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American Journal of Epidemiology Advance Access originally published online on December 8, 2006
American Journal of Epidemiology 2007 165(5):505-513; doi:10.1093/aje/kwk040
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American Journal of Epidemiology Copyright © 2006 by the Johns Hopkins Bloomberg School of Public Health All rights reserved; printed in U.S.A.

ORIGINAL CONTRIBUTIONS

Reproductive Risk Factors for Cutaneous Melanoma in Women: A Case-Control Study

C. Suzanne Lea1, Elizabeth A. Holly2, Patricia Hartge3, Jennifer S. Lee4,5, DuPont Guerry, IV6, David E. Elder6, Allan Halpern7, Richard W. Sagebiel8 and Margaret A. Tucker5

1 Statistics and Epidemiology Program, Research Triangle Institute International, Research Triangle Park, NC
2 Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA
3 Epidemiology and Biostatistics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD
4 Division of Endocrinology and Metabolism, Department of Medicine, University of California San Francisco, San Francisco, CA
5 Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD
6 Pigmented Lesion Study Group, School of Medicine, University of Pennsylvania, Philadelphia, PA
7 Dermatology Section, Memorial Sloan-Kettering Cancer Center, New York, NY
8 Melanoma Clinic, University of California San Francisco, San Francisco, CA

Correspondence to Dr. Margaret Tucker, Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 6120 Executive Boulevard, EPS7122, Rockville, MD 20892-7236 (e-mail: tuckerp{at}mail.nih.gov).

Received for publication April 15, 2006. Accepted for publication July 26, 2006.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Reproductive hormonal factors may have a potential role in cutaneous melanoma. This study estimated the risk of melanoma in women related to self-reported changes in nevi during pregnancy, while using oral contraceptives and/or hormone replacement therapy. Trained interviewers administered a questionnaire obtaining information about oral contraceptive use, hormone replacement therapy, reproductive history, sun exposure, occupation, and medical history from 318 Caucasian women newly diagnosed between 1991 and 1992 from two pigmented lesion clinics in San Francisco, California, and Philadelphia, Pennsylvania. A total of 395 frequency-matched control participants were recruited from hospital-affiliated outpatient clinics. Clinicians conducted skin examinations to assess the number and type of nevi, extent of freckling, solar damage, and skin type. For women aged less than 55 years, there was an association between a livebirth 5 years before diagnosis (odds ratio = 2.6, 95% confidence interval: 1.3, 5.3) and between number of births and melanoma risk (for ≥3 births: odds ratio = 3.3, 95% confidence interval: 1.7, 6.5; ptrend < 0.001). Changes in nevi during recent pregnancies were a risk factor for melanoma, based upon small numbers (odds ratio = 2.9, 95% confidence interval: 1.1, 8.1). Oral contraceptive use and hormone replacement therapy were not associated with melanoma risk.

case-control studies; contraceptives, oral; hormone replacement therapy; melanoma; nevus, pigmented; parity

Abbreviations: HRT, hormone replacement therapy; OC, oral contraceptive


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Striking differences in age-specific patterns of cutaneous melanoma incidence between women and men have suggested modulation of melanoma risk by sex (1, 2). Exogenous hormone use (oral contraceptives (OCs) and hormone replacement therapy (HRT)) and reproductive factors have been investigated in multiple studies (3). Although variations in estrogen and progesterone levels have been the primary focus of investigations of these differences, behavioral patterns also may play a role (4).

A majority of case-control studies, including a meta-analysis (3), concluded that OC use is unlikely to increase a woman's risk for melanoma (5–20), although other studies have reported associations between melanoma and some exogenous hormone use (1, 9, 19, 21–24). Epidemiologic studies using indicators of endogenous hormonal variation, such as number of children, age at menarche or menopause, and age at first birth, also have shown mixed results for melanoma risk (9, 12–14, 17, 20, 21), and multiple case reports of skin changes or melanoma occurring during or shortly after pregnancy have been published (25–27). The purpose of the present analysis was to address the role of reproductive factors and exogenous hormone use in the etiology of melanoma.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
This case-control study recruited women from referral centers in the San Francisco Bay area, California (48 percent), and Philadelphia area, Pennsylvania (52 percent), to examine factors associated with melanoma risk. Detailed study methods have been published (4, 28–32) and are summarized briefly below. The project was approved by the institutional review boards of the National Cancer Institute, Bethesda, Maryland; Westat, Inc., Rockville, Maryland; University of California San Francisco, San Francisco, California; and University of Pennsylvania, Philadelphia, Pennsylvania.

Eligible study participants included Caucasian women between 20 and 79 years of age with incident, invasive cutaneous melanoma diagnosed between January 1, 1991, and December 31, 1992. Patients were examined at the Pigmented Lesion Clinic at the Hospital of the University of Pennsylvania (Philadelphia, Pennsylvania) or at the Melanoma Clinic of the University of California San Francisco (San Francisco, California). Patients were enrolled in the study at their initial evaluation related to their index melanoma diagnosis. All diagnoses were confirmed by histologic review (W. H. Clark, D. E. Elder, R. W. Sagebiel). After exclusions (nine women with a previous melanoma and four non-Whites), 318 women met the case definition. A total of 395 frequency-matched (age, race, geographic study location) control participants were recruited from outpatient clinics with catchment areas similar to the melanoma clinics at the University of California San Francisco and University of Pennsylvania (28, 29). No pregnant women were enrolled.

After obtaining written, informed consent, trained staff conducted interviews in English that lasted approximately 45 minutes and included participants' history of sun exposure, occupation, residence, medication use, including OC and HRT use, reproductive life, and family history of melanoma.

We inquired about changes in nevi during each pregnancy among women who had been pregnant in the past 5 years, during the use of OCs, or during the use of HRT for any reason. Participants were asked if there had been changes in the number or appearance of any moles; whether new moles had appeared; and whether existing moles had become darker, larger, or more irregular in outline, had disappeared, or had been removed by a physician. Recall of these events during pregnancy was elicited from women who had been pregnant only during the previous 5 years to minimize recall bias. Each participant's examiner recorded the number of nevi greater than 2 mm in size by categories of different sizes, the number of dysplastic nevi, freckling pattern, skin color, and solar damage.

Expert senior examiners confirmed the dysplastic nevus status for each participant. Pairwise agreement among expert clinicians occurred, on average, 87 percent of the time (29). Lesions not agreed upon by examiners were not counted as dysplastic nevi but were deemed indeterminate (29).

We evaluated a variety of recognized clinical, phenotypic, and sun exposure risk factors for model inclusion. Atypical nevi, freckling, and education were risk factors for melanoma in earlier analyses of these data (29). However, family history, phenotypic features, and sun exposure factors were not confounders for primary variables in this report. Unless otherwise stated, statistical models include categorical variables for age group (<55, 55–64, ≥65 years), educational level (less than high school, post-high school, and college graduate), study location (San Francisco, California, or Philadelphia, Pennsylvania), confirmed dysplastic nevus status (absent vs. present), total number of nevi (0–100 or >100), and extent of freckling (none to few or moderate to extensive). Persons with no or indeterminate clinically dysplastic nevi were categorized as having no dysplastic nevi, and persons with histologic evidence but no clinical evidence of dysplastic nevi and those with one or more clinically verified dysplastic nevi were categorized as having dysplastic nevi (29). The "ever pregnant" category included women who did not give birth.

The referent group in analyses for exogenous hormone use (OCs and HRT) was women who reported never having taken exogenous reproductive hormones. For OC and HRT use, restricting analyses to women aged 55 years or more showed little difference from the analyses with all ages combined; thus, no stratification by age is presented for OC or HRT use. Total reproductive life was computed as the duration of menstruation minus the duration of OC use (if any). For menopausal women, the duration of menstruation was computed from the age at first period to the age at last period. For premenopausal women, the duration of menstruation was computed from the age at first period to the age at interview.

Odds ratios with 95 percent confidence intervals were computed with SAS, version 8.2, software (SAS Institute, Inc., Cary, North Carolina) to estimate the relative risk of melanoma (hereafter called "risk") by use of logistic regression models while controlling for confounding variables. Odds ratios are not presented for cells with fewer than five observations. A significance level of 0.05 (two sided) was used for all tests. Skin changes were assessed in separate models that included stratum-specific estimates for no exogenous hormone use, use with no skin changes, and use with skin changes for OCs and HRT. This same paradigm applied to analyses of skin changes during pregnancy. Study participants with unknown parameters for any factor in the multivariate model were excluded from analyses. All histologic types of melanoma were combined, because no differences by histologic type were found.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
Seventy-seven percent of cases were diagnosed with superficial spreading melanoma, 12 percent with nodular melanoma, and 11 percent with a mixture of other melanoma types. Four cases did not have the melanoma subtype available. There were no significant differences between cases and controls by age, study location, or education, except that more controls than cases had graduated from college. More cases than controls had dysplastic nevi, total nevi, freckling, light hair and eyes, and total number of sunburns. More controls than cases reported ever having been pregnant (table 1). There were no differences in the mean values between cases and controls by age at menarche or menopause, age at first or last use of either type of exogenous hormones, duration of use or time since use for OCs or HRT, or age at first or last pregnancy (table 2). Twenty-three percent of cases and twenty-three percent of controls reported never having used exogenous hormones of any kind.


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  		TABLE 1. Characteristics of women with cutaneous melanoma and controls, San Francisco Bay area, California, and Philadelphia, Pennsylvania, 1991–1992

 

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  		TABLE 2. Oral contraceptive use, hormone replacement therapy, and reproductive and pregnancy factors by case and control status, San Francisco Bay area, California, and Philadelphia, Pennsylvania, 1991–1992

 
Sixty-five percent of cases and 60 percent of controls reported a history of OC use, whereas 19 percent of cases and 25 percent of controls reported any HRT use. The odds ratios showed no significant associations between melanoma and ever/never OC use, duration of OC use, age at first use, years since first and last OC use, and calendar year of first OC use. The majority of women reported OC use after 1970. The odds ratios for the association between melanoma and ever/never HRT use, duration of HRT use, age at first HRT use, and years since first and last HRT use were inverse and had confidence limits that overlapped unity.

Odds ratios for the use of OCs and/or HRT use were consistently elevated in relation to a history of changed appearance of nevi (larger, darker, or more irregular), development of new nevi, and having had nevi removed by a physician, although cell sizes for these comparisons were small (table 3).


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  		TABLE 3. Adjusted odds ratios and 95% confidence intervals for cutaneous melanoma and skin changes during oral contraceptive use and hormone replacement therapy, San Francisco Bay area, California, and Philadelphia, Pennsylvania, 1991–1992

 
Women with melanoma were more likely to have been pregnant compared with controls (odds ratio = 1.7, 95 percent confidence interval: 1.0, 2.6) (table 4). The timing of pregnancy, whether 5 years or less or more than 5 years before diagnosis or interview, conferred an elevated odds ratio among women aged less than 55 years when compared with women who never had been pregnant. In parous women, risk of melanoma increased with an increasing number of livebirths, nearly tripling with two or more livebirths (ptrend < 0.001) and increasing more than threefold in women aged less than 55 years at diagnosis. There was no effect of parity in women aged 55 years or more at diagnosis. Among women who were aged less than 55 years at diagnosis, having a livebirth within the last 5 years conferred a 2.6-fold higher risk than no previous livebirth. The total years of reproductive life were not associated with risk.


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  		TABLE 4. Adjusted odds ratios and 95% confidence intervals for cutaneous melanoma and reproductive factors by age category at diagnosis or interview, San Francisco Bay area, California, and Philadelphia, Pennsylvania, 1991–1992

 
Women with melanoma who had been pregnant 5 years before diagnosis or interview reported change in the number or appearance (larger, darker, or more irregular) of existing nevi, and they reported the appearance of new nevi (table 5). However, the numbers were small, and confidence intervals were correspondingly wide.


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  		TABLE 5. Adjusted odds ratios and 95% confidence intervals for cutaneous melanoma and skin changes by pregnancy within last 5 years, San Francisco Bay area, California, and Philadelphia, Pennsylvania, 1991–1992

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
These data indicate that pregnancy and an increasing number of livebirths were associated with an elevated risk of cutaneous melanoma before the age of 55 years. There were suggestive findings based on small numbers that nevus changes and pregnancy within the 5 years prior to melanoma diagnosis were associated with increased risk. Some nevus changes were related to exogenous OC and HRT use and melanoma risk.

Although these parity results are not consistent with those from some previous studies (8–10, 12–14, 16, 17, 19, 20, 33), few of the earlier studies had adequate numbers to restrict analyses to women aged less than 55 years at diagnosis and pregnancy within 5 years prior to diagnosis. Further, some of the inconsistencies among previous studies may be related to geographic and temporal factors in reproductive behavior.

Our results suggest that changes in nevi during pregnancy may identify a group of women at increased risk of melanoma. The changes in nevi include the "A," "B," "C," "D," and "E" warning signs for melanoma, such as "A" for asymmetry, "B" for irregular borders, "C" for color changes, "D" for increases in size or diameter, and "E" for evolution over time (34). Our results support the suggestion that nevus changes should be tracked during pregnancy in high-risk women. It is biologically plausible that pregnancy would be causally related to pigmentation and growth of nevi. Levels of melanocyte-stimulating hormone that stimulate the production of melanin and related pigmentation increase during pregnancy. A burst of melanocyte-stimulating hormone production primarily during the first trimester may increase cell division. Growth hormone, also elevated, can activate the melanocyte-stimulating hormone signaling pathway, intensifying the effect.

Pregnancy status may allow clinical expression of previously damaged melanocytes and their clonal progeny (35), possibly through the immunosuppression that permits tolerance of the fetus. Our results that higher risk of melanoma during recent pregnancy correlated with increasing number of children may be related to sunlight exposure during maternal outdoor activity with her other children.

In studies presenting clinical cases, changes in the appearance of nevi have been documented during pregnancy (26, 27, 36, 37). In an earlier observational study that assessed skin changes during pregnancy, the authors found no increased effect on melasma of the face or nonfacial areas of the skin during pregnancy (16). Our results are consistent with these earlier results.

Whereas the number of cases and controls and detailed phenotyping are major strengths of this study, there are possible limitations. Since this study was clinic based, it may not necessarily be representative of the general population (29), and some residual confounding may exist. Small cell sizes generated by cross-classification of nevi changes and exogenous hormone use resulted in wide confidence intervals that overlapped unity. The exogenous reproductive hormone use and nevus changes reported while using OCs and/or HRT may be differentially recalled in cases and controls, resulting in the potential for bias. However, we found no consistent differences between cases and controls. Since skin assessment was restricted to pregnancy within 5 years of diagnosis, recall bias was minimized.

OC use does suggest a possible elevated risk among a small proportion of women who reported a changed appearance of nevi or development of new nevi. Careful examination and further research are warranted on this smaller subgroup. Results further suggest that pregnancy may be a marker for a modest elevation of melanoma risk, especially in multiparous women. These findings should serve as a reminder that women (and their partners) should do regular skin self-examination to detect changing or otherwise suspicious pigmented lesions.


   ACKNOWLEDGMENTS
 
This research was supported by the Intramural Research Program of the National Institutes of Health and the National Cancer Institute and by funding from National Cancer Institute grants CP33045 and CPO568 to the University of California San Francisco (E. A. Holly, Principal Investigator).

Conflict of interest: none declared.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

  1. Holly EA, Cress RD, Ahn DK. (1994) Cutaneous melanoma in women: ovulatory life, menopause, and use of exogenous estrogens. Cancer Epidemiol Biomarkers Prev 3:661–8.[Abstract]
  2. Ries LAG, Harkins D, Krapcho M, et al. (2006) SEER cancer statistics review, 1975 –2003(National Cancer Institute, Bethesda, MD) (http://seer.cancer.gov/csr/1975_2003/).
  3. Karagas MR, Stukel TA, Dykes J, et al. (2002) A pooled analysis of 10 case-control studies of melanoma and oral contraceptive use. Br J Cancer 86:1085–92.[CrossRef][ISI][Medline]
  4. Fears TR, Bird CC, Guerry D 4th, et al. (2002) Average midrange ultraviolet radiation flux and time outdoors predict melanoma risk. Cancer Res 62:3992–6.[Abstract/Free Full Text]
  5. Adam SA, Sheaves JK, Wright NH, et al. (1981) A case-control study of the possible association between oral contraceptives and malignant melanoma. Br J Cancer 44:45–50.[ISI][Medline]
  6. Bain C, Hennekens CH, Speizer FE, et al. (1982) Oral contraceptive use and malignant melanoma. J Natl Cancer Inst 68:537–9.[ISI][Medline]
  7. Helmrich SP, Rosenberg L, Kaufman DW, et al. (1984) Lack of an elevated risk of malignant melanoma in relation to oral contraceptive use. J Natl Cancer Inst 72:617–20.[ISI][Medline]
  8. Holman CDJ, Armstrong BK, Heenan PJ. (1984) Cutaneous malignant melanoma in women: exogenous sex hormones and reproductive factors. Br J Cancer 50:673–80.[ISI][Medline]
  9. Gallagher RP, Elwood JM, Hill GB, et al. (1985) Reproductive factors, oral contraceptives and risk of malignant melanoma: Western Canada Melanoma Study. Br J Cancer 52:901–7.[ISI][Medline]
  10. Green A and Bain C. (1985) Hormonal factors and melanoma in women. Med J Aust 142:446–8.[ISI][Medline]
  11. Gallagher RP, Elwood JM, Hill GB. (1986) Risk factors for cutaneous malignant melanoma: the Western Canada Melanoma Study. Recent Results Cancer Res 102:38–55.[Medline]
  12. Osterlind A, Tucker MA, Stone BJ, et al. (1988) The Danish case-control study of cutaneous malignant melanoma. III. Hormonal and reproductive factors in women. Int J Cancer 42:821–4.[ISI][Medline]
  13. Zanetti R, Franceschi S, Rosso S, et al. (1990) Cutaneous malignant melanoma in females: the role of hormonal and reproductive factors. Int J Epidemiol 19:522–6.[Abstract/Free Full Text]
  14. Hannaford PC, Villard-Mackintosh L, Vessey MP, et al. (1991) Oral contraceptives and malignant melanoma. Br J Cancer 63:430–3.[ISI][Medline]
  15. Palmer JR, Rosenberg L, Strom BL, et al. (1992) Oral contraceptive use and risk of cutaneous malignant melanoma. Cancer Causes Control 3:547–54.[CrossRef][ISI][Medline]
  16. Holly EA, Cress RD, Ahn DK. (1995) Cutaneous melanoma in women. III. Reproductive factors and oral contraceptive use. Am J Epidemiol 141:943–50.[Abstract/Free Full Text]
  17. Westerdahl J, Olsson H, Masback A, et al. (1996) Risk of malignant melanoma in relation to drug intake, alcohol, smoking and hormonal factors. Br J Cancer 73:1126–31.[ISI][Medline]
  18. Gefeller O, Hassan K, Wille L. (1998) Cutaneous malignant melanoma in women and the role of oral contraceptives. Br J Dermatol 138:122–4.[CrossRef][ISI][Medline]
  19. Smith MA, Fine JA, Barnhill RL, et al. (1998) Hormonal and reproductive influences and risk of melanoma in women. Int J Epidemiol 27:751–7.[Abstract/Free Full Text]
  20. Naldi L, Altieri A, Imberti GL, et al. (2005) Cutaneous malignant melanoma in women. Phenotypic characteristics, sun exposure, and hormonal factors: a case-control study from Italy. Ann Epidemiol 15:545–50.[CrossRef][ISI][Medline]
  21. Holly EA, Weiss NS, Liff JM. (1983) Cutaneous melanoma in relation to exogenous hormones and reproductive factors. J Natl Cancer Inst 70:827–31.[ISI][Medline]
  22. Beral V, Evans S, Shaw H, et al. (1984) Oral contraceptive use and malignant melanoma in Australia. Br J Cancer 50:681–5.[ISI][Medline]
  23. Le MG, Cabanes PA, Desvignes V, et al. (1992) Oral contraceptive use and risk of cutaneous malignant melanoma in a case-control study of French women. Cancer Causes Control 3:199–205.[CrossRef][ISI][Medline]
  24. Feskanich D, Hunter DJ, Willett WC, et al. (1999) Oral contraceptive use and risk of melanoma in premenopausal women. Br J Cancer 81:918–23.[CrossRef][ISI][Medline]
  25. Slingluff CL Jr, Reintgen DS, Vollmer RT, et al. (1990) Malignant melanoma arising during pregnancy. A study of 100 patients. Ann Surg 211:552–7.[ISI][Medline]
  26. Elling SV and Powell FC. (1997) Physiological changes in the skin during pregnancy. Clin Dermatol 15:35–43.[CrossRef][ISI][Medline]
  27. Mackie RM. (1999) Pregnancy and exogenous hormones in patients with cutaneous malignant melanoma. Curr Opin Oncol 11:129–31.[CrossRef][Medline]
  28. Hartge P, Holly EA, Halpern A, et al. (1995) Recognition and classification of clinically dysplastic nevi from photographs: a study of interobserver variation. Cancer Epidemiol Biomarkers Prev 4:37–40.[Abstract]
  29. Tucker MA, Halpern A, Holly EA, et al. (1997) Clinically recognized dysplastic nevi: a central risk factor for cutaneous melanoma. JAMA 277:1439–44.[Abstract]
  30. Goldstein AM, Chidambaram A, Halpern A, et al. (2002) Rarity of CDK4 germline mutations in familial melanoma. Melanoma Res 12:51–5.[CrossRef][ISI][Medline]
  31. Millen AE, Tucker MA, Hartge P, et al. (2004) Diet and melanoma in a case-control study. Cancer Epidemiol Biomarkers Prev 13:1042–51.[Abstract/Free Full Text]
  32. Jl Rutter, Bromley CM, Goldstein AM, et al. (2004) Heterogeneity of risk for melanoma and pancreatic and digestive malignancies: a melanoma case-control study. Cancer 101:2809–16.[CrossRef][ISI][Medline]
  33. Karagas MR, Zens MS, Stukel TA, et al. (2006) Pregnancy history and incidence of melanoma in women: a pooled analysis. Cancer Causes Control 17:11–19.[CrossRef][ISI][Medline]
  34. Abbasi NR, Shaw HM, Rigel DS, et al. (2004) Early diagnosis of cutaneous melanoma: revisiting the ABCD criteria. JAMA 292:2771–6.[Abstract/Free Full Text]
  35. McLean DI and Gallagher RP. (1997) Hormones, immunology, nevi, and melanoma. Arch Dermatol 133:783–4.[CrossRef][ISI][Medline]
  36. Ellis DL. (1991) Pregnancy and sex steroid hormone effects on nevi of patients with dysplastic nevus syndrome. J Am Acad Dermatol 25:467–82.[ISI][Medline]
  37. Grimes PE. (1995) Melasma: etiologic and therapeutic considerations. Arch Dermatol 131:1453–7.[Abstract]

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