspring was intermediate between the two backcrosses. The data suggest that either a locus (or loci) other than L and B has a role in Rous tumor regression in this species or the immune response region of the B blood group-major histocompatibility complex differs in the two lines even though the serological and/or graft vs. host regions have not been shown to differ.

Animals↗
PubMed1978

Differentiation of progressive versus regressive Rous virus-induced avian sarcomas according to tumor and infiltrating lymphocyte fine structure.

Electron microscope examination of progressing and regressing Rous virus-induced sarcomas in an inbred line of White Leghorns revealed that regressing tumors contained moderate to marked lymphocyte infiltration, frequent contact between lymphocytes and tumor cells, and extensive areas of necrosis. Lymphocytes infiltrating regressing tumors exhibited a polar accumulation of organelles at the point of contact between lymphocyte and target cell. On the other hand, progressing tumors contained low to moderate numbers of lymphocytes, infrequent lymphocyte-tumor cell interaction and less evidence of tumor cell degeneration. Lymphocytes from progressing tumors lacked the polar organization of organelles. This experimental system is offered as a means of studying the role of lymphocytes in tumor regression.

Animals↗
PubMed1978

Lymphocytotoxicity of chickens bearing Rous sarcomas.

A 51Cr uptake microcytotoxicity assay was used to determine the cytotoxicity of lymphocytes from chickens bearing Rous sarcomas. Differences in lymphocyte cytotoxicity among individual chickens were statistically significant. Lymphocytes from chickens regressing (or having regressed) their tumors were significantly more cytotoxic than lymphocytes from hosts with progressing tumors. Lymphocytes from chickens with progressing tumors tended to enhance tumor cell growth in vitro.

Animals↗
PubMed1975

Effect of regression of Rous sarcoma tumors upon egg production in an inbred line of White Leghorns.

Reserach was conducted to determine whether development and subsequent regression of a Rous sarcoma virus (RSV) induced wing-web tumor influenced egg production. Fifty-seven six-week old pullet chicks of inbred line 6 of the United States Department of Agriculture, Regional Poultry Research Laboratory, East Lansing, Michigan, were inoculated subcutaneously in the left wing-web with 0.1 ml. of a 10-minus 3 dilution of a pseudotype of Bryan high titer RSV designated BH-RSV (RAV-1). Thirty chicks were left uninoculated. Each chick was examined for tumor growth at regular intervals to 10 weeks post-inoculation. A tumor was considered regressed if it disappeared completely. Ninteen regressor and 22 uninoculated females were placed in laying cages at 4.5 months of age and egg production data obtained over seven 28-day periods. The difference in hen-day egg production between regressors and uninoculated controls favored regressors by 2.7 eggs/bird and was statistically significant. Physiological stimulus from cellular immunity, linkage and pleiotropy are discussed as possible caused of the higher egg production in regressors.

Animals↗
PubMed1975

Genetic differences in susceptibility to ulcerative enteritis in Japanese quail.

Six lines of Japanese quail were derived from a single foundation population. Four of the lines were selected on the basis of family mean three week body weight, two were unselected and all lines were randomly mated. Quail were housed in wire batteries during the brooding, rearing and laying periods. During the brooding period, hover temperature and floor space per chick were similar from line to line. For the rearing and laying periods, floor space per chick was approximately the same from line to line. During an outbreak of ulcerative enteritis (diagnosed on the basis of gross and histopathology) in generation 31 and again in generation 34, mortality ranged from zero for males of one control line to approximately 50 percent for females of one selected line. Analysis of variance showed that incidence of mortality differed significantly among lines and between sexes. Mortality was generally higher in selected than in control lines and in females than in males. It is suggested that susceptibility to ulcerative enteritis in quail may be a polygenically inherited trait and that the breeding which accompanied selection for body size may have made some loci homozygous for susceptibility alleles.

Animals↗