SUPPLEMENT
Management of Colorectal Carcinoma in Children
and Young Adults
John Goldberg, MD* and Wayne L. Furman, MDw
Summary: Colorectal Carcinoma (CRC) is rare in patients less than
20 years of age. Although presenting symptoms are similar to
adults, this diagnosis is rarely considered in the initial differential
diagnosis of young patients. We will review what is published about
the incidence, epidemiology, and clinical presentation of CRC in
children, adolescents and young adults. Because of its rarity in this
age group, few pediatric oncologists will have experience with
CRC, and clinical trials will rarely be available. The treatment of
CRC in adults is evolving rapidly and consultation with medical
oncologists experience in treating adults with CRC is essential to
develop the best treatment plan for a young patient diagnosed with
CRC.
Key Words: colorectal carcinoma, children, young adults, manage-
ment guidelines
(J Pediatr Hematol Oncol 2012;34:S76–S79)
OVERVIEW
Although colorectal carcinoma (CRC) is the third
most common cancer in adults,1 it is exceptionally rare in
children, adolescents, and young adults, with an incidence
of only about 1 per million persons below 20 years of age
(Fig. 1).2 Because of the extreme rarity of the tumor in this
age group, it may be difficult to develop a treatment plan
when CRC is diagnosed. Pediatric case series, which are
limited by relatively small numbers of patients and by re-
ferral bias, cannot serve as the basis of definitive treatment
recommendations.3,4 Here we will briefly review what is
known about the incidence, epidemiology, and clinical
presentation of CRC in children, adolescents, and young
adults and summarize the clinical options described in the
peer-reviewed literature to provide a basis for management
decisions by pediatric oncologists.
INTRODUCTION
In 2010, approximately 142,000 patients in the United
States were diagnosed with CRC and approximately 51,000
died of CRC.1 However, fewer than 100 cases are diagnosed
each year in children, adolescents, and young adults (Fig. 1).4
CRC accounts for 2.1% of malignancies in the 15- to 29-
Received for publication January 24, 2012; accepted February 1, 2012.
From the *University of Miami Miller School of Medicine, Miami, FL;
and wDepartment of Oncology, St Jude Children’s Research Hos-
pital, Memphis, TN.
Supported by grants CA23099 and by the American Lebanese Syrian
Associated Charities (ALSAC).
The authors declare no conflict of interest.
Reprints: Wayne L. Furman, MD, Department of Oncology, St Jude
Children’s Research Hospital, 262 Danny Thomas Place, Memphis,
TN 38105 (e-mail: wayne.furman@stjude.org).
Copyright r 2012 by Lippincott Williams & Wilkins
S76 | www.jpho-online.com J Pediatr Hematol Oncol
year-old age group5 and has been reported in children as
young as 9 months.2
In adults, CRC is more common in developed coun-
tries. Although the cause of this disparity is not well un-
derstood, dietary differences have been suggested as a major
factor. Other factors reported to be associated with an in-
creased incidence of CRC in adults include obesity,6 a high-
calorie diet, high consumption and/or overcooking of red
meat, excess alcohol consumption, sedentary lifestyle, and
cigarette smoking.7 However, the disparate incidence in
developed and undeveloped countries is more likely to re-
flect complex interactions among multiple factors, including
genetics, lifestyle, and environment, as well as diet.2 Most
of these factors are unlikely to exert a major effect in chil-
dren. Although case series offer clues about the biological
nature of CRC in patients under 20 years of age,3,8 defini-
tive conclusions cannot be drawn from the small numbers
of patients studied.
In adults, most cases of CRC occur sporadically, al-
though approximately 20% to 30% have a possible genetic
cause.9 Only about 5% of patients have a well-defined in-
herited genetic syndrome. The most common of these (3% to
5% of all patients) is hereditary nonpolyposis CRC or Lynch
syndrome; the second most common (˜1%) is familial ad-
enomatous polyposis (FAP) or Gardner syndrome. The re-
mainder are syndromes involving hamartomatous polyps,
such as Peutz-Jeghers syndrome and familial juvenile poly-
posis.4 The incidence of these well-defined genetic syndromes
in children with CRC cannot be clearly determined from
available pediatric series.3,4,10–20 Because nearly every patient
with FAP will eventually develop CRC if left untreated, the
standard of care is prophylactic colectomy. However, the
optimal timing of colectomy in children with FAP is un-
known.13,21 Colonic polyps appear at a median age of 16
years22 but have been seen in children as young as 5 years.23
The majority of children with FAP who developed CRC had
a severe polyposis phenotype (more than 1000 colonic pol-
yps).12 CRC arises from the mucosal surface of the bowel; in
adults, it usually arises from preexisting adenomas that are
thought to progress to invasive carcinoma in a stepwise
manner over a decade or more.5,24 The applicability of this
model to children with CRC is unknown. There are several
factors that argue for a different pathogenesis in children: (1)
CRC has been seen in children as young as 9 months; (2)
premalignant adenomas are rarely seen in proximity to
sporadic CRC in children; and (3) CRC in children tends to
be of mucinous histology.2,4
CLINICAL PRESENTATION
Most large series suggest that children tend to present
with late-stage disease and mucinous histology and that they
have a relatively poor outcome.3,4,10–12,14–20,25 However, a
recent review of data from the Surveillance, Epidemiology,
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J Pediatr Hematol Oncol  Volume 34, Supplement 2, May 2012
2500
Other cancers
Colorectal cancers
Incidence per Year per Million
2000
1500
1000
500
0
<5
FIGURE 1. Incidence of colorectal carcinoma relative to other cancers: SEER, 1975 to 2000.5 SEER indicates Surveillance, Epidemiology,
and End Results.
and End Results (SEER) program suggests that these find-
ings may reflect reporting bias.5 Early signs of CRC are
difficult to distinguish from common causes of abdominal
complaints. Anemia, vague abdominal pain, bleeding, weight
loss, and change in bowel habits have been reported as pre-
senting complaints for children with colon cancer.2–4 In a
recent review of 77 children with CRC who presented to
St Jude Children’s Research Hospital, patients had experienced
symptoms for a median of 3 months and most were anemic.3
All of the presenting complaints are so common in pediatric
care that the possible diagnosis of CRC may be overlooked,
whereas in an older adult the same complaints would prompt
colonoscopy; this factor may be partially responsible for data
suggesting later-stage disease at diagnosis in children. As in
most other series (summarized in Saab and Furman4), 66 of
77 patients (86%) at St Jude presented with advanced-stage
disease, 48 (62%) had mucinous histology, 33 (43%) had
>10% signet-ring cells, and the 10-year event-free survival
estimate overall was only 17.7% ± 5.1%.3 All of these pa-
rameters are “worse” than those reported in adults with
CRC.1,26 However, while vigilance for pediatric CRC re-
mains important, adult-type screening exams (eg, colono-
scopy, routine fecal occult blood testing, and sigmoidoscopy)
are not likely to be cost-effective and will generally identify
many false positives in the absence of known risk factors.
DIAGNOSIS AND STAGING
Histopathologic examination of tissue is required for
diagnosis. The procedure used to obtain tissue is best de-
termined in consultation with surgical colleagues and de-
pends on the patient’s clinical situation. Decisions about
how tissue is to be obtained should take into account that
surgery is the most important component of effective
therapy. Complete evaluation of a patient with suspected
CRC should include a chest x-ray, CT of the chest, abdo-
men, and pelvis, and a bone scan. Barium enema is some-
times used to help identify areas of concern before the
diagnosis is made. At this point, the utility of fluorodeox-
yglucose positron emission tomography (FDG-PET) scans
is unclear. This method appears to be less useful in de-
r 2012 Lippincott Williams & Wilkins
Management of Colorectal Carcinoma
6.3%
1.7% 2.7% 3.8% 5.0%
0.6% 1.0%
5–9 10–14 15–19 20–24 25–29 30–34 35–39 40–44
Age at Diagnosis (Years)
tecting lesions of mucinous histology.27 Because mucinous
lesions appear to predominate in children, FDG-PET scans
may be less helpful in these patients. Other tests to consider
include a total colonoscopy to identify other lesions or
polyps, complete blood count, blood chemistry panel with
liver enzymes, and typically a carcinoembryonic antigen
(CEA) assay. Although this antigen is useful in adults28 to
monitor disease and predict recurrence or progression, it is
less likely to be useful in most pediatric cases. In a study by
Rao et al,29 CEA levels in 9 of 23 pediatric patients did not
correspond with either residual disease or disease pro-
gression. In a follow-up study, the same group concluded
that CEA is not an effective marker for monitoring most
children with CRC.30
Staging guidelines for adult patients should be applied
to children with CRC. Currently the American Joint Com-
mission on Cancer guidelines (http://www.cancerstaging.
org/staging/posters/colon8.5x11.pdf)31 provide the most widely
used staging system.
MANAGEMENT RECOMMENDATIONS
Only 1 small prospective clinical trial has been reported
for CRC in pediatric patients,25 and therefore treatment
recommendations must be adapted from experience in adults.
Surgery is the mainstay of treatment, and patients whose
tumors cannot be completely surgically resected are rarely
cured. Resection should follow guidelines established in
adults. The basic surgical principles are removal of the major
vascular pedicle supplying the tumor along with its lym-
phatics, and en bloc resection of any organs or structures
attached to the tumor. At least a 5 cm margin of normal
bowel should be obtained on either side of the tumor to
minimize the possibility of an anastomotic recurrence.32
Adequate lymph node resection is imperative, as some pa-
tients with stage III tumors can be cured by surgery alone. In
particular, primary and secondary draining lymph node
echelons should be removed. The number of lymph nodes
examined by the pathologist is prognostic of survival,33 and
therefore a minimum of 12 negative lymph nodes should be
examined to define node-negative disease.34 The surgeon
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Goldberg and Furman
must also remember that the pattern of spread of mucinous
CRC may be intraperitoneal. Therefore, extensive explora-
tion of the peritoneal surface, including that overlying Gerota
fascia and the diaphragm, should be undertaken during
laparotomy. All peritoneal nodules should be removed if
feasible. If the diagnosis was not made preoperatively and
CRC is found in a patient being urgently explored for an
acute abdomen, the surgeon should convert the procedure to
a standard colon cancer resection with excision of draining
lymphatics, which may necessitate closing the original wound
(eg, an appendectomy incision) and using a midline
approach. Cases of localized recurrence may benefit from
reexcision. Hyperthermic perfusion of the peritoneal cavity
after colon resection and peritonectomy has been applied in
only a few cases, and there are insufficient data to recom-
mend this approach for all patients.
Unfortunately for many children, adolescents, and
young adults, CRC is rarely considered in the initial dif-
ferential diagnosis, and therefore the initial surgical ap-
proach is often inadequate. In those cases, reexploration of
the abdomen, with the goals of bowel resection with ad-
equate margins and adequate lymph node sampling, should
be performed at a center experienced in this type of surgery.
Because of the rarity of CRC in children, few pediatric
oncologists will have any substantial experience with this
disease. Consultation with medical oncologists experienced
in evaluating adults with CRC is essential. The treatment
for children should be adapted from current adult treat-
ment recommendations. For stage II disease, in general the
benefit of adjuvant chemotherapy is still being studied.
Currently, adjuvant chemotherapy does not appear to im-
prove survival by more than 5%.34–36 Careful observation
is a reasonable recommendation for most adults who have
no evidence of disease after resection; however, adjuvant
therapy may be recommended for those with any poor
prognostic features, such as poorly differentiated histology,
perforation, T4 lesion, peritumoral lymphovascular in-
volvement, or inadequate lymph node sampling.34,35
As noted above, most pediatric patients with CRC
present with 1 or more of the poor prognostic features. For
example, in the largest available pediatric series, the 8 chil-
dren with stage II disease had only a 37.5% ± 15% 10-year
event-free survival estimate,3 although 5-year disease-free
survival is 60% to 80 + % in most adult studies.35 The best
option for children with CRC is participation in a clinical
trial, although this opportunity is rarely available for pedia-
tric patients with CRC. The relative prevalence of 1 or more
negative prognostic factors at diagnosis and young age by
definition suggest that adjuvant chemotherapy be strongly
considered (and carefully discussed by the oncologist with the
family) for many children, adolescents, and young adults with
stage II disease. Chemotherapy has demonstrated a clear
survival benefit for adults with stage III or IV disease,34,37
and children should be treated in a similar fashion. Although
the FOLFOX regimen38,39 or one of its derivatives, such as
modified FOLFOX-6,40 is the current regimen of choice,37
chemotherapy for advanced-stage disease is under active in-
vestigation and changing rapidly. Addition of the targeted
agents bevacizumab,41,42 cetuximab,43 and panitumumab44–46
to standard chemotherapy regimens has shown benefit in se-
lected patient groups. There is accumulating evidence that
some patients who present with stage IV disease can be
cured, if complete surgical resection can eventually be at-
tained.47 In considering options for a pediatric patient with
advanced-stage disease, one should carefully review the
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J Pediatr Hematol Oncol  Volume 34, Supplement 2, May 2012
current medical literature and consult with an adult on-
cologist experienced in treating CRC before recommending
a specific regimen.
FOLLOW-UP RECOMMENDATIONS
Careful observation is recommended for the child with
sporadic CRC who completes all planned treatment. How-
ever, few data are available to predict the risk of recurrence in
such children or the risk of second malignancies later in life.
Because CRC is both rare in children and extremely difficult
to cure, the number of survivors is small. Although to date no
large-scale randomized trials have documented the efficacy of
a standard postoperative monitoring program in adults,
young patients have a long period of latency for relapse and
should undergo posttreatment screening with regular colo-
noscopy and radiologic evaluations at least as frequently as
recommended for adults.34,48 Screening with CEA at rea-
sonable intervals could be considered for children who had
high CEA levels at presentation. Although the 5-year survival
estimate for early-stage colon cancer is excellent at about
90%, patients with metastatic disease have less than a 10%
likelihood of 5-year survival. It is not clear how long relapse
surveillance should be continued for patients who survive
metastatic pediatric CRC. The child should be followed in a
clinic specializing in the long-term sequelae of treatment for
childhood cancer, regardless of other follow-up plans.
CONCLUSIONS
CRC in children, adolescents, and young adults is rare.
Although presenting symptoms are similar to those in
adults, CRC is often not considered in the initial evaluation
of a young patient. Because of its rarity in children, few
pediatric oncologists have any substantial experience with
CRC, and clinical trials are rarely available. The majority
of reported cases present with advanced-stage disease and
have mucinous or signet-ring cell carcinomas,4 whereas
only 5% to 15% of adults present with these histologic
subtypes.49 Treatment of young patients should be adapted
from adult guidelines. Surgery is the mainstay of treatment,
and patients who cannot be rendered surgically free of
disease are rarely cured. The treatment of CRC in adults is
evolving rapidly,50 and consultation with medical oncolo-
gists experienced in treating adults with CRC is essential.
ACKNOWLEDGMENT
The authors thank Sharon Naron for editorial assistance.
REFERENCES
1. American Cancer Society. Cancer Facts and Figures 2010.
Atlanta, GA: American Cancer Society; 2011.
2. Pappo AS, Rodriguez-Galindo C, Furman WL. Management of
infrequent cancers of childhood. In: Pizzo PA, Poplack DG, eds.
Principles and Practice of Pediatric Oncology. Vol 6th. Phila-
delphia, PA: Lippincott Williams & Wilkins; 2011:1098–1123.
3. Hill DA, Furman WL, Billups CA, et al. Colorectal carcinoma
in childhood and adolescence: a clinicopathologic review.
J Clin Oncol. 2007;25:5808–5814.
4. Saab R, Furman WL. Epidemiology and management options for
colorectal cancer in children. Paediatr Drugs. 2008;10:177–192.
5. Spunt S, Furman WL, La Quaglia MP, et al. Colon and rectal
cancer. In: Bleyer A, O’Leary M, Ries L, eds. Cancer
Epidemiology in Older Adolescents and Young Adults 15 to 29
Years of Age, Including SEER Incidence and Survival: 1975–2000.
r 2012 Lippincott Williams & Wilkins
J Pediatr Hematol Oncol  Volume 34, Supplement 2, May 2012
NIH Pub. No. 06-5767. Bethesda, MD: National Cancer
Institute; 2006:123–133.
6. Donohoe CL, Pidgeon GP, Lysaght J, et al. Obesity and
gastrointestinal cancer. Br J Surg. 2010;97:628–642.
7. Libutti SK, Saltz LB, Rustgi AK, et al. Cancer of the colon. In:
DeVita VT, Hellman S, Rosenberg SA, eds. Cancer Principles
& Practice of Oncology. Vol 7th. Philadelphia, PA: Lippincott
Williams & Wilkins; 2005:1061–1109.
8. Datta RV, Laquaglia MP, Paty PB. Genetic and phenotypic
correlates of colorectal cancer in young patients. N Engl J Med.
2000;342:137–138.
9. Grady WM. Genetic testing for high-risk colon cancer patients.
Gastroenterology. 2003;124:1574–1594.
10. Andersson A, Bergdahl L. Carcinoma of the colon in children:
a report of six new cases and a review of the literature.
J Pediatr Surg. 1976;11:967–971.
11. Chantada GL, Perelli VB, Lombardi MG, et al. Colorectal
carcinoma in children, adolescents, and young adults. J Pediatr
Hematol Oncol. 2005;27:39–41.
12. Durno C, Aronson M, Bapat B, et al. Family history and
molecular features of children, adolescents, and young adults
with colorectal carcinoma. Gut. 2005;54:1146–1150.
13. Durno CA, Gallinger S. Genetic predisposition to colorectal
cancer: new pieces in the pediatric puzzle. J Pediatr Gastro-
enterol Nutr. 2006;43:5–15.
14. Ferrari A, Rognone A, Casanova M, et al. Colorectal
carcinoma in children and adolescents: the experience of the
Istituto Nazionale Tumori of Milan, Italy. Pediatr Blood
Cancer. 2008;50:588–593.
15. Karnak I, Ciftci AO, Senocak ME, et al. Colorectal carcinoma
in children. J Pediatr Surg. 1999;34:1499–1504.
16. Laquaglia MP, Heller G, Filippa DA, et al. Prognostic factors
and outcome in patients 21 years and under with colorectal
carcinoma. J Pediatr Surg. 1992;27:1085–1089.
17. Middelkamp JN, Haffner H. Carcinoma of the colon in
children. Pediatrics. 1963;32:558–571.
18. Radhakrishnan CN, Bruce J. Colorectal cancers in children
without any predisposing factors. A report of eight cases and
review of the literature. Eur J Pediatr Surg. 2003;13:66–68.
19. Sharma AK, Gupta CR. Colorectal cancer in children: case report
and review of literature. Trop Gastroenterol. 2001;22:36–39.
20. Taguchi T, Suita S, Hirata Y, et al. Carcinoma of the colon
in children: a case report and review of 41 Japanese cases.
J Pediatr Gastroenterol Nutr. 1991;12:394–399.
21. Alkhouri N, Franciosi JP, Mamula P. Familial adenomatous
polyposis in children and adolescents. J Pediatr Gastroenterol
Nutr. 2010;51:727–732.
22. Corredor J, Wambach J, Barnard J. Gastrointestinal polyps in
children: advances in molecular genetics, diagnosis, and
management. J Pediatr. 2001;138:621–628.
23. Distante S, Nasioulas S, Somers GR, et al. Familial adenom-
atous polyposis in a 5 year old child: a clinical, pathological, and
molecular genetic study. J Med Genet. 1996;33:157–160.
24. Markowitz SD, Bertagnolli MM. Molecular origins of cancer:
molecular basis of colorectal cancer. N Engl J Med.
2009;361:2449–2460.
25. Pratt CB, Rao BN, Merchant TE, et al. Treatment of
colorectal carcinoma in adolescents and young adults with
surgery, 5-fluorouracil/leucovorin/interferon-alpha 2a and
radiation therapy. Med Pediatr Oncol. 1999;32:459–460.
26. Consorti F, Lorenzotti A, Midiri G, et al. Prognostic
significance of mucinous carcinoma of colon and rectum: a
prospective case-control study. J Surg Oncol. 2000;73:70–74.
27. Berger KL, Nicholson SA, Dehdashti F, et al. FDG PET evalua-
tion of mucinous neoplasms: correlation of FDG uptake with
histopathologic features. Am J Roentgenol. 2000;174:1005–1008.
28. Goldstein MJ, Mitchell EP. Carcinoembryonic antigen in the
staging and follow-up of patients with colorectal cancer.
Cancer Invest. 2005;23:338–351.
29. Rao BN, Pratt CB, Fleming ID, et al. Colon carcinoma in
children and adolescents. A review of 30 cases. Cancer. 1985;
55:1322–1326.
r 2012 Lippincott Williams & Wilkins
Management of Colorectal Carcinoma
30. Angel CA, Pratt CB, Rao BN, et al. Carcinoembryonic antigen
and carbohydrate 19-9 antigen as markers for colorectal carcinoma
in children and adolescents. Cancer. 1992;69:1487–1491.
31. American Joint Committee on Cancer Staging Handbook. In:
Edge SB, Byrd DR, Compton CC, et al, eds. AJCC Cancer
Staging Manual. Vol 7th. Springer: American Joint Committee
on Cancer; 2010.
32. Rodriguez-Bigas MA, Hoff PM, Crane CH. Carcinoma of the
colon and rectum. In: Kuff DW, Bast RC Jr, Hait WN, et al, eds.
Cancer Medicine 7. London: BC Decker Inc.; 2006:1369–1391.
33. Gunderson LL, Jessup JM, Sargent DJ, et al. Revised TN
categorization for colon cancer based on national survival
outcomes data. J Clin Oncol. 2010;28:264–271.
34. Cited with permission from the NCCN Clinical Practice
guidelines in Oncology (NCCN Guidelines(r))[Colon Cancer]
(version 3.2012) (c) 2012 National Comprehensive Cancer
Network, Inc. Available at: NCCN.org. Accessed [February
28, 2012]. To view the most recent and complete version of the
NCCN Guidelines(r), go on-line to NCCN.org.
35. Benson AB III, Schrag D, Somerfield MR, et al. American Society
of Clinical Oncology recommendations on adjuvant chemotherapy
for stage II colon cancer. J Clin Oncol. 2004;22:3408–3419.
36. Figueredo A, Charette ML, Maroun J, et al. Adjuvant therapy
for stage II colon cancer: a systematic review from the Cancer
Care Ontario Program in evidence-based care’s gastrointestinal
cancer disease site group. J Clin Oncol. 2004;22:3395–3407.
37. Saltz LB. Adjuvant therapy for colon cancer. Surg Oncol Clin
N Am. 2010;19:819–827.
38. Andre T, Boni C, Mounedji-Boudiaf L, et al. Oxaliplatin,
fluorouracil, and leucovorin as adjuvant treatment for colon
cancer. N Engl J Med. 2004;350:2343–2351.
39. Andre T, Boni C, Navarro M, et al. Improved overall survival
with oxaliplatin, fluorouracil, and leucovorin as adjuvant
treatment in stage II or III colon cancer in the MOSAIC trial.
J Clin Oncol. 2009;27:3109–3116.
40. Tournigand C, Andre T, Achille E, et al. FOLFIRI followed
by FOLFOX6 or the reverse sequence in advanced colorectal
cancer: a randomized GERCOR study. J Clin Oncol.
2004;22:229–237.
41. Hurwitz H, Fehrenbacher L, Novotny W, et al. Bevacizumab
plus irinotecan, fluorouracil, and leucovorin for metastatic
colorectal cancer. N Engl J Med. 2004;350:2335–2342.
42. Hurwitz HI, Yi J, Ince W, et al. The clinical benefit of
bevacizumab in metastatic colorectal cancer is independent
of K-ras mutation status: analysis of a phase III study of
bevacizumab with chemotherapy in previously untreated
metastatic colorectal cancer. Oncologist. 2009;14:22–28.
43. Cunningham D, Humblet Y, Siena S, et al. Cetuximab
monotherapy and cetuximab plus irinotecan in irinotecan-
refractory metastatic colorectal cancer. N Engl J Med.
2004;351:337–345.
44. Addeo R, Caraglia M, Cerbone D, et al. Panitumumab: a new
frontier of target therapy for the treatment of metastatic
colorectal cancer. Expert Rev Anticancer Ther. 2010;10:499–505.
45. Giusti RM, Shastri KA, Cohen MH, et al. Drug approval
summary: panitumumab (Vectibix). Oncologist. 2007;12:577–583.
46. Van CE, Peeters M, Siena S, et al. Open-label phase III trial of
panitumumab plus best supportive care compared with best
supportive care alone in patients with chemotherapy-refractory
metastatic colorectal cancer. J Clin Oncol. 2007;25:1658–1664.
47. VanderMeer TJ, Callery MP, Meyers WC. The approach to the
patient with single and multiple liver metastases, pulmonary
metastases, and intra-abdominal metastases from colorectal
carcinoma. Hematol Oncol Clin North Am. 1997;11:759–777.
48. Desch CE, Benson AB III, Somerfield MR, et al. Colorectal
cancer surveillance: 2005 update of an American Society of Clini-
cal Oncology practice guideline. J Clin Oncol. 2005;23:8512–8519.
49. Negri FV, Wotherspoon A, Cunningham D, et al. Mucinous
histology predicts for reduced fluorouracil responsiveness and sur-
vival in advanced colorectal cancer. Ann Oncol. 2005;16:1305–1310.
50. Cunningham D, Atkin W, Lenz HJ, et al. Colorectal cancer.
Lancet. 2010;375:1030–1047.
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