Carcinogenesis vol.27 no.7 pp.1310–1315, 2006
doi:10.1093/carcin/bgi276
Advance Access publication November 25, 2005
Green tea, black tea and breast cancer risk: a meta-analysis of
epidemiological studies
Can-Lan Sun , Jian-Min Yuan, Woon-Puay Koh1 and
Mimi C.Yu
The Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA
and 1Department of Community, Occupational and Family Medicine,
National University of Singapore, Singapore 117597
To whom correspondence should be addressed. Tel: þ612 626 5367;
Fax: þ612 625 8950;
Email: canlans@umn.edu
Introduction
Tea is one of the most popular beverages consumed around the
world, second only to water. Polyphenols are the naturally
occurring compounds in fresh tea leaves and account for its
pungency and unique flavor. The four primary polyphenols in
fresh tea leaves are epigallocatechin gallate (EGCG), epigallocatechin, epicatechin gallate and epicatechin, with the most
abundant being EGCG. These four catechins account for up to
30% of dry weight of the fresh tea leaves (1). Varying methods
Abbreviations: CI, confidence interval; EGCG, epigallocatechin gallate;
HCC, hospital-based case–control study; OR, odds ratio; PCC, populationbased case–control study; RR, relative risk.
#
Methods
Literature search strategy
To search for observational studies of tea consumption in relation to breast
cancer risk, we conducted a literature search in MEDLINE database for all
English-language papers published from January 1, 1966 to August 31, 2004.
For outcome, we identified articles using medical-subject-heading term,
‘breast neoplasm’, or keywords, ‘breast cancer, breast tumor or mammary
gland tumor.’ For exposure, we identified articles using medical-subjectheading terms, ‘tea, flavonoids or catechin’, or keywords, ‘green tea, black
The Author 2005. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org 1310
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Experimental studies have shown that tea and tea polyphenols have anti-carcinogenic properties against breast
cancer. A number of epidemiologic studies, both case–
control and cohort in design, have examined the possible
association between tea intake and breast cancer development in humans. This meta-analysis included 13 papers
which examined populations in eight countries and provided data on consumption of either green tea or black tea,
or both in relation to breast cancer risk. Summary odds
ratios (ORs) for highest versus non/lowest tea consumption
level were calculated based on fixed and random effects
models. Heterogeneity between studies was examined via
the Q statistics. For green tea, the combined results from
the four studies indicated a reduced risk of breast cancer
for highest versus non/lowest intake (OR ¼ 0.78, 95%
CI ¼ 0.61–0.98). For black tea, conflicting results were
observed in case–control versus cohort studies. The combined results from the eight case–control studies showed a
minor inverse association between black tea consumption
and risk of breast cancer (OR ¼ 0.91, 95% CI ¼ 0.84–0.98).
This inverse association was stronger in hospital-based
(OR ¼ 0.77, 95% CI ¼ 0.50–1.19) than population-based
case–control studies (OR ¼ 0.94, 95% CI ¼ 0.81–1.09). Five
cohort studies demonstrated a modest increase in risk
associated with black tea intake (OR ¼ 1.15, 95% CI ¼
1.02–1.31). The results of this meta-analysis indicate a
lower risk for breast cancer with green tea consumption.
Available data suggest a possible late-stage, promotional
effect of black tea on breast carcinogenesis.
of processing the tea leaves after harvest lead to three major
types of tea with different kinds and concentrations of polyphenols. To make green tea, fresh tea leaves are steamed or
pan-dried at high temperature right after plucking, resulting in
minimal oxidation of the naturally occurring catechins in the
tea leaves. Alternatively, fresh tea leaves are rolled or crushed
during the manufacture of black tea to encourage oxidation
and polymerization of the polyphenols in a process commonly
known as fermentation, resulting in the generation of other
distinct polyphenols such as thearubigins and theaflavins. An
intermediate stage of enzymatic oxidation yields Oolong tea.
In general, the amounts of native polyphenols in green tea are
30–40% weight of the water-extractable materials, as compared with 3–10% in black tea (2). About 78% of the tea
production worldwide is black tea, which is the main tea
beverage consumed in the US and Europe. Green tea, which
is the main tea beverage in Japan and parts of China, accounts
for 20% of worldwide production, while the remaining 2% of
tea production is Oolong tea which is consumed mainly in
Southern China and Taiwan.
There has been extensive in vitro research regarding the
possible cancer prevention mechanisms by green and black
tea extracts and their polyphenols using human breast cancer
cell lines. These studies suggested that multiple mechanisms
are involved, including induction of apoptosis (3) and cell
cycle arrest (4), down-regulation of telomerase (5), inhibition
of vascular endothelial growth factor (6) and suppression of
aromatase activity (7). Both green and black tea extracts also
have demonstrated cancer preventive properties in carcinogeninduced or transplanted mammary tumors in experimental
animal studies. Green tea extracts or catechins fed to rodents
after administration of chemical carcinogens decreased the
size and multiplicity of mammary tumors (8,9). Although
less extensively studied, black tea extracts, given before carcinogen challenge, have been shown to reduce the tumor
number, size and multiplicity in carcinogen-treated rats on a
high fat diet (10,11).
Over the last three decades, a number of epidemiologic
studies were conducted to investigate the association between
tea consumption and breast cancer risk. This report presents
results of a meta-analysis of all published data on this topic,
including testing for homogeneity between studies, and computation of summary odds ratios for breast cancer in relation to
green tea and black tea separately.
Tea and breast cancer risk
tea, thearubigin, theaflavin or catechin.’ For study design, we identified
articles using medical-subject-heading terms or keywords, ‘case–control
studies’, ‘retrospective studies’, ‘cohort studies’ or ‘prospective studies.’
Articles satisfying the exposure, outcome and study design criteria were
pulled. In addition, all bibliographies of retrieved papers were screened for
further relevant publications.
For inclusion into the meta-analysis, the identified articles have to provide
information on (i) the number of breast cancer cases studied and (ii) the odds
ratio (OR) or relative risk (RR), and its corresponding 95% confidence interval
(CI), for highest versus non/lowest level of tea intake. In total, 20 papers (12–
31) were identified and reviewed by two authors (Sun and Yuan). Nagano et al.
(23) and Wu et al. (29) were excluded since these two data sets were merely
subsets of Key et al. (16) and Wu et al. (30), respectively. Franceschi et al. (14)
and La Vecchia et al. (17) were excluded since the two case–control data sets
were subsequently combined in Tavani et al. (28). The reports by Ewertz et al.
(12), Lawson et al. (18) and Stocks (26) were excluded due to insufficient
information on ORs and 95% CIs. Thus, the meta-analysis of green tea and
breast cancer included the following three papers: Key et al. (16), Suzuki et al.
(27) and Wu et al. (30); the meta-analysis of black tea and breast cancer
included the following 13 papers: Ewertz and Gill (13), Goldbohm et al.
(15), Key et al. (16), Lubin et al. (19), Mannisto et al. (20), Mclaughlin et al.
(21), Michels et al. (22), Rosenberg et al. (24), Schairer et al. (25), Suzuki
et al. (27), Tavani et al. (28), Wu et al. (30) and Zheng et al. (31).
by design (cohort versus case–control) and found that results across studies
with the same design were homogeneous. We used the fixed effect model to
calculate the summary OR and its 95% CI across homogeneous studies. We
used the random effect model to calculate the summary OR and its 95% CI
across heterogeneous studies.
Results of the meta-analysis may be biased if the probability of a study being
published is dependent on its results. In other words, studies with strong
positive findings may be more likely to be published. In an attempt to detect
publication or related bias, we first visually explored asymmetry in funnel
plots, i.e. plots of effect estimates against their estimated precision (34). In the
absence of publication bias, the funnel plots should be symmetrical with
estimates from larger studies in the center, flanked equally on either side by
the less precise estimates. The funnel plots would be skewed (i.e. asymmetrical) in the presence of publication bias. We then formally tested the degree of
asymmetry of the funnel plot using Egger’s un-weighted regression asymmetry
test (35). We considered the funnel plot to be asymmetrical if the intercept of
the regression line deviated from zero with a P-value of 50.10. We should note
that these tests for asymmetry possess relatively low power to detect real
publication bias when the number of individual studies included in the metaanalysis is small (25), which is the case in the current review.
Meta-analysis
Study-specific ORs and 95% CIs for highest versus non/lowest tea consumption level were extracted from each paper. For all studies, the reported relative
risk estimate was adjusted for age and race/ethnicity, if applicable. On the
other hand, only some studies reported relative risk estimates that had taken
into account the established menstrual and reproductive risk factors for breast
cancer. Those studies were Goldbohm et al. (15), Mannisto et al. (20),
Mclaughlin et al. (21), Michels et al. (22), Suzuki et al. (27), Tavani et al.
(28), Wu et al. (30) and Zheng et al. (31). Lubin et al. (19) and Mannisto et al.
(20) employed both hospital and population control groups. The results based
on comparison with population controls were used in the meta-analysis. Mannisto et al. (20) reported pre- and post-menopausal specific OR (95% CI)
estimates separately. We calculated a single OR (95% CI) estimate for total
subjects by means of a weighted average of pre-menopausal OR (95% CI) and
post-menopausal OR (95% CI), with weights being the inverse of the respective subgroup variance. For cohort studies, the percentages of subjects in the
highest and non/lowest consumption levels were calculated either as the proportions of the numbers of subjects in these two categories over the total
number of study subjects (15,27,31), or as the proportions of person-years in
these two categories over the total person-years (16,22). For case–control
studies, the proportions (expressed in percentages) of control subjects in
the highest and non/lowest consumption categories were stated. Statistical
computing was performed using the STATA statistical software (College
Station, TX).
We examined possible heterogeneity in results across studies using the
Q statistic (32). We defined statistical significance as P 5 0.10 rather than
the conventional level of 0.05 because of the low power of this test (33). The
null hypothesis that the studies are homogeneous would be rejected if P is
50.10. When we noted a significant heterogeneity among study results with
respect to the black tea–breast cancer risk association, we stratified studies
Green tea
Four studies were included in the meta-analysis on green tea
consumption and breast cancer risk, consisting of three cohort
studies from Japan (16,27) [results from two separate cohort
studies were reported in ref. (27)] and one population-based
case–control study from Los Angeles (30). Table I and Figure 1
present the relative risk or odds ratio for each of the studies
along with their summary OR.
Results
Suzuki 2004b
Key 1999
Wu 2003
Combined
.2
.5
1
1.5
2
2.5
RR
Fig. 1. Meta-analysis of green tea consumption and breast cancer risk.
Table I. Green tea consumption and breast cancer risk
Study (reference)
Design Study
period
Population No. of cases/ No. of
Lowest
no. of
exposure exposure
non-cases
levels
level
Cohort studies
Suzuki 2004: Cohort 1 (27) Cohort 1984–1992 Japan
Suzuki 2004: Cohort 2 (27) Cohort 1990–1997 Japan
Key 1999 (16)
Cohort 1969–1993 Japan
103/14 306
119/20 476
405/34 332
4
4
3
51 cup/day
51 cup/day
1 cup/day
Highest
exposure
level
Percent in
RR (95% CI)
lowest, highest for highest versus
exposure levels lowest exposure level
5 cups/day
5 cups/day
5 cups/day
18%, 43%
29%, 26%
13%, 28%
Summary OR: cohort studies
Population-based case–control (PCC) study
Wu 2003 (30)
PCC
1995–1998 USA
Summary OR: all studies
1.17 (0.67–2.05)
0.61 (0.36–1.06)
0.86 (0.62–1.21)
0.85 (0.66–1.09)
501/593
3
Non-drinkers 485.7 ml/day 22%, 10%
0.47 (0.26–0.85)
0.78 (0.61–0.98)
Test for homogeneity among all studies: Q ¼ 5.95 based on 3 degrees of freedom P ¼ 0.11. Summary OR was based on fixed effect models.
Test for homogeneity among all cohort studies: Q ¼ 2.71 based on 2 degrees of freedom P ¼ 0.26. Summary OR was based on fixed effect models.
Test for homogeneity between study designs (cohort versus case–control): Q ¼ 3.26 based on 1 degree of freedom P ¼ 0.07.
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Suzuki 2004a
C.-L.Sun et al.
There was no significant heterogeneity among the study
results (P ¼ 0.11). Overall summary OR showed an 20%,
statistically significant reduction in risk of breast cancer
associated with high intake of green tea (summary OR ¼
0.78, 95% CI ¼ 0.61–0.98). The risk reduction was stronger
among Asian women in Los Angeles, California (OR ¼ 0.47,
95% CI ¼ 0.26–0.85) (30) than among native Japanese in
Japan (summary OR for cohort studies ¼ 0.85, 95% CI ¼
0.66–1.09). There was no indication of publication bias from
either visualization of the funnel plot or the Egger’s test
(intercept ¼ 0.19, P ¼ 0.83) (Figure 2).
Begg's funnel plot with pseudo 95% confidence limits
.5
-.
5
-1
0
.1
.2
.3
s.e. of: LOGRR
Fig. 2. Funnel plot of green tea consumption and breast cancer risk.
Table II. Black tea consumption and breast cancer risk
Study (reference)
Cohort studies
Suzuki 2004 (27)
Michels 2002 (22)
Key 1999 (16)
Goldbohm 1996 (15)
Zheng 1996 (31)
No. of cases/ No. of Lowest
levels exposure
no. of
level
non-cases
Design Study
period
Population
Cohort
Cohort
Cohort
Cohort
Cohort
Japan
222/34 782
Sweden
1271/57 765
Japan
342/34 332
The Netherland 507/1376
USA
1015/10 056
1984–1997
1987–1997
1969–1993
1986–1990
1986–1993
3
5
3
6
4
Never
1 cup/week
1 cup/week
51 cup/day
Never/monthly
Highest
exposure
level
RR (95% CI)
Percent
for highest
in lowest,
highest levels versus lowest level
Daily
4þ cups/day
5þ cups/day
5þ cups/day
2þ cup /day
NA
32%,
62%,
11%,
58%,
8%
15%
19%
9%
Summary OR: all cohort studies
Summary OR: cohort studies excluding the two Japanese studies
Population-based case–control (PCC) studies
Wu 2003 (30)
PCC
1995–1998
Mannisto 1999 (20)
PCC
1990–1995
McLaughlin 1992 (21) PCC
1982–1984
Ewertz 1990 (13)
PCC
1983–1984
Scharier 1987 (25)
PCC
1973–1980
Lubin 1985 (19)
PCC
1975–1979
USA
Finland
USA
Denmark
USA
Israel
501/593
310/454
1617/1617
1474/1322
1510/1882
804/804
Summary OR: HCC studies
Summary OR: all case–control studies
Summary OR: all studies
(0.77–2.69)
(0.91–1.40)
(0.82–1.48)
(0.86–1.99)
(0.92–1.41)
1.15 (1.02–1.31)
1.15 (1.00–1.33)
3
5
2
5
6
4
Non-drinkers
0
Never
0
0
0
487.5 ml/day
4150 g/day
Ever
5þ cups/day
5þ cups/day
4þ cups/day
22%,
20%,
21%,
17%,
33%,
28%,
11%
20%
79%
7%
0.6%
10%
Summary OR: PCC studies
Hospital-based case–control (HCC) studies
Tavani 1998 (28)
HCC
1983–1994 Italy
Rosenberg 1985 (24)
HCC
1975–1982 USA
1.44
1.13
1.10
1.31
1.14
0.81
0.89
0.97
0.99
0.60
0.80
(0.49–1.34)
(0.50–1.57)
(0.81–1.16)
(0.69–1.42)
(0.20–1.90)
(0.40–1.80)
0.94 (0.81–1.09)
5882/5399
2645/1476
2
4
No
0
1 cup/day
5þ cups/day
21%, 79%
55%, 6%
0.94 (0.85–1.03)
0.60 (0.50–0.90)
0.77 (0.50–1.19)
0.91 (0.84–0.98)
0.98 (0.88–1.09)
Test for heterogeneity among all studies: Q ¼ 20.54 based on 12 degrees of freedom P ¼ 0.06. Summary OR was based on random effect model.
Test for heterogeneity among all cohort studies: Q ¼ 0.98 based on 4 degrees of freedom P ¼ 0.91. Summary OR was based on fixed effect model.
Test for heterogeneity among all case–control studies: Q ¼ 9.70 based on 7 degrees of freedom P ¼ 0.21. Summary OR was based on fixed effect model.
Test for heterogeneity between study designs (cohort and case–control): Q ¼ 9.75 based on 1 degrees of freedom P ¼ 0.002.
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LOGRR
0
Black tea
Thirteen studies, including five cohort studies (15,16,22,
27,31) and eight case–control studies (13,19–21,24,25,28,30),
were included in the meta-analysis on black tea consumption
and breast cancer risk. Two cohort studies were conducted in
Europe (15,22), one in the US (31) and the remaining two
in Japan (16,27). Three case–control studies were conducted
in Europe (13,20,28), four in the US (21,24,25,30) and one in
the Middle East (19).
There was statistically significant heterogeneity in results
across the 13 studies (P ¼ 0.06). The summary OR based on all
studies indicated no association between black tea consumption and breast cancer risk (summary OR ¼ 0.98; 95% CI ¼
0.88–1.09) (Table II and Figure 3). There was no indication of
publication bias from either visualization of the funnel plot
or the Egger’s test (intercept ¼ 0.03, P ¼ 0.71) (Figure 4).
Although the results across all studies were heterogeneous,
results from either cohort studies alone (P ¼ 0.91) or case–
control studies alone (P ¼ 0.21) did not reject the homogeneity
hypothesis. The summary OR from all cohort studies showed a
modest increase (summary OR ¼ 1.15, 95% CI ¼ 1.02–1.31)
while the summary OR from all case–control studies showed a
modest decrease in risk of breast cancer (summary OR ¼ 0.91,
95% CI ¼ 0.84–0.98) associated with high black tea intake.
There was a statistically significant difference in the summary
OR from the cohort studies and the one calculated from the
case–control studies. Exclusion of the two cohort studies from
Japan, where black tea consumption is rare, did not materially
change the cohort study summary OR (summary OR ¼ 1.15,
95% CI ¼ 1.00–1.33). When we separated the populationbased case–control studies from their hospital-based
Tea and breast cancer risk
Suzuki 2004
Michels 2002
Key 1999
Goldbohm 1996
Zheng 1996
Wu 2003
Mannisto 1999
McLaughlin 1992
Ewertz 1990
Scharier 1987
Lubin 1985
Tavani 1998
Rosenberg 1985
Combined
.5
.2
RR
1
1. 5
2
2. 5
Begg's funnel plot with pseudo 95% confidence limits
LOGRR
1
0
-1
0
.2
s.e. of:LOGRR
.4
.6
Fig. 4. Funnel plot of black tea consumption and breast cancer risk.
counterparts, we noted a stronger association from hospitalbased (summary OR ¼ 0.77, 95% CI ¼ 0.50–1.19)
than population-based studies (summary OR ¼ 0.94, 95% CI
¼ 0.81–1.09). Since menstrual (such as age at menarche,
menopausal status) and reproductive (such as parity, age at
first birth) factors are established major risk factors for breast
cancer, we separated the case–control studies by whether any
menstrual/reproductive risk factors were adjusted for in the
statistical analysis. We noted a stronger association in the four
studies (13,19,24,25) that did not adjust for any menstrual or
reproductive risk factors (summary OR ¼ 0.73, 95% CI ¼
0.59–0.91) compared with the four studies (20,21,28,30) that
did (summary OR ¼ 0.94, 95% CI ¼ 0.87–1.02).
Discussion
This meta-analysis evaluated the association between green
tea and black tea consumption and breast cancer risk based on
all published epidemiological studies. There is suggestion that
green tea but not black tea consumption is related to a
decreased risk of breast cancer. Although we failed to observe
any publication bias visually or in formal statistical testing, we
would caution that the number of published studies on this
topic is too small for the results to be conclusive.
Overall, there is no evidence of heterogeneity among the
four studies (16,27,30) on green tea and breast cancer risk. In
addition, there is no evidence of heterogeneity across the three
cohort studies whose summary result indicates a modest breast
cancer risk reduction associated with high green tea intake
(summary OR ¼ 0.85, 95% CI ¼ 0.66–1.09). Although Key
et al. (17) examined tea intake in a specialized cohort, majority
of subjects were atomic bomb survivors of Hiroshima and
Nagasaki, Japan, there is no evidence that these subjects’
unique experience in August 1945 could have a confounding
effect on the observed green tea-breast cancer association
noted in that study. Patterns of green tea intake were comparable between the three Japanese cohorts (16,27) (see Table I).
However, the single case–control study by Wu et al. [The
Los Angeles Asian Breast Cancer Study, ref. (30)] showed a
considerably stronger green tea–breast cancer association relative to the overall cohort study result, and the test for homogeneity between study design (cohort versus case–control)
reached borderline statistical significance (P ¼ 0.07). There
are some important differences between the cohort studies in
Japan and the Los Angeles Asian Breast Cancer Study. The
Japanese cohort studies suffer from a relative lack of unexposed subjects. In Japan, where green tea drinking is pervasive,
only 2% of the population are non-drinkers of green tea (23).
In contrast, 22% of the controls in Wu et al. were either nondrinkers or occasional (51 cup/month) drinkers of green tea
(30). In the Japanese studies, only intake frequency was asked
while Wu et al. assessed both frequency and usual amounts
drunk each time. Wu et al. also reported that the beneficial
effect of green tea on breast cancer risk was primarily observed
among women with low soy intake (30) and soy intake was
high in Japan (36). Thus, differences in the prevalence and
range of exposure to green tea and other dietary cofactors may
explain, at least partly, the disparate findings between the
study among Asians in Los Angeles (30) and those among
natives of Japan (16,27).
In contrast to green tea, there is no overall protective effect
of black tea on breast cancer risk. Interestingly, all five
cohort studies (15,16,22,27,31) reported increased risk, with
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Fig. 3. Meta-analysis of black tea consumption and breast cancer risk.
C.-L.Sun et al.
1314
Given the relative paucity of human data, prospective cohort
studies with a wide range of green tea exposure and longer
duration of follow-up are needed to affirm the protective effect
of green tea on human breast cancer development. Current
epidemiological data do not support a role for black tea in
protection against breast cancer in humans. Cohort studies
with longer duration of follow-up are needed to elucidate the
effect of black tea on different stages of breast cancer development. Since genetic and lifestyle/dietary cofactors may
influence the effect of green/black tea on breast carcinogenesis
(29,30,43), future studies should address the possible interaction effects between tea and other dietary/genetic cofactors.
Conflict of Interest Statement: None declared.
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a statistically significant summary OR of 1.15. The summary
OR did not change materially after exclusion of the two Japanese studies (16,27), where black tea intake is relatively rare
and thus raising doubts on a causal interpretation of the
observed positive black tea–breast cancer association. All
three US/Europe-based cohort studies assessed tea intake at
the time of baseline interview. The follow-up periods of these
three cohort studies ranged from 4 to 10 years. Recently, we
noted higher levels of circulating estrogens in black tea drinkers than in non-tea drinkers, while estrogen levels were lower
in green tea drinkers than in non-tea drinkers (37). It is well
established in experimental studies that estrogen is a strong
promoter of mammary carcinogenesis [reviewed in (38)].
Hence, we speculate that the overall cohort findings are compatible with the notion of black tea intake having a late-stage,
promotional effect on breast cancer, possibly via its effect on
circulating estrogen levels. The summary OR for breast cancer
associated with high consumption of back tea based on case–
control studies was 0.91 (95% CI ¼ 0.84–0.98). However, we
noted a weaker association in population-based (summary OR
¼ 0.94, 95% CI ¼ 0.81–1.09) versus hospital-based studies
(summary OR ¼ 0.77, 95% CI ¼ 0.50–1.19). We also noted a
weaker association in studies adjusted for major menstrual/
reproductive risk factors for breast cancer (summary OR ¼
0.94, 95% CI ¼ 0.87–1.02) than those which made no attempt
to adjust for any menstrual/reproductive risk factors for breast
cancer. Therefore, we conclude that the overall evidence do
not support black tea drinking as having a protective effect on
breast cancer.
There has been extensive research into the possible anticarcinogenic mechanisms of tea and its polyphenols, and
many of these mechanistic studies relate specifically to the
catechins. In experimental studies involving breast cancer cell
lines, EGCG, the major catechin in green tea, has been shown
to suppress cell viability and induce apoptosis by downregulation of telomerase (5), and to inhibit angiogenesis by
reducing expression of vascular endothelial growth factor in a
dose-dependent manner (6). Epigallocatechin, another major
catechin in green tea, also has strong effects in inducing apoptosis and inhibiting growth of breast cancer cells in vitro (3).
Green tea catechins can increase hepatic glucuronidation of
estrone and estradiol in animal studies (39) and have been
shown to inhibit human placental aromatase, an enzyme
which converts androstenedione to estrone (40). Hence, if the
beneficial effect of tea on breast cancer risk comes mainly
from the tea catechins, an explanation for the relative lack of
risk reduction associated with black tea drinking can be due to
the much lower level of catechins in black tea compared with
green tea (up to 10-fold difference in catechin contents) (2).
Compared with green tea, black tea has been shown to be a less
potent inhibitor of tumor progression in a mouse model of
a hormone-dependent human breast tumor (41). In addition,
as mentioned previously, levels of circulating estrogens were
higher in Singapore Chinese women who drank black tea
regularly relative to their non-tea drinking counterparts,
while lower levels of circulating estrogens were found
among regular green tea drinkers compared with non-tea
drinkers (37). Furthermore, in a study of Caucasian women
in The Netherlands, serum levels of prolactin, another female
hormone implicated in breast carcinogenesis, has been shown
to correlate positively with black tea consumption (42).
In summary, the current epidemiologic literature supports
the hypothesis that green tea protects against breast cancer.
Tea and breast cancer risk
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Received July 6, 2005; revised October 27, 2005;
accepted November 12, 2005
1315
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