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Janet F Y Lee

Publications and source records attributed to Janet F Y Lee.

14 recordsLinked to original sources
PubMed2007

Critical appraisal on the role and outcome of emergency colectomy for uncomplicated right-sided colonic diverticulitis.

BACKGROUND: Emergency colectomy is well accepted for treating complicated right-sided colonic diverticulitis. However, the role of colectomy for uncomplicated diverticulitis is not well defined. The aim of this study was to evaluate the short-term and long-term surgical outcome of uncomplicated right-sided diverticulitis in our locality. PATIENTS AND METHODS: Retrospective chart review of patients operated for right-sided diverticulitis over a 20-year period was conducted. Recurrent attacks of right-sided diverticulitis, re-operation rate and re-hospitalisation rate were the long-term parameters of interest. An updated telephone interview was carried out for all surviving patients. RESULTS: Seventy-four patients (35 males and 39 females), median age 35.5 (range 16-70) years, were operated for uncomplicated diverticulitis. Thirty patients underwent colectomy, whereas the others underwent appendectomy with diverticulectomy (n = 8) or appendectomy alone (n = 36). All short-term parameters were less favourable for the colectomy group, including higher complication rate, slower return of gastrointestinal function, higher requirement of parenteral analgesic and longer hospital stay. Without colectomy, only 2 patients developed recurrent diverticulitis necessitating hospitalisation, both of whom resolved on conservative treatment. On the other hand, 1 patient required re-operation after colectomy because of intestinal obstruction. The overall re-hospitalisation rate was comparable between the colectomy and the non-colectomy group (16.7% vs. 13.6%). CONCLUSIONS: Emergency colectomy can eradicate suspicious lesions and eliminate risk of recurrent diverticulitis but at the expense of higher morbidity rates. As the natural course of uncomplicated right-sided colonic diverticulitis is usually benign, conservative treatment with minimal surgery may be a better therapeutic option.

Adolescent↗
PubMed2006

Emergency laparoscopically assisted right hemicolectomy for obstructing right-sided colon carcinoma.

BACKGROUND: We report our preliminary experience in urgent laparoscopically assisted right hemicolectomy for obstructing right-sided colon carcinoma. MATERIALS AND METHODS: From January to April 2005, seven consecutive patients with obstructing right-sided colon carcinoma underwent emergency laparoscopically assisted right or extended right hemicolectomy. Patient demographic data, operative details, and short-term clinical outcomes were prospectively collected and analyzed. RESULTS: The median duration of obstructing symptoms prior to admission was 3 days (range, 1-6 days). Two patients underwent palliative resection and five patients underwent curative resection. The median operative time was 180 minutes (range, 125-350 minutes). There were no conversions to the open procedure. Median blood loss was 30 mL (range, negligible-300 mL). The median times to resuming diet, first bowel motion, and full ambulation were 4 days (range, 3-10 days), 5 days (range, 3-7 days), and 4 days (range, 4-5 days), respectively. The median duration of hospital stay was 7 days (range, 6-19 days). One patient with ischemic heart disease developed acute coronary syndrome postoperatively and died on postoperative day 19. The remaining patients had no complications. The median tumor length was 3.5 cm (range, 2-5 cm) and the median number of lymph nodes removed was 17 (range, 16-36). CONCLUSION: Emergency laparoscopically assisted right hemicolectomy for obstructing right-sided colon carcinoma is feasible and safe, with favorable short-term clinical outcomes and an acceptable number of lymph nodes removed.

Adenocarcinoma↗
PubMed2006

Simultaneous laparoscopic resection of rectal cancer and liver metastasis.

Simultaneous resection of colorectal tumor and liver metastasis has been advocated because of the benefits of avoiding a second operation, reduced morbidity, shorter treatment time, and similar outcomes. We report a case of simultaneous laparoscopic resection. The operative time was 350 minutes and the estimated blood loss was 500 mL. The patient required parenteral analgesia for less than 48 hours. Flatus was passed on postoperative day 3, and a solid diet was resumed on postoperative day 5. He was fully mobile on postoperative day 4 and was discharged 3 days later. With the advance of laparoscopic technology and technique, simultaneous resection becomes an attractive option.

Colorectal Neoplasms↗
PubMed2004

Promoter hypermethylation of tumor-related genes in the progression of colorectal neoplasia.

Gene promoter hypermethylation is increasingly recognized to play an important role in cancer development through silencing of gene transcription. This study determined the methylation profiles of primary colorectal cancers and adenomas to elucidate the role of epigenetic changes in different stages of colorectal carcinogenesis. We examined the methylation profiles of 47 sporadic colorectal cancers, 36 colonic adenomas from patients without cancer and 34 colonic biopsies from patients without colonic lesions. Paired adjacent dysplasia tissues obtained from 17 cancer patients were also examined. Promoter hypermethylation in 10 tumor-related genes (APC, ATM, GSTP1, HLTF, MGMT, hMLH1, p14, p15, SOCS-1 and TIMP-3) were studied by methylation-specific PCR. Promoter hypermethylation was frequently detected in more than 40% of colonic cancers and adenomas in APC, ATM, HLTF, MGMT and hMLH1 genes (p < 0.0001 vs. normal). While low level of methylation was detected in p14, p15 and TIMP-3, there was no methylation detected in GSTP1 and SOCS-1. The frequencies of methylation were comparable between tumors and adenomas, and advanced and nonadvanced adenoma. In contrast, K-ras mutation was only detected in advanced adenomas and cancers. Concurrent methylation in >/= 3 genes was found in 66.7% adenomas and 68.1% cancers but not in normal colonic tissues. Methylation was associated with reduced protein expressions in colorectal adenomas and cancers. Moreover, methylation in ATM was more common in older cancer patients (p = 0.002), but there was no significant association between promoter hypermethylation and other clinicopathologic characteristics of cancer. Our study demonstrated the early and specific involvement of promoter hypermethylation in the colorectal adenoma-carcinoma sequence.

Adenoma↗
PubMed2004

Laparoscopic resection of rectosigmoid carcinoma: prospective randomised trial.

BACKGROUND: Although laparoscopic resection of colorectal carcinoma improves post-operative recovery, long-term survival and disease control are the determining factors for its application. We aimed to test the null hypothesis that there was no difference in survival after laparoscopic and open resection for rectosigmoid cancer. METHODS: From Sept 21, 1993, to Oct 21, 2002, 403 patients with rectosigmoid carcinoma were randomised to receive either laparoscopic assisted (n=203) or conventional open (n=200) resection of the tumour. Survival and disease-free interval were the main endpoints. Patients were last followed-up in March, 2003. Perioperative data were recorded and direct cost of operation estimated. Data were analysed by intention to treat. FINDINGS: The demographic data of the two groups were similar. After curative resection, the probabilities of survival at 5 years of the laparoscopic and open resection groups were 76.1% (SE 3.7%) and 72.9% (4.0%) respectively. The probabilities of being disease free at 5 years were 75.3% (3.7%) and 78.3% (3.7%), respectively. The operative time of the laparoscopic group was significantly longer, whereas postoperative recovery was significantly better than for the open resection group, but these benefits were at the expense of higher direct cost. The distal margin, the number of lymph nodes found in the resected specimen, overall morbidity and operative mortality did not differ between groups. INTERPRETATION: Laparoscopic resection of rectosigmoid carcinoma does not jeopardise survival and disease control of patients. The justification for adoption of laparoscopic technique would depend on the perceived value of its effectiveness in improving short-term post-operative outcomes.

Aged↗
PubMed2003

15-hydroxy-eicosatetraenoic acid arrests growth of colorectal cancer cells via a peroxisome proliferator-activated receptor gamma-dependent pathway.

Peroxisome proliferator-activated receptor gamma (PPARgamma) inhibits cell growth via promoting apoptosis. Human colorectal cancer tissues had abundant PPARgamma but the incidence of apoptosis was very low, suggesting a defect in the PPARgamma pathway. Here, we found that 15-hydroxy-eicosatetraenoic acid (15S-HETE), an endogenous ligand for PPARgamma, was significantly decreased in the serum of patients with colorectal cancer. Treatment of colon cancer cells with 15S-HETE inhibited cell proliferation and induced apoptosis, which was preceded by an increase in TGF-beta-inducible early gene (TIEG) and a decrease in Bcl-2. The action of 15S-HETE could be blocked when PPARgamma was suppressed. Overexpression of Bcl-2 prevented the apoptosis. The levels of TIEG and 15-lipoxygenase (15-LOX), the enzyme responsible for 15S-HETE production, was decreased in colorectal cancer. Therefore, colorectal cancer is associated with decreased 15S-HETE. Treatment of colon cancer cells with 15S-HETE inhibits cell proliferation and induces apoptosis in a PPARgamma-dependent pathway involving augmentation of TIEG and reduction of Bcl-2 expression.

Apoptosis↗
PubMed2003

Induction of colon cancer cell death by 7-hydroxystaurosporine (UCN-01) is associated with increased p38 MAPK and decreased Bcl-xL.

UCN-01, a selective inhibitor of protein kinase C, is known to inhibit the growth of cancer cells. Although it is currently undergoing clinical evaluation, information about its effect on human colon cancer is limited and the mechanism responsible is lacking. The objective of this study was to examine the cytotoxicity of UCN-01 to human colon cancer cells in vitro and its effect on the apoptotic molecules. HT-29, a radiation- and chemotherapy-resistant human colon cancer cell, was used in the study. Cell death/apoptosis was determined by the MTT assay and DNA fragmentation measurement. NF-kappaB activity was measured by an enzyme immunoassay method. Western blot was employed to examine the expression of relevant apoptotic molecules. The result showed that UCN-01 could induce apoptosis of human colon cancer cells in a time- and dose-dependent manner. It markedly reduced the expression of Bcl-xL, but enhanced the level of p38 MAPK. In addition to Bcl-xL and p38 MAPK, UCN-01 also increased both caspase-3 and peroxisome proliferator activated receptor gamma protein levels. HT-29 cells transfected with exogenous Bcl-xL showed a significant increase in NF-kappaB activity and prevented apoptosis induced by UCN-01. The overexpression of Bcl-xL also reversed other relevant molecular changes observed in UCN-01-treated cells. In conclusion, UCN-01 exerted an antitumor effect in human colon cancer cells by inducing apoptosis. The mechanism responsible appeared to be related to reduction of Bcl-xL and increased p38 MAPK. The overexpression of Bcl-xL can significantly prevent apoptosis induced by UCN-01.

Apoptosis↗
PubMed2002

Activation of Kupffer cells inhibits tumor growth in a murine model system.

Kupffer cells, a liver organ-specific macrophage, play an important role in preventing the development of malignant tumors. The mechanism responsible for their tumoricidal activities is not completely known. In our study, we established in vivo models involving a rat malignant cell line, rat Kupffer cells and tumor implantation in nude mice. A series of relevant in vitro experiments were also carried out to determine possible pathways. LPS-activated Kupffer cells produced significant amounts of NO, TNFalpha and IFNgamma. Malignant cells treated with either Kupffer cells or culture supernatant of the activated Kupffer cells had an increase in caspase-8 activity. Implanted tumors originated from malignant cells treated with either Kupffer cells or culture supernatant of the activated Kupffer cells grew much smaller than those from malignant cells without treatment or treated with control supernatants. The alteration of anti-apoptotic Bcl-2 was inversely associated with the change of pro-apoptotic caspase-8 and their levels in the tumor tissues matched the size of the tumors and treatments they received. It appeared that the above changes resulted in an increase in cellular DNA damage and apoptosis seen in malignant cells. Therefore, Kupffer cells execute their anti-tumor effect via increasing the production of NO, TNFalpha and IFNgamma and these cytotoxic molecules inhibit the growth of tumor by damaging cellular DNA and inducing apoptosis that was featured by downregulation of Bcl-2 but upregulation of caspase-8.

Animals↗
PubMed2002

Apoptosis induced by activation of peroxisome-proliferator activated receptor-gamma is associated with Bcl-2 and NF-kappaB in human colon cancer.

Peroxisome-proliferator activated receptor-gamma (PPARgamma) has been demonstrated to exert an inhibitory effect on cell growth in most cell types studied, but its role in colon cancer is still uncertain. The molecular mechanism between the activation of PPARgamma and its consequence is unknown. In the present report, we show that the expression of PPARgamma was significantly increased in tumor tissues from human colon cancer compared with non-tumor tissues and that PPARgamma ligands, 15-Deoxy-delta(12,14)prostaglandin J2 or ciglitizone, induced apoptosis in HT-29 cells, a human colon cancer cell line. The occurrence of apoptosis induced by PPARgamma ligands was sequentially accompanied by reduced levels of NF-kappaB and Bcl-2. Over-expression of Bcl-2 significantly protected the cells from apoptosis. This study suggested that a PPARgamma-Bcl-2 feedback loop may function to control the life-death continuum in colonic cells and that a deficiency in generation of PPARgamma ligands may precede the development of human colon cancer.

Apoptosis↗
PubMed2002

Increased apoptosis in infiltrating mononuclear cells of colorectal cancer: a mechanism for tumor escape.

CONTEXT: Disturbance in apoptosis has been proposed as one of the mechanisms involved in the immune response targeting tumor outgrowth. How colorectal cancer cells escape from attack by the immune system is not yet fully understood. OBJECTIVE: To investigate apoptotic molecules associated with colorectal cancer counterattack. DESIGN AND SETTING: Tissue samples of colon from 12 patients with colorectal cancer were collected and analyzed by immunostaining. In addition to tumorous tissues, corresponding nontumorous specimens of colon were obtained as controls. MAIN OUTCOME MEASURES: We examined the expression of Bcl-2, Bcl-xl, Bax, caspase-3, and inducible nitric oxide synthase in infiltrating mononuclear cells of colorectal cancer tissues and also in colorectal cancer tissues. The TUNEL assay was used to detect in situ apoptosis. RESULTS: Apoptosis was barely detectable in specimens of colorectal cancer, which was consistent with an increase in Bcl-2 level and a decrease in caspase-3 level. In contrast, infiltrating mononuclear cells of tumorous tissues showed a marked increase in apoptosis compared with those of nontumorous tissues. The increased apoptosis might have resulted from an imbalance of antiapoptotic and proapoptotic molecules, as reflected by reduction of Bcl-2 level and elevation of Bax level. The elevated caspase-3 levels found in this study could be a downstream effector of the Bcl-2 and Bax apoptotic pathways. A significant increase in inducible nitric oxide synthase observed in the infiltrating mononuclear cells might contribute to immunosuppression seen in colorectal cancer. CONCLUSION: It is tempting to speculate that aberrant expression of apoptotic molecules and inducible nitric oxide synthase in infiltrating mononuclear cells provides the underlying mechanism through which colorectal cancer cells escape attack by the immune system and subsequently grow without control.

Apoptosis↗
PubMedDate not supplied

MRC CLASICC trial.

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Colectomy↗