close

Вход

Забыли?

вход по аккаунту

?

96

код для вставкиСкачать
1358
CANCER October 1, 1997 / Volume 80 / Number 7
TABLE 1
Survival and LRF in Prognostic Subgroups of Patients with Breast
Carcinoma Treated with Mastectomy Alonea
Prognostic
subgroup
No. of patients
10-year overall
survival (%)
10-year LRF
(%)
T1 N0 BIb
T2 N0 BI
T2 N0 BIII
T2 N(1?3) BI
T2 N(1?3) BII
T2 N�BII
T2 N�BIII
30
80
110
39
104
63
37
96
92
65
73
50
41.5
24
7
8
23
27
29
63
70
Marks and Prosnitz were quite right in stating that
??final resolution of the controversy regarding the survival impact of postmastectomy RT would require a
very large prospective trial.?? In such a trial, with the
application of modern, ??safe?? RT technique, an unresolved issue of the optimal combination of RT and
adjuvant systemic therapy could also be addressed. A
question arises as to whether such trial would be feasible nowadays, when a high proportion of patients are
treated with breast-conserving therapy and there is an
increasing interest in neoadjuvant approaches.
REFERENCES
LRF: locoregional failure.
a
Adapted from Korzeniowski et al.2
b
Histologic grade according to Bloom classification.
1.
2.
TABLE 2
Effectiveness of RT in Preventing Local (Chest Wall) and Regional
(Lymph Node) Failures in Relation to Lymph Node Involvement
3.
No. of metastatic
lymph nodes
Therapy
No. of
10-year Effect of 10-year
patients LF rate RT (%)b RF rate
Effect of
RT (%)b
4.
1?3
265
85
173
77
82%
5.
�
OP
OP / RT
OP
OP / RT
15.5%
4%
23%
10.5%
74%
54%
19%
3.5%
35%
5%
86%
6.
RT: radiation therapy; LF: local failure; RF: regional failure; OP: operation alone.
a
Adapted from Korzeniowski.5
b
Effectiveness of RT � 100% 0 failure rate with RT/failure rate without RT 1 100% (e.g., in patients
with 1?3 lymph nodes involved, RT with 50 Gy prevents the development of chest wall recurrence in
74% of patients).
chest wall failures than in preventing lymph node failures, and that this effectiveness decreases with the
number of positive lymph nodes. This observation is
keeping in with more recent reports of Fletcher et al.,6
who also found that 50 Gy to the chest wall was relatively ineffective in patients with massive lymph node
involvement, and who even recommended the use of
higher doses.7
All the above considerations consistently lead to
the conclusion that patients with 1 ? 3 positive lymph
nodes are in fact more likely to benefit from postmastectomy RT in terms of improvement of survival than
those with 4 or more lymph nodes involved. First, they
are at lower risk of distant dissemination; and if it
exists, it is more likely to be controlled with adjuvant
systemic therapy. Second, RT, due to smaller tumor
burden, may be more effective in eradicating subclinical locoregional disease, thus improving disease free
and overall survival.
/ 7b71$$1349
09-10-97 13:20:26
cana
7.
Marks LB, Prosnitz LR. ??One to three?? or ??four or more???
Selecting patients for postmastectomy radiation therapy.
Cancer 1997;79:668?70.
Korzeniowski S, Dyba T, Sko?yszewski J. Classical prognostic
factors for survival and loco-regional control in breast cancer patients treated with radical mastectomy alone. Acta Oncol 1994;33:759?65.
Bonadonna G, Valagussa P, Moliterni A, Zambetti M, Brambilla C. Adjuvant cyclophosphamide, methotrexate and fluorouracil in node positive breast cancer: the results of 20
years of follow-up. N Engl J Med 1995;332:901?6.
Fletcher GH. Local results of irradiation in the primary management of localized breast cancer. Cancer 1972;29:545?51.
Korzeniowski S. The value of postoperative radiotherapy in
patients with breast cancer treated with radical mastectomy
[Ph.D. thesis]. Krako?w: Centrum Onkologii, 1991.
Fletcher GH, McNeese MD, Oswald MJ. Long-range results
for breast cancer patients treated by radical mastectomy and
postoperative radiation without adjuvant chemotherapy: an
update. Int J Radiat Oncol Biol Phys 1989;17:11?4.
McNeese, Fletcher GH, Levitt SH. Breast cancer. In: Levitt
SH, Tapley ND, editors. Technological basis of radiation
therapy: practical clinical application. 2nd edition. Philadelphia: Lea and Febiger, 232?47.
Stanis?aw Korzeniowski, M.D., Ph.D.
Department of Radiation Therapy
Centre of Oncology
Maria Sk?odowska-Curie Memorial Institute
Krako?w, Poland
Assessment of Microsatellite
Alterations in Young Patients with
Gastric Adenocarcinoma
W
e read with interest the article by Hayden et al.1
about their search for microsatellite instability
(MI) in 10 young patients (age � years) with gastric
adenocarcinoma, using a panel of 12 microsatellite
markers. The majority of cases in the series were advanced gastric adenocarcinomas, and the authors did
not detect MI. The results fit with the absence of MI
W: Cancer
Correspondence
1359
TABLE 1
Summary of the Clinicopathologic Data from 11 Cases of Early Onset Gastric Carcinomas
Case no.
Gender
Age (yrs)
Site
Histologic typea
T
N
MIb
29
33
48
115
140
145
150
161
169
195
212
F
M
M
M
M
M
M
F
F
M
M
29
37
34
29
36
38
26
40
39
39
40
A
A
A
A
A
A
A
A
B
B
A
Unclassified (solid)
Unclassified (solid)
Mixed
Intestinal (glandular)
Unclassified (solid)
Mixed
Intestinal (glandular)
Intestinal (glandular)
Diffuse (isolated cell)
Mixed
Intestinal (glandular)
T1
T3
T1
T2
T3
T3
T4
T3
T4
T4
T3
N2
N1
N0
N0
N1
N1
N2
N1
N3
N1
N1
0
0
0
0
/
0
0
0
0
0
0
F: female; M: male; A: antrum; B: body; T, N: UICC classification.
a
According to the classifications of Lauren (and, in parentheses, Carneiro et al.)9
b
Accessed using at least five dinucleotide repeats and a mononucleotide repeat (BAT26).10
in the few cases of gastric carcinoma in patients
younger than 40 years reported in the literature,2 ? 4 at
variance with a prevalence ranging from 20% to 33%
in patients older than 40 years.2,3
We recently enlarged our series and found MI in
1 of 11 (9.1%) patients age � years with gastric carcinoma and no history of hereditary nonpolyposis colorectal carcinoma (HNPCC) (Table 1). Taking together
the results of Hayden et al.1 and our own (Table 1),
the following conclusions may be drawn.
First, the low prevalence of MI in the gastric carcinomas of young patients cannot be ascribed to the
low number of loci analyzed in each case, nor to a
high concentration of early carcinomas in any of the
series.
Second, the low prevalence of MI cannot be ascribed to the site of the tumors because all of them
were located in the distal stomach, and MI is much
more frequent in carcinomas of the distal stomach5
than in those of the proximal stomach.6
Finally, the low prevalence of MI in the gastric
carcinomas of young patients cannot be ascribed to
an excess of diffuse-type carcinomas, which are known
to exhibit a low frequency of MI,5,7 because the majority of the tumors were of the intestinal, mixed, or solid
types.
We thus concur with Hayden et al. that, at variance
with the findings for early onset colorectal carcinomas,8 genetic instability does not appear to be involved in the etiopathogenesis of most gastric carcinomas occurring in young patients.
It remains to be seen whether gastric carcinomas
arising within the context of HNPCC (and/or in patients with germline mutations in mismatch repair
genes) will occur in young patients or follow the typical
/ 7b71$$1349
09-10-97 13:20:26
cana
clinicopathologic profile of sporadic gastric carcinomas with MI, which tend to occur in elderly patients
and are associated with a good prognosis.5
REFERENCES
1.
2.
3.
4.
5.
6.
7.
8.
9.
Hayden JD, Cawkwell L, Sue-Ling H, Johnston D, Dixon MF,
Quirke P, et al. Assessment of microsatellite alterations in
young patients with gastric adenocarcinoma. Cancer 1997;
79:684?7.
Seruca R, Dos Santos NR, David L, Consta?ncia M, Barroca
H, Carneiro F, et al. Sporadic gastric carcinomas with microsatelite instability display a particular clinicopathologic profile. Int J Cancer 1995;64:32?6.
Mironov NM, Aguelon MA, Patapova G, Omori Y, Gorbunov
OV, Klimenkov AA, et al. Alterations of (CA)n DNA repeats
and tumor suppressor genes in human gastric cancer. Cancer Res 1994;54:41?4.
Zelada-Hedman M, Iselius L, Gunve?n P, Weger A, Nordenskjold M, Skoog L, et al. Genetic rearrangements in sporadic
and familial gastric carcinomas detected with microssatelite
markers. Eur J Surg Oncol 1994;20:667?73.
Dos Santos NR, Seruca R, Consta?ncia M, Seixas M, SobrinhoSimo?es M. Microsatellite instability at multiple loci: clinicopathologic implications and prognosis. Gastroenterology
1996;110:38?44.
Gleeson CM, Sloan JM, McGuigan JA, Ritchie AJ, Weber JL,
Russel SEH. Widespread microsatellite instability occurs infrequently in adenocarcinoma of the gastric cardia. Oncogene 1996;12:1653?62.
Chung Y, Song J, Lee J, Jung Y, Seo E, Choi S, et al. Microsatellite instability?associated mutations associate preferentially with the intestinal type of primary gastric carcinomas
in a high-risk population. Cancer Res 1996;56:4662?5.
Liu B, Farrington SM, Petersen GM, Hamilton SR, Parsons
R, Papadopoulos N, et al. Genetic instability occurs in the
majority of young patients with colorectal cancer. Nat Med
1995;1:348?52.
Carneiro F, Seixas M, Sobrinho-Simo?es M. New elements for
an updated classification of the carcinomas of the stomach.
Pathol Res Pract 1995;191:571?584.
W: Cancer
1360
CANCER October 1, 1997 / Volume 80 / Number 7
10. Hoang JM, Cottu PH, Thuille B, Salmon RJ, Thomas G, Hamelin
R. BAT-26 an indicator of the replication error phenotype in
colorectal cancers and cell lines. Cancer Res 1997;15:300?3.
4.
Raquel Seruca, M.D.
Institute of Molecular Pathology and Immunology of
the University of Porto (IPATIMUP)
Porto, Portugal
Manuel Sobrinho-Simo?es, M.D.
Institute of Molecular Pathology and Immunology of
the University of Porto (IPATIMUP)
Department of Pathology
Medical Faculty
University of Porto
Porto, Portugal
Author Reply
W
e welcome the correspondence from Dr. Seruca
and Dr. Sobrinho-Simo?es confirming our observation of a paucity of microsatellite instability in young
patients with gastric adenocarcinoma.1 We recently
studied gastric adenocarcinomas in 17 more young
patients younger than 40 years from Braga, Portugal
(unpublished data). A mutator phenotype suggestive
of the hereditary nonpolyposis colorectal carcinoma
syndrome2 was found in only one case (6%). However,
low level microsatellite instability occurring in less
than 29% of markers analyzed3 was detected in 6 more
cases (35%). Although the significance of low frequency microsatellite instability is as yet undetermined, there may be subtle differences in the molecular pathology of gastric carcinoma occurring in young
patients from relatively high and low risk populations
that require exploration. The data reported so far suggest that the prevalence of a hereditary nonpolyposis
colorectal carcinoma ? associated mutator phenotype
is lower in early onset gastric carcinoma than in early
onset colorectal carcinoma.4 It remains to be determined whether or not the few early onset gastric carcinomas with a mutator phenotype harbor underlying
DNA mismatch repair gene mutations.
REFERENCES
1.
2.
3.
Hayden JD, Cawkwell L, Sue-Ling H, Johnston D, Dixon MF,
Quirke P, et al. Assessment of microsatellite alterations in
young patients with gastric adenocarcinoma. Cancer 1997;
79:684?7.
Aaltonen LA, Peltoma?ki P, Leach FS, Sistonen P, Pylkkanen
L, Mecklin J-P, et al. Clues to the pathogenesis of familial
colorectal cancer. Science 1993;260:812?6.
Gleeson CM, Sloan JM, McGuigan JA, Ritchie AJ, Weber JL,
Russell SEH. Widespread microsatellite instability occurs in-
/ 7b71$$1349
09-10-97 13:20:26
cana
frequently in adenocarcinoma of the gastric cardia. Oncogene 1996;12:1653?62.
Liu B, Farrington SM, Petersen GM, Hamilton SR, Parsons
R, Vogelstein B, et al. Genetic instability occurs in the majority of young patients with colorectal cancer. Nat Med
1995;1:348?52.
Jeremy D. Hayden, B.Sc., M.B., Ch.B.
Iain G. Martin, M.D., F.R.C.S.
Division of Surgery and Molecular Oncology
University of Leeds
Leeds, United Kingdom
Association of Stein?Leventhal
Syndrome with the Incidence of
Postmenopausal Breast Carcinoma
in a Large Prospective Study of
Women in Iowa
A
recent article by Anderson et al.1 published in Cancer reported the results from a cohort study including 472 women with a history of Stein ? Leventhal syndrome (SLS). No association emerged between SLS
and risk of breast carcinoma (14 cases overall).
SLS is characterized by menstrual irregularities,
infertility, a high level of androgens, and obesity,
which are clinical and hormonal conditions associated
with the risk of breast carcinoma. Other studies have
shown inconsistent data regarding the association between SLS and the risk of breast carcinoma.2,3 Thus,
it is also important to examine further the issue in
consideration of the recent hypothesis of an association between SLS and insulin resistance and hyperinsulinemia4 (i.e., possible risk factors for breast carcinoma). Therefore, we analyzed data from a large case ?
control study on breast carcinoma conducted between
June 1991 and February 1994 in six Italian areas: the
provinces of Pordenone and Gorizia, the urban areas
of Milan and Genoa, the province of Forl?? in northern
Italy, the province of Latina near Rome in central Italy,
and the urban area of Naples in southern Italy. Study
methods have been described previously.5,6
The cases studied were 2569 women (median age
55 years; range, 23 ? 74 years) with incident (i.e., diagnosed within 1 year before the interview), histologically confirmed breast carcinoma who were admitted
to the major teaching and general hospitals in the
areas under surveillance. The controls were 2588
women (median age, 56 years; range, 20 ? 74 years)
who were admitted for acute conditions (22% for traumas, 33% for other orthopedic disorders, 16% for acute
W: Cancer
Документ
Категория
Без категории
Просмотров
2
Размер файла
63 Кб
Теги
1/--страниц
Пожаловаться на содержимое документа