Volume 71 - 2008 - Fasc.4 - Case series
Surgery and intracavitary chemotherapy for Peritoneal Carcinomatosis from Colorectal Origin
A subset of patients with colorectal cancer (CRC) develops synchronous or metachronous isolated peritoneal disease. The development of peritoneal carcinomatosis (PC) can be conceptual- ized as a series of well defined steps including cell shedding, adhe- sion to mesothelial cells and underlying matrix, and invasion of submesothelial tissue. Surgical cytoreduction combined with hyperthermic intraperitoneal chemoperfusion (HIPEC) has evolved as the standard of care in patients with mucinous appen- diceal tumors including the pseudomyxoma peritonei syndrome. Recently, this approach was extended to patients with peritoneal carcinomatosis (PC) from non appendiceal CRC. In this review, we discuss the biological rationale, clinical methods, and oncological outcomes associated with cytoreduction and intracavitary chemotherapy in CRC patients suffering from peritoneal disease spread. (Acta gastroenterol. belg., 2008, 71, 000-000).
The role of oral fluoropyrimidines in the treatment of advanced gastric cancer
Although the incidence of gastric cancer is declining during the second half of the 20th century, it remains the second leading cause of cancer death worldwide.
The majority of patients with gastric cancer will require pallia- tive treatment at some point in the course of their disease. Approximately 50% of patients already have advanced incurable disease at the time of initial presentation, and even those who undergo potentially curative resection have high rates of distant as well as local recurrence.
Chemotherapy in advanced gastric cancer demonstrated a sig- nificant survival benefit over best supportive care alone. Median overall survival increased from 3-5 to 8-12 months.
Today, a platinum based regimen is considered as first-line treatment in advanced gastric cancer. Different regimens are investigated and used in routine practice.
Similarly to fluorouracil, capecitabine is well tolerated in combi- nation with a range of cytotoxic drugs. As a single agent, it has not undergone large scale randomised studies. S-1, another oral fluo- ropyrimidine, is a potential challenger to the role of capecitabine, but is lacking phase III data in Western population. (Acta gastro- enterol. belg., 2008, 71, 361-366).
Dysplasia and colorectal cancer in inflammatory bowel disease : a result of inflammation or an intrinsic risk ?
Patients with inflammatory bowel disease (IBD) face an increased lifetime risk of developing colorectal cancer (CRC). Although CRC in IBD only accounts for 1-2% of all cases of CRC in the general population, it is responsible for approximately 15% of the mortality of patients with Crohn's disease (CD) and ulcera- tive colitis (UC). Independent factors associated with increased risk include long disease duration, extensive colonic involvement, young age at onset of IBD, severity of inflammation, primary sclerosing cholangitis, backwash ileitis and a family history of CRC. Many of these factors emphasise the role of inflammation as an underlying mechanism. Despite the differences between the molecular abnormalities found in colitis-associated dysplasia in comparison with sporadic CRC, IBD-associated cancer has a similar dysplasia-cancer sequence, similar frequencies of major chromosomal abnormalities, microsatellite instability and similar glycosylation changes. These similarities seem to outweigh the differences and make it reasonable to suggest that not only IBD- associated CRC but even sporadic colon cancer might be largely secondary to inflammation. Oxidative stress, apoptosis, COX-2 activity and a possible common inherited defective glycosylation are thought to play a key role in the pathogenesis of colitis-associ- ated CRC. DNA alterations initiated in colonic crypts can expand to adjacent crypts through crypt fission.
There seems little doubt that the increased risk of cancer in inflammatory bowel diseases is a result of the disease rather than an inherited phenomenon. An understanding of the definition and pathogenesis of CRC in IBD is crucial to optimise patient manage- ment. Further investigation is therefore necessary. (Acta gastro- enterol. belg., 2008, 71, 367-372).
The role of oral fluoropyrimidines in the treatment of advanced gastric cancer
Although the incidence of gastric cancer is declining during the second half of the 20th century, it remains the second leading cause of cancer death worldwide.
The majority of patients with gastric cancer will require pallia- tive treatment at some point in the course of their disease. Approximately 50% of patients already have advanced incurable disease at the time of initial presentation, and even those who undergo potentially curative resection have high rates of distant as well as local recurrence.
Chemotherapy in advanced gastric cancer demonstrated a sig- nificant survival benefit over best supportive care alone. Median overall survival increased from 3-5 to 8-12 months.
Today, a platinum based regimen is considered as first-line treat- ment in advanced gastric cancer. Different regimens are investigat- ed and used in routine practice.
Similarly to fluorouracil, capecitabine is well tolerated in combi- nation with a range of cytotoxic drugs. As a single agent, it has not undergone large scale randomised studies. S-1, another oral fluo- ropyrimidine, is a potential challenger to the role of capecitabine, but is lacking phase III data in Western population. (Acta gastro- enterol. belg., 2008, 71, 000-000).
Dysplasia and colorectal cancer in inflammatory bowel disease : a result of inflammation or an intrinsic risk ?
Patients with inflammatory bowel disease (IBD) face an increased lifetime risk of developing colorectal cancer (CRC). Although CRC in IBD only accounts for 1-2% of all cases of CRC in the general population, it is responsible for approximately 15% of the mortality of patients with Crohn's disease (CD) and ulcera- tive colitis (UC). Independent factors associated with increased risk include long disease duration, extensive colonic involvement, young age at onset of IBD, severity of inflammation, primary scle- rosing cholangitis, backwash ileitis and a family history of CRC. Many of these factors emphasise the role of inflammation as an underlying mechanism. Despite the differences between the molecular abnormalities found in colitis-associated dysplasia in comparison with sporadic CRC, IBD-associated cancer has a similar dysplasia-cancer sequence, similar frequencies of major chromosomal abnormalities, microsatellite instability and similar glycosylation changes. These similarities seem to outweigh the differences and make it reasonable to suggest that not only IBD- associated CRC but even sporadic colon cancer might be largely secondary to inflammation. Oxidative stress, apoptosis, COX-2 activity and a possible common inherited defective glycosylation are thought to play a key role in the pathogenesis of colitis-associ- ated CRC. DNA alterations initiated in colonic crypts can expand to adjacent crypts through crypt fission.
There seems little doubt that the increased risk of cancer in inflammatory bowel diseases is a result of the disease rather than an inherited phenomenon. An understanding of the definition and pathogenesis of CRC in IBD is crucial to optimise patient manage- ment. Further investigation is therefore necessary. (Acta gastro- enterol. belg., 2008, 71, 000-000).
Surgery and intracavitary chemotherapy for peritoneal carcinomatosis from colorectal origin
A subset of patients with colorectal cancer (CRC) develops synchronous or metachronous isolated peritoneal disease. The development of peritoneal carcinomatosis (PC) can be concep- tualized as a series of well defined steps including cell shedding, adhesion to mesothelial cells and underlying matrix, and invasion of submesothelial tissue. Surgical cytoreduction combined with hyperthermic intraperitoneal chemoperfusion (HIPEC) has evolved as the standard of care in patients with mucinous appen- diceal tumors including the pseudomyxoma peritonei syndrome. Recently, this approach was extended to patients with peritoneal carcinomatosis (PC) from non appendiceal CRC. In this review, we discuss the biological rationale, clinical methods, and oncological outcomes associated with cytoreduction and intracavitary chemotherapy in CRC patients suffering from peritoneal disease spread. (Acta gastroenterol. belg., 2008, 71, 373-378).
