Incidence Of Lymphatic Vessel Invasion Research Articles

Early Barrett's carcinoma: the depth of infiltration of the tumour correlates with the degree of differentiation, the incidence of lymphatic vessel and venous invasion

The incidence of regional lymph node metastasis in early Barrett's carcinoma is determined by the depth of infiltration of the tumour. The present study investigated the possible relationship between the depth of infiltration of the tumour, its degree of differentiation and the incidence of lymphatic vessel and venous invasion in early Barrett's carcinoma. To this end, a total of 805 endoscopically resected specimens obtained from 472 patients with early Barrett's carcinomas were analysed. The results of this analysis revealed that increasing depth of tumour infiltration is associated with an increase in the incidence of poorly differentiated carcinomas--from 0.8% for lesions limited to the mucosa (m1) to 41.4% when the depth of infiltration extended to the lower third of the submucosa (sm3). A similar correlation was also found for the incidence of lymphatic vessel invasion (m1, 0.6%; sm3, 44.8%) and for venous invasion (m1, 0%; sm3, 13.8%). All of these observations proved to be statistically highly significant (p < 0.001). In conclusion, the results show that the degree of differentiation, as well as the incidence of lymphatic vessel and venous invasion, correlates with the depth of infiltration of the early carcinoma in Barrett's oesophagus.

Attenuation by cyclic phosphatidic acid of peritoneal metastasis of azoxymethane-induced intestinal cancers in Wistar rats.

The effect of cyclic phosphatidic acid, a unique analogue of lysophosphatidic acid, on the induction of bombesin-enhanced peritoneal metastases from intestinal adenocarcinomas induced by azoxymethane was investigated in male Wistar rats. Rats were given 10 weekly injections of azoxymethane (7.4 mg/kg body weight, s.c.) and of bombesin (40 microg/kg body weight, s.c.) every other day from the start of the experiment, and from week 16, they received injections of cyclic phosphatidic acid (3 or 6 mg/kg body weight, s.c.) every other day until the end of the experiment in week 45. Cyclic phosphatidic acid at both dosages significantly decreased the incidence of bombesin-enhanced cancer metastases to the peritoneum but had little or no effect on the location, histologic type, depth of involvement or infiltrating growth patterns of the tumors. Cyclic phosphatidic acid at either dose decreased significantly the incidence of lymphatic vessel invasion of adenocarcinomas and the activity of RhoA protein in the tumors, both of which were enhanced by bombesin. Our findings indicate that cyclic phosphatidic acid inhibits cancer metastasis through inhibition of RhoA protein activation.

Induction by bombesin of peritoneal metastasis of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

We investigated the effect of the gastrointestinal regulatory peptide, bombesin, on the development of peritoneal metastasis from gastric cancers induced in rats by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and on Rho activity in the gastric cancers. Rats were allocated to three groups. All groups received MNNG (100 micrograms/ml) solution for 25 weeks from the start of the experiment. Group 1 (controls) received olive oil injections from the start of MNNG treatment; group 2 animals received alternate-day s.c. injections of bombesin (40 micrograms/kg body weight) in olive oil from the start of the experiment until the end of the experiment at week 52; and group 3 received the s.c. bombesin injection on alternate days from week 26 until week 52. The effect of bombesin on Rho activity in gastric cancer was examined by Western blotting. Bombesin given from the start of the experiment (group 2) and after the MNNG treatment (group 3) both significantly increased the incidence of gastric cancer metastasis, compared with controls, at week 52: The incidence of metastasis was significantly higher in group 2 than in group 3. Bombesin from the start of the experiment (group 2) significantly increased the incidence of tumors with deeper invasion or more infiltrative growth pattern, or lymphatic vessel tumor invasion, while bombesin after MNNG treatment (group 3) significantly increased the incidence of lymphatic vessel invasion. Bombesin also increased the activity of Rho protein in the tumors. Bombesin significantly increased the incidence of peritoneal metastasis from gastric cancers through the activation of Rho protein.

Genistein attenuates peritoneal metastasis of azoxymethane-induced intestinal adenocarcinomas in Wistar rats

The effects of the soybean isoflavonoid genistein on the development of bombesin-enhanced peritoneal metastasis from intestinal adenocarcinomas induced by azoxymethane (AOM) were investigated in male inbred Wistar rats. From the beginning of the experiment, rats were given 10 weekly s.c. injections of AOM (7.4 mg/kg body weight) and s.c. injections of bombesin (40 microg/kg body weight) every other day, and from week 16, s.c. injections of genistein (5 or 10 mg/kg body weight) every other day until the end of the experiment in week 45. Bombesin significantly increased the incidence of intestinal tumors and of cancer metastasis to the peritoneum. Although genistein administered at either dose had little or no effect on the enhancement of intestinal carcinogenesis by bombesin or on the location, histologic type, depth of involvement, labeling index, or growth pattern of intestinal cancers, it significantly decreased the incidence of cancer metastasis. Genistein also significantly decreased the incidence of lymphatic vessel invasion of adenocarcinomas, which was enhanced by bombesin. Our findings indicate that genistein attenuates cancer metastasis by inhibiting cancer cell invasion into lymphatic vessels through activities that do not affect the growth of intestinal cancers.

Genistein attenuates peritoneal metastasis of azoxymethane-induced intestinal adenocarcinomas in Wistar rats.

The effects of the soybean isoflavonoid genistein on the development of bombesin-enhanced peritoneal metastasis from intestinal adenocarcinomas induced by azoxymethane (AOM) were investigated in male inbred Wistar rats. From the beginning of the experiment, rats were given 10 weekly s.c. injections of AOM (7.4 mg/kg body weight) and s.c. injections of bombesin (40 microg/kg body weight) every other day, and from week 16, s.c. injections of genistein (5 or 10 mg/kg body weight) every other day until the end of the experiment in week 45. Bombesin significantly increased the incidence of intestinal tumors and of cancer metastasis to the peritoneum. Although genistein administered at either dose had little or no effect on the enhancement of intestinal carcinogenesis by bombesin or on the location, histologic type, depth of involvement, labeling index, or growth pattern of intestinal cancers, it significantly decreased the incidence of cancer metastasis. Genistein also significantly decreased the incidence of lymphatic vessel invasion of adenocarcinomas, which was enhanced by bombesin. Our findings indicate that genistein attenuates cancer metastasis by inhibiting cancer cell invasion into lymphatic vessels through activities that do not affect the growth of intestinal cancers.

Suppression by apigenin of peritoneal metastasis of intestinal adenocarcinomas induced by azoxymethane in Wistar rats.

The effect of a naturally occurring flavonoid apigenin on the development of bombesin-enhanced peritoneal metastasis from intestinal adenocarcinomas induced by azoxymethane was investigated in male Wistar rats. From the start of the experiment, rats were given weekly s.c. injections of azoxymethane (7.4 mg/kg body weight) for 10 weeks and s.c. injection of bombesin (40 microg/kg body weight) every other day, and from week 16, s.c. injections of apigenin (0.75 or 1.5 mg/kg body weight) every other day until the end of the experiment in week 45. Bombesin significantly increased the incidence of intestinal tumors and cancer metastasis to the peritoneum in week 45. It also significantly increased the labeling index of intestinal cancers. Although administration of apigenin at either dose with bombesin had little or no effect on the enhancement of intestinal carcinogenesis by bombesin, the location, histologic type, depth of involvement, infiltrating growth patterns and labeling index, it was found to decrease significantly the incidence of cancer metastasis. Apigenin significantly decreased the incidence of lymphatic vessel invasion of adenocarcinomas, which was enhanced by bombesin. In vitro experiments revealed that apigenin inhibited bombesin-enhanced phosphorylation of mitogen-activated protein kinase (MAPK), but not matrix metalloprotease (MMP)-9 expression. Our findings indicate that apigenin inhibits cancer metastasis through inhibition of phosphorylation of MAPK.

Incidence and prognostic significance of vascular and neural invasion in squamous cell carcinomas of the esophagus

The prognostic influence of blood-vessel invasion (BVI), lymphatic-vessel invasion (LVI) and neural invasion (NI) was evaluated retrospectively in a series of 161 patients with squamous cell carcinoma (SCC) of the esophagus who underwent esophageal resection. Evidence of BVI, LVI and NI was found in 32.9%, 48.5% and 26.1%, respectively. Incidence of BVI, LVI and NI was significantly higher in high pT categories (pT3 and pT4) than in low pT categories (pT1 and pT2) and in patients with distant metastases than in patients without distant metastases. Incidence of LVI and NI in lymph-node-positive patients was significantly higher than in lymph-node-negative patients. The 5-year survival rate was significantly lower in patients with BVI or LVI than in patients without BVI or LVI. Patients with evidence of NI showed no significant differences in 5-year survival from patients without evidence of NI. By stepwise multivariate Cox regression analysis, BVI and LVI were shown to be independent prognostic factors. A search for vascular invasion may therefore provide additional prognostic precision in SCC of the esophagus.

The correlation between tumor size and lymphatic vessel invasion in resected peripheral stage I non-small-cell lung cancer: A potential risk of limited resection

We attempted to clarify whether a correlation exists between tumor size and the incidence of lymphatic vessel invasion in peripheral non-small-cell lung cancer without regional lymph node metastasis. The study included 212 resected non-small-cell lung cancers classified as pathologic stage I disease and located on the periphery of the lung. The incidence of lymphatic vessel invasion was relatively correlated with the maximum diameter of the tumor as follows: 25% (1/4) for tumor size 1.0 cm or less, 40% (19/48) for size 1.1 to 2.0 cm, 49% (28/58) for size 2.1 to 3.0 cm, and 57% (58/102) for tumor size 3.1 cm or more. The incidence of lymphatic vessel invasion of tumors measuring 3 cm or less in greatest dimension was 44% (48/110). The degree of lymphatic vessel invasion of 20 resected tumor samples measuring 3 cm or less in greatest diameter with hilar lymph node metastasis was also examined for comparison. This figure was as high as 85%. These observations suggest that even small peripheral tumors without any regional lymph node metastasis have a relatively high rate of lymphatic vessel invasion and thus pose a potential risk of local recurrence after a limited resection, especially in a wedge resection of the tumor. (J THORAC CARDIOVASC SURG 1994;108:684-6)

ｓｔａｇｅ ＩＩ大腸癌における予後影響因子の検討

Histopathological factors that influence the prognosis of stage II carcinoma of colon and rectum were studied using 50 surgical materials, all cases of which had been appeared to be curably operated.They were divided into two groups. The group A, included worse prognostic 25 cases with local recurrence and/or distant metastasis. The group B included better prognostic 25 cases without any recurrence and/or metastasis for 5 years after surgical treatment. The comparative study between A and B groups was made about degree of main histological differentiation of carcinoma, hisological dedifferentiating features at the edge of invasion of subserosa and serosa, infiltrative mode, depth of invasion and both lymphatic and venous vascular invasion.The results are as followings.As to main histological differentiation, well differentiated adenocarcinoma (well) acco-unted for llcases, moderately differentiated adenocarcinoma (mod) for 11 and mucinous carcino-ma (muc) for 3 in group A. In group B, well accounted for 16, mod for 7 and muc for 2. Group A revealed the dedifferentiated feature at the edge of invasion of subserosa and serosa more clearly in contrast to group B. Concerning infiltrative mode (inf), expansive growth (a) accounted for 8 and expansive and infiltrative growth (β) for 17 in group A. In group B, a accounted for 16 and β for 9.The depth of invasion was ss (a1) in 9 and s (a2) in 16 in group A and ss (a1) in 21 and s (a2) in 4 in group B. The incidence of venous invasion was 96% in group A and 64% of group B. The incidence of lymphatic vessel invasion showed no significant difference between them.The results suggest that degree of main histological differentiation, at the invasive borders, infiltrative mode, depth of invasion and venous invasion are important histopathological factors to predict the prognosis of stage II carcinoma of the colon and rectum.

Clinical significance of ras p21 overexpression for patients with an advanced colorectal cancer

The expression of ras oncogene product p21 was examined in 45 paraffin-embedded sections of primary advanced colorectal cancers, using the anti-v-H-ras p21 monoclonal antibody Y13-259. Fourteen of these specimens (31 percent) were stained positively. The incidence of lymphatic vessel invasion of cancer cells and lymph node metastasis correlated statistically with the overexpression of ras p21. The depth of invasion and incidence of liver metastasis in the p21-positive group were more prominent than in the p21-negative group. Statistically significant differences were evident in operative curability and clinical stage at initial surgery and in the long-term survival rate between these groups (P less than 0.05). We propose that ras p21 overexpression may serve as a marker to predict the prognosis of colorectal cancer.

Lymphatic vessel invasion is an independent prognostic factor for survival in colorectal cancer

To assess whether lymphatic vessel invasion (LVI) is an independent prognostic factor in colorectal cancer, we retrospectively reviewed the records of 462 patients who underwent potentially curative surgery for carcinoma of the colon and rectosigmoid/rectum (rs/rectum) at the New England Deaconess Hospital from 1965–1978. Sixty-one patients were identified as having tumors with lymphatic vessel invasion (LVI+), and they were compared with the remaining group of 401 patients who had tumors without lymphatic vessel invasion (LVI-). The incidence of lymphatic vessel invasion was significantly increased in tumors with blood vessel invasion (24% vs. 5%, p = 0.000001). Patients with LVI+ tumors also had a significantly increased incidence of positive nodes (59% vs. 25%, p = 0.0004), the average number of positive nodes (4.8 vs. 2.2, p = 0.0003), and a lower 5-year survival rate (colon: 57% vs. 84%, p = 0.0001; rs/rectum: 38% vs. 71%, p = 0.004). There was a significant ( p ≤ 0.05) increase in local (16% vs. 7%), abdominal (33% vs. 9%), and distant (13% vs. 4%) failure as a component of failure in patients with LVI+ colon cancer and a significant increase in abdominal (33% vs. 11%) and distant (13% vs. 8%) failure as a component of failure in patients with LVI+ rectosigmoid/rectal cancer. Proportional hazards analysis demonstrated that lymphatic vessel invasion was an independent prognostic factor for survival.