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Metastasis to the parotid region is rare, and originates primarily from head and neck squamous cell carcinoma and melanoma of the skin. Renal clear cell adenocarcinoma has considerable metastatic potential and the parotid gland is one possible destination. Histopathologic study is important to differentiate this entity from primary clear cell parotid neoplasm.
A 57-year-old man was admitted to the hospital because of multiple subcutaneous masses with pain, mild dyspnea, and bloody sputum. He had been asymptomatic until one month earlier, when he began to have a dry cough and myalgia of the right forearm. A chest radiograph showed cardiomegaly. Whole-body computed tomographic scan, cytologic examination of the sputum, and histological examination of a subcutaneous nodule on the scalp resulted in the diagnosis of lung cancer with multiple organ metastases, including those to skeletal muscle and myocardium. Despite chemotherapy, he died suddenly on the 45th hospital day. Autopsy revealed that about half of the myocardium had been replaced by metastatic tumors, so we speculated that he died from heart failure due to cardiac muscle metastasis.
The influence of local irradiation on the development of metastases and primary tumor volume was studied in Lewis lung carcinoma growing intramuscularly in the hind leg of C57BL/6 mice. The time course of development of metastases was determined from the size of the lung colonies at autopsy by determining the growth rate of the colonies. Irradiation within five days after tumor cell injection inhibited the incidence of metastases in accordance with irradiation dose. For irradiation more than seven days after the injection, promotion of metastases was observed around the time of the experiment as a function of irradiation dose and tumor volume. After the irradiation phase, the development of metastases was inhibited in accordance with radiation dose. When delay in metastasis was defined as additional days needed to develop two or ten colonies compared with controls, the relationship between delay and dose was linear. At the regrowth phase of the primary tumor, the incidence of metastases from the irradiated tumor was reduced in comparison with that from unirradiated tumors of the same size. Inhibition of metastases was observed only at 5 Gy and showed slight dose-dependency. Mechanisms in the development of metastases as they related to these findings are also discussed.
Spontaneous regression of metastases from cancer of kidney is an exceptional event, original but non-specific to this neoplasm. Observed principally in secondary pulmonary localizations this phenomenon occurs most frequently after nephrectomy. A personal case is presented of regression of pulmonary images considered as being metastatic after irradiation of a pelvic metastasis from renal adenocarcinoma, and a literature review carried out. The various pathogenic hypotheses are discussed and the place of nephrectomy for metastatic renal cancer (Robson's stage IV) debated.
The proteolytic activities of human tumor cell lines deriving from bronchial squamous cell carcinoma, a lung metastasis of an embryonal rhabdomyosarcoma and a pleural mesothelioma were measured by use of chromogenic substrates. N-acetyl-alanine aminopeptidase activity, plasminogen activator activity, H-D-Ile-Pro-Arg-p-NA splitting activity as well as plasmin-like activity, cathepsin G-like activity and plasma-kallikrein-like activity were found in cell lysates. The enzymatic activity of N-acetyl-alanine aminopeptidase, plasminogen activator and H-D-Ile-Pro-Arg-p-NA splitting activity changed during culturing. Plasminogen activator and H-D-Ile-Pro-Arg-p-NA splitting activity decreased to very low values, whereas N-acetyl-alanine aminopeptidase activity leveled at 1 x 10(-5) mU/cell. Unlike other proteolytic activities, plasminogen activator was released into the medium. Plasminogen activator activity could be measured in culture medium which contained no fetal calf serum.
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Once metastatic cells successfully seed at distant sites, their clinical detection and danger to the host are dependent on growth to form gross metastases. Metastatic tumor cells proliferate in response to local paracrine growth factors and inhibitors, and their growth also depends on production and responses to autocrine growth factors. A major organ-derived (paracrine) growth factor from lung tissue-conditioned medium has been isolated that differentially stimulates the growth of cells metastatic to brain or lung. Characterization of this mitogen demonstrated that it is a transferrin or a transferrin-like glycoprotein. Furthermore, antibodies to transferrin can remove significant growth activity from lung tissue-conditioned medium. Cells that are metastatic to brain or lung express greater numbers of transferrin receptors on their surfaces than cells that are poorly metastatic or metastatic to liver. Growth responses of metastatic cells and organ preferences of colonization appear to change during progression to more malignant states. At early stages of metastatic progression there is a tendency for many common malignancies to metastasize and grow preferentially at particular sites, suggesting that paracrine growth mechanisms may dominate the growth signals at this stage of progression. In contrast, at later stages of metastatic progression widespread dissemination to various tissues and organs occurs, and autocrine growth mechanisms may dominate the growth responses of metastatic cells. Ultimately, the progression of malignant cells to completely autonomous (acrine) states can occur, and at this stage of metastatic progression cell growth may be completely independent of autocrine and paracrine growth factors or inhibitors.
BACKGROUND: There is a greater controversy regarding the indication of radiotherapy of the pelvic lymphatics in patients with suspected lymph node metastases in locally advanced prostate cancer (T2b-4 N0) on the one hand and in patients with pathologically proven lymph node metastases in locoregional advanced prostate cancer (Tx pN+) on the other hand following definitive radiotherapy and radical prostatectomy. This paper investigates the possible indications for radiotherapy of the pelvic lymphatics in the light of data from the literature. PATIENTS AND METHODS: Because data from several retrospective studies concerning radiotherapy of the pelvic lymphatics indicated a better outcome, the RTOG conducted 2 prospective randomised studies (RTOG 75-06, 77-06) to address these questions. However, the results of these studies showed no better survival or cause specific survival for patients treated for the paraaortal or pelvic lymphatics and therefore, radiotherapy of the pelvic lymphatics was no more advocated. A reanalysis showed several problems of the study design and it was concluded that the studies couldn't prove the question of elective radiotherapy of the pelvic lymphatics. In RTOG 77-06 patients with T1b/T2 tumors were investigated. Therefore, there is no prospective study investigating the elective radiotherapy in patients with T3-tumors, who are at high risk of pelvic lymph node metastases. RESULTS: Today there is no indication for treating the paraaortal lymphatics in patients with locoregional advanced prostate cancer. Many radiotherapists perform the elective radiotherapy of pelvic lymphatics when the risk of metastases is above 15 to 20% because retrospective data indicate a better outcome. On the other hand, many others don't treat them because RTOG 75-06 and 77-06 didn't demonstrate a better outcome. Laparoscopic lymphadenectomy with low morbidity seems to be helpful as in pN0 patients radiotherapy is not necessary. Where performing laparoscopic pelvine lymphadenectomy is impossible the probability of the frequency of lymph node metastases can be estimated using the clinical tumor stage, the Gleason-score and the pretherapeutic PSA. In case of proven metastases (pN+) some retrospective data indicate that patients with micrometastasis could profit from aggressive treatment. In case of proven metastases and extirpation by lymphadenectomy it seems that patients with hormonal therapy and radiotherapy have a longer tumor-free interval. However, there are no data from randomized trials. CONCLUSIONS: Every radiotherapist has to make his own decision for radiotherapy of the pelvic lymphatics as there is no standard treatment. Two randomised studies are open and recruiting patients. These are one study of the ARO, investigating patients with histologically proven lymph node metastases and one study of the RTOG (RTOG 9413), investigating patients with an estimated risk of lymph node metastases > 15%. In case of radiotherapy of the pelvic lymphatics a dose of 45 Gy for suspected metastases and 50.4 Gy for proven metastases is recommended.
Angiogenic factors including endothelin-1 (ET-1) play a key role in the progression of breast metastases to bone. We investigated the impact of ET-1 on the development of bone metastases in an immunocompetent murine skin-fold chamber model. Murine mammary carcinoma 4T1 was injected in a skin-fold chamber implanted on CB6 mice along with bone explants. Furthermore, mice were treated with or without a dual selective antagonist of both ET-1 receptors. The progression of the vascularization within the chamber was monitored over time by intravital microscopy (IVM). The tumor growth and the development of bone metastases were assessed by cytokeratin-19 gene expression and histological studies. Results indicate that this new model associated with IVM allows for the continuous monitoring of the change in vascularization associated with the development of bone metastases. Additionally, treatment with an antagonist of both ET-1 receptors was associated with the presence of significantly less vessels near the tumor mass compared to control mice. These changes were correlated with smaller tumor masses and reduced bone invasion (P < 0.05). Thus, in an immunocompetent murine model of breast carcinoma metastases to bone, our data support the hypothesis that vascularization plays a role in tumor development and progression and that ET-1 specifically modulates the angiogenesis associated with breast metastases to the bone.
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B16-F10 is a B16 mouse melanoma subline that preferentially metastasizes to the lung following intravenous injection. Previously we isolated TI-241 (LRF-1 homologue related to Jun-Fos) gene that was expressed higher in the high metastatic clone B16-F10 than the low metastatic clone F1. Transfection of TI-241 into F1 converted it into a high-metastatic cell. We studied the effect of antisense oligonucleotide designed to reduce the expression of TI-241 in B16-F10 cells, and observed an unexpected increase in the TI-241 level. The increase in the expression was maximal at 30 h, then it decreased during further culture with or without TI-241 antisense oligonucleotide. This increased TI-241 expression by antisense oligonucleotide was also observed in B16-F1 cells whereas sense oligonucleotide did not affect the expression. B16-F10 cells cultured with TI-241 antisense oligonucleotide showed enhanced experimental metastatic potential to the mouse lungs compared with untreated B16-F10 and B16-F10 cultured with TI-241 sense oligonucleotide.
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