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Results for “prostate adenocarcinoma”

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At least 19 recordsLinked to original sources

PubMedDate not supplied

Tumor-specific immunity in patients with prostatic adenocarcinoma or benign prostatic hyperplasia.

Twenty patients were skin tested with solubilized components of autologous prostatic adenocarcinoma or benign prostatic hypertrophy (BPH). Four of ten patients bearing adenocarcinoma of the prostate exhibited tumor-specific cutaneous responsiveness to solubilized autologous tumor-specific antigens (TSA). One responding patient also responded to solubilized allogeneic TSA. A single patient bearing prostatic carcinoma responded only to solubilized components of allogeneic BPH. Nine of ten patients with BPH exhibited no response to solubilized components of autologous BPH. The patient responding to the extract of autologous BPH, however, also had clinical stage B adenocarcinoma of the prostate. These observations suggest host responsiveness to TSA of prostatic carcinoma. Possible clinical significance and mechanisms to explain the findings are discussed.

Adenocarcinoma↗

PubMedDate not supplied

Characterization of the Dunning R3327H prostatic adenocarcinoma: an appropriate animal model for prostatic cancer.

The Dunning R3327H rat prostatic adenocarcinoma appears to be an appropriate animal model for studying prostatic cancer. This report contains a detailed characterization of this tumor at the morphologic, biochemical, and therapeutic levels. Electron micrographic, histologic, and histochemical studies clearly establish the adenocarcinoma nature of this tumor. The histology of the R3327H tumor is similar to well-differentiated human prostatic cancer. The biochemical and enzymatic profile of the tumor indicates its origin from the rat dorsolateral prostate. The cell kinetics and growth rates of this tumor following a variety of hormonal manipulations (castration, estrogens, androgens, and antiandrogens) have established that 70%-90% of the cells in this tumor require androgens for their growth. However, 10%-30% of the cells are capable of growth in the absence of androgens. Both cell types are present in the initial tumor inoculum and these different cell types possess similar growth rates. The predominance of the androgen-sensitive cells accounts for the relatively greater size of the tumor achieved in the intact male animal at a given growth time. After the tumor is well established in an intact animal, subsequent estrogen therapy or castration resulted in a marked diminution in tumro volume. This was followed by a subsequent relapse. In addition, estramustine phosphate was also shown to cause shrinkage in the tumor volume.

Adenocarcinoma↗

PubMed1979

Patterns of spontaneous metastasis manifested by three rat prostate adenocarcinomas.

Three transplantable rat prostate adenocarcinoma cell lines were assessed for patterns of metastasis, ie, routes of dissemination and larger organ(s) selected for implantation. Two lines (I and III) were disseminated only through ipsilateral lymphatic channels to the lungs. The third cell line (II) was disseminated through lymphatic and blood channels to lungs, liver, and kidneys. The pattern of spontaneous metastasis is a characteristic of the tumor cell; but there is evidence that the rate and extent of metastasis can be modified experimentally.

Adenocarcinoma↗

PubMed1977

Investigations on prostatic adenocarcinomas in rats.

Metastatic prostate adenocarcinomas, derived from aging germfree Wistar rats, have been propagated in rats and in tissue culture. A protocol has been developed and demonstrated for assay of treatments which retard or which accelerate the rate and extent of tumor growth and of metastasis in tumor-bearing rats. The pattern of spread has been retarded by cyclophosphamide, aspirin, indomethacin, and Corynebacterium parvum. The spread pattern has been accelerated by oral administrations of sodium barbiturate.

Adenocarcinoma↗

PubMed1979

The Nb rat: prostatic adenocarcinoma model.

The Noble rat prostatic adenocarcinoma is an animal model which is used to study human prostatic carcinoma. It mimics the human condition in histology, in biochemistry with the production of acid phosphatase, and in tumor growth which is relatively constant. Additionally, it is hormonally dependent and metastasizes. This animal model should provide an avenue for the evaluation of cytotoxic chemotherapeutic agents heretofore receiving little attention from the urologic community.

Adenocarcinoma↗

PubMed1978

Extended total excision of prostatic adenocarcinoma.

Cases of locally advanced prostatic adenocarcinoma (stages B and C) managed by exenteration or prostatocystectomy were reviewed. Local control and survival rates seem to justify this approach in selected cases, especially when conservative measures, such as hormonal therapy and irradiation, have been exhausted.

Adenocarcinoma↗

PubMed1975

Transplantable metastasizing prostate adenocarcinomas in rats.

Three spontaneous prostate adenocarcinomas from aged, randombred, germfree Lobund Wistar rats were transplanted, without change, through several series of conventional Lobund Wistar rats. One tumor type differed histologically from the other two tumor types. Rats with subcutaneously transplanted tumors developed metastatic tumors in the lymph nodes and lungs. No microbial agent was detected in the tumor cells.

Adenocarcinoma↗

PubMed1975

Double primary prostatic adenocarcinoma.

Two cases of double primary prostatic adenocarcinoma are described. A periurethral papillary adenocarcinoma coexisted with the common acinar type of cancer, which tends to arise deep in the corpus of the gland. We are of the opinion that the patterns observed in these tumors are not mere variations of one neoplasm, but rather two dissimilar growths of diverse cell origin, varried histology, and possibly also of disparate biologic potential.

Adenocarcinoma, Papillary↗

PubMed1979

The impact of current staging procedures in assessing disease extent of prostatic adenocarcinoma.

We studied 454 patients with prostatic adenocarcinoma who were assigned a preliminary clinical stage on the basis of serum acid phosphatase, routine bone survey and physical examination. Subsequently, they were assigned a final clinical stage after radioisotopic bone scanning, lymphangiography and staging pelvic lymph node dissection. Only 53, 54, 57 and 26 per cent, respectively, of patients initially assigned the preliminary clinical stage of IB, II, III or IVA remained at that stage after the additional studies.

Adenocarcinoma↗

PubMed1977

In vitro propagation of prostate adenocarcinoma cells from rats.

Two rat adenocarcinomas were physically dispersed and propagated in vitro. Epithelial and fibroblast cell lines were cloned from them and the monolayer cell lines derived therof were further characterized. The cells produced acid phosphatase in early in vitro cell passages, and later they turned negative. Fibroblast-like cells produced no tumors when implanted in syngeneic Lobund Wistar rats, but as few as 10 epithelial cells produced metastasizing adenocarcinomas in them. A third prostate tumor has yielded a line of epithelial cells which reproduced the original tumor type in inoculated rats, but the cells have not yet been characterized. Rat prostate adenocarcinomas provided a useful model system for in vitro and in vivo studies on prostate cancer and on metatasis.

Acid Phosphatase↗

PubMed1979

Immunobiology and therapeutic manipulation of heterotransplanted Nb rat prostatic adenocarcinoma. Chemotherapy of autonomous tumor, 102 Pr, heterotransplanted into congenitally athymic (nude) mice and syngeneic Nb rats.

Nb rat prostatic adenocarcinomas, previously induced by the administration of testosterone and estrogen, have been serially studied as heterotransplants into congenitally athymic (nude) mice and into groups of Nb rats. This animal system has been used to evaluate the chemotherapeutic efficacy of 5-fluorouracil and Ftorafur. The use of both species was to determine if there would be any significant difference in relative tumor growth in nude mice which lack functional T cells as opposed to intact Nb rats. The autonomous tumor, 102 Pr, is the subject of the thesis presented herein. One donor Nb rat bearing 102 Pr prostatic adenocarcinoma served as the donor for this experiment. The nude mice and Nb rats received the transplant on the same date and were subjected to the chemotherapies outlined above and were treated after there was sufficient increase in tumor volume from the 2 mm3 wedge to assure growth and neovascularity (greater than 60 mm3). Statistically significant data was presented revealing 5-fluorouracil to be efficacious in the treatment of these tumors. Also presented is data revealing differences in growth versus time in the respective recipient animal hosts. It is suggested herein that this combination animal model system could be used for screening potential cytotoxic chemotherapeutic agents.

Adenocarcinoma↗

PubMed2026

Methyltransferase 3 promotes v-set and transmembrane domain-containing 2-like protein expression to intensify ferroptosis-mediated prostate adenocarcinoma progression through the m6A methylation modification.

BACKGROUND: Prostate adenocarcinoma (PRAD) is a common malignancy with high incidence in men. The role of v-set and transmembrane domain-containing 2-like protein (VSTM2L) in PRAD remains largely unreported. METHODS: Gene expression was analyzed using The Cancer Genome Atlas (TCGA), the Tumor Immune Estimation Resource (TIMER) 2.0, and the University of Alabama at Birmingham CANcer data analysis Portal (UALCAN) databases, and validated by quantitative real-time PCR (qRT-PCR) and western blot. Cell proliferation was assessed by 5-ethynyl-2'-deoxyuridine (EdU) staining. Apoptosis and mitochondrial membrane potential were examined by flow cytometry. Intracellular iron, Fe2+, and reactive oxygen species (ROS) levels were measured using commercial kits and flow cytometry. The role of VSTM2L in tumor growth was evaluated using xenograft mouse models, with protein expression in tumors evaluated by immunohistochemistry (IHC). The N6-methyladenosine (m6A) modification sites on VSTM2L mRNA were predicted using the sequence-based RNA adenosine methylation site predictor (SRAMP) website. The interaction between methyltransferase 3 (METTL3) and VSTM2L was confirmed by methylated RNA immunoprecipitation (MeRIP) and dual-luciferase reporter assay. Correlation analysis was performed using the TCGA database. RESULTS: VSTM2L was overexpressed in PRAD tissues and cell lines. Silencing VSTM2L inhibited PRAD cell proliferation, promoted apoptosis, and enhanced ferroptosis and oxidative stress in vitro. Consistently, VSTM2L knockdown suppressed tumor growth in vivo. Mechanically, METTL3 mediated m6A methylation to stabilize VSTM2L mRNA. Furthermore, METTL3 promoted proliferation and inhibited apoptosis, ferroptosis, and oxidative stress in PRAD cells via a VSTM2L-dependent manner. CONCLUSION: METTL3 promotes PRAD progression by stabilizing VSTM2L expression through m6A methylation, thereby inhibiting ferroptosis. This study establishes a direct link between RNA methylation and ferroptosis in PRAD, revealing the METTL3/VSTM2L axis as a novel regulatory pathway and a potential therapeutic target.

Male↗

PubMed1978

Steroid hormone receptor characterization of several histologic variants of a rat prostatic adenocarcinoma.

Several histologic variants of the transplantable R-3327 prostatic adenocarcinoma carried in male Copenhagen rats have been characterized and the histologic types have been correlated with steroid hormone receptor content. One type is clearly an adenocarcinoma; this tumor is hormonally responsive and contains substantial amounts of both androgen and estrogen receptors. In contrast, another histologic type, a fibrosarcoma, is hormonally nonresponsive and does not contain either receptor. A third histologic variant is classified as a carcinosarcoma and contains histological elements of both adenocarcinoma and fibrosarcoma and is also hormonally responsive. This tumor contains lower receptor levels than the adenocarcinomas but more than the fibrosarcomas. The androgen receptor appears to be identical in the different histologic forms of the tumor: the sedimentation coefficient is 7.8S and the dissociatiln constant for methyltrienolone is 4 x 10(-9) M. Similarly, the estrogen receptor from the different histologic forms of the tumor has a sedimentation coefficient of 8.3S and the dissociation constant for estradiol is 7 x 10(-10) M. These findings clearly distinguish the cytosol binding macromolecules from plasma binding proteins, and classify them as steroid hormone receptors. Further, rat serum was devoid of androgen and estrogen binding in the 8S region. Normal prostate tissue from Copenhagen rats contained low levels of an androgen receptor, but no estrogen receptor. It is possible that during growth and/or passage of the R-3327 tumor, the hormonally responsive adenocarcinoma cells do not survive and there is a gradual emergence of the nonresponsive fibrosarcoma. If, as we suspect, the receptors are found in the epithelial cells and not the stromal cells, there clearly should be considerable variation of receptor content in the different intermediary histologic forms of the tumor.

Adenocarcinoma↗

PubMed1979

Therapeutic manipulation of Nb rat prostatic adenocarcinomas: chemotherapeutic evaluation of autonomous tumors.

Nb rat autonomous prostatic adenocarcinomas were transplanted into several groups of synergeneic Nb rats. Chemotherapy using 5-fluorouracil, methotrexate, Adriamycin, and cyclophosphamide was evaluated. Significance was seen with the use of these agents with varying doses. Cyclophosphamide and 5-fluorouracil treated animals had complete tumor regression whereas Adriamycin and methotrexate treated animals had cessation of tumor volume increase in some groups after chemotherapy; however, neither agent causes complete tumor regression.

Adenocarcinoma↗

PubMed1977

An animal model for the study of prostatic adenocarcinoma.

After the injection of the potent carcinogen 9,10-dimethyl-1,2-benzanthracene (DMBA) male rats (Fisher/Furth), mice (Strong A/J), and Golden hamsters, which had been previously conditioned by castration and in which the prostate had become histologically atrophic, developed tumors consistent with prostatic adenocarcinoma. One month after castration, intravenous injections of DMBA were given in the vena cava or jugular vein once a month for 3 months. Three to four months later, histologic evidence of prostate adenocarcinoma was consistently found in each of the groups of castrated animals (11 rats, 22 mice, and 11 hamsters) which survived the experiment. The glands were enlarged grossly and ureteral obstructions were also noted. Metastasis to the lung also occurred in five mice, three rats, and one hamster.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1977

Development of an epithelial tissue culture line from human prostatic adenocarcinoma.

The development of a tissue culture line of human prostatic adenocarcinoma is described. The culture (HPC-36), derived from tumor tissue explants, is a pure epithelial culture with characteristics of neoplastic cells, including a large nuclear size relative to the amount of cytoplasm, multiple nucleoli within the nucleus, many mitotic figures, the formation of multinucleated giant cells and the loss of contact inhibition. The cells also stained positively for acid phosphatase and have been grown in monolayer and suspension cultures. The HPC-36 cells presently are being studied to determine whether they are true descendants of the cancer cells.

Acid Phosphatase↗

PubMed1978

HPC-36: an epithelial tissue culture line derived from human prostate adenocarcinoma.

The development of a tissue culture line of human prostate adenocarcinoma has been described. The culture (HPC-36), derived from tumor tissue explants, is purely epithelial, with characteristics of neoplastic cells. These include a large nuclear size relative to the amount of cytoplasm, multiple nucleoli within the nucleus, many mitotic figures, the formation of multinucleated giant cells, and loss of contact inhibition. The cells also stained positively for acid phosphatase and have been grown in monolayer and suspension cultures. The HPC-36 cells are presently being studied to determine whether they are true descendants of the cancer cells.

Acid Phosphatase↗

PubMed1975

Ectopic ACTH production in disseminated prostatic adenocarcinoma.

The second fully documented case of ACTH-producing prostatic adenocarcinoma with elevated plasma and tissue levels of ACTH is presented. The distinguishing characteristics of ACTH-producing extrapituitary neoplasms and the various modes of therapy are discussed.

17-Hydroxycorticosteroids↗