Hakim A A
Department of Medicine, Stritch School of Medicine, Evanston, Illinois.
J Surg Oncol. 1989 Jan;40(1):21-31. doi: 10.1002/jso.2930400107.
The main objective of this study was to differentiate between lymph nodes infiltrated by estrogen receptor-positive (ER+) and estrogen receptor-negative (ER-) breast carcinoma. Lymph nodes were obtained from 40 postmenopausal cancer patients, 10 from each disease stage. Six patients from each group had estrogen receptor-positive (BCaER+) and four estrogen receptor-negative (BCaER-) tumors. Both tumor-containing (T) and uninvolved (N) lymph nodes from the same patient were examined by the following parameters: magnitude of lymph node nucleic acid hybridization with cDNA probes from breast cancer MCF-7ER+ and MCF-7ER- cells; and binding capacity of 3H-estradiol, 125I-EGF, and 125I-PDGF binding and protein kinase C activities of the lymph nodes. Concomitant with the appearance of transformed cells, several events occur: Tumor cells induce stimulation of mononuclear cells and macrophages and evoke T- and B-cell proliferation, leading to the synthesis of tumor cell membrane-associated antibodies. In estrogen receptor-positive (ER+) breast carcinoma, estrogens and host hormonal modulatory mechanisms stimulate production and release of epithelial growth (EGF) and platelet-derived growth factors (PDGF). These factors are characterized by protein kinase C activities. There is infiltration of tumor cells into the lymph node and infiltration of leukocytes into the tumor site. In the lymph node, tumor progression depends on tumor cell proliferation rate and metastatic aggressiveness. The experiments described in this study document the changes that occur in lymph nodes, with differences between nodes infiltrated with BCaER+ and BCaER- breast carcinomas. Hybridization of 32P-cDNA from MCF-7ER+ cells with cellular RNA from BCaER+ involved (T) lymph nodes is greater than with cellular RNA from uninvolved (N) lymph nodes. The magnitude of hybridization correlated (P less than 0.005) with the disease stage.
本研究的主要目的是区分雌激素受体阳性（ER+）和雌激素受体阴性（ER-）乳腺癌浸润的淋巴结。从40名绝经后癌症患者获取淋巴结，每个疾病阶段10名。每组6名患者患有雌激素受体阳性（BCaER+）肿瘤，4名患有雌激素受体阴性（BCaER-）肿瘤。对同一患者的含肿瘤（T）和未受累（N）淋巴结进行以下参数检测：淋巴结与来自乳腺癌MCF-7ER+和MCF-7ER-细胞的cDNA探针的核酸杂交程度；以及3H-雌二醇、125I-表皮生长因子（EGF）和125I-血小板衍生生长因子（PDGF）的结合能力，还有淋巴结的蛋白激酶C活性。伴随转化细胞的出现，会发生若干事件：肿瘤细胞诱导单核细胞和巨噬细胞的刺激，并引发T细胞和B细胞增殖，导致肿瘤细胞膜相关抗体的合成。在雌激素受体阳性（ER+）乳腺癌中，雌激素和宿主激素调节机制刺激上皮生长因子（EGF）和血小板衍生生长因子（PDGF）的产生和释放。这些因子具有蛋白激酶C活性。有肿瘤细胞浸润到淋巴结以及白细胞浸润到肿瘤部位。在淋巴结中，肿瘤进展取决于肿瘤细胞增殖率和转移侵袭性。本研究中描述的实验记录了淋巴结中发生的变化，BCaER+和BCaER-乳腺癌浸润的淋巴结之间存在差异。来自MCF-7ER+细胞的32P-cDNA与BCaER+受累（T）淋巴结的细胞RNA的杂交程度大于与未受累（N）淋巴结的细胞RNA的杂交程度。杂交程度与疾病阶段相关（P<0.005）。
