ライフサイエンスコーパス: cervical cancer

1 y to improve prevention of HPV infection and cervical cancer.

2 ion affected survival in women with invasive cervical cancer.

3 d help to identify women with higher risk of cervical cancer.

4 may be an effective therapeutic modality for cervical cancer.

5 STAT3/IRF1 pathway for chemosensitization in cervical cancer.

6 raepithelial neoplasia and invasive squamous cervical cancer.

7 ociated with an increased risk of developing cervical cancer.

8 ts from the cohort of patients with advanced cervical cancer.

9 ly involved in initiation and progression of cervical cancer.

10 theless, functional p53 has been observed in cervical cancer.

11 lity of antiangiogenesis therapy in advanced cervical cancer.

12 n is a very effective treatment strategy for cervical cancer.

13 usceptibility to HPV infections that lead to cervical cancer.

14 nic PI3K mutation-mediated AKT activation in cervical cancer.

15 efer the cotesting approach to screening for cervical cancer.

16 can induce complete regression of metastatic cervical cancer.

17 average-risk women younger than 21 years for cervical cancer.

18 in several studies as a diagnostic marker of cervical cancer.

19 f ACT could mediate regression of metastatic cervical cancer.

20 reatments that can decrease the incidence of cervical cancer.

21 radicating tumors in the TC-1 mouse model of cervical cancer.

22 g certain cancers such as bladder cancer and cervical cancer.

23 recognized as the main etiologic factor for cervical cancer.

24 wide health threat and an etiologic agent of cervical cancer.

25 in the treatment of metastatic or recurrent cervical cancer.

26 apy in patients with metastatic or recurrent cervical cancer.

27 erall survival (OS) of women with stage IIIB cervical cancer.

28 only a few high- and low-risk HPV types for cervical cancer.

29 enesis, a mediator of disease progression in cervical cancer.

30 ts with recurrent, persistent, or metastatic cervical cancer.

31 extremely rare and aggressive neuroendocrine cervical cancer.

32 (HPV) screening will be the primary test for cervical cancer.

33 including human papillomavirus (HPV)-caused cervical cancer.

34 e agents of many human cancers, most notably cervical cancer.

35 ificant potential for the treatment of human cervical cancer.

36 has been established as the primary cause of cervical cancer.

37 and CIN and ultimately incidence of invasive cervical cancer.

38 females at higher risk for HPV infection and cervical cancer.

39 ovel recurrent HPV integrations at PTPN13 in cervical cancer.

40 erapeutic efficacy of Cucurbitacin D against cervical cancer.

41 accine protects against an additional 15% of cervical cancers.

42 pment for clinical treatment of prostate and cervical cancers.

43 levels of FOXM1 often observed in poor-risk cervical cancers.

44 s including penile, vulva, oropharyngeal and cervical cancers.

45 ICs and high-income countries for breast and cervical cancers.

46 2 years, persistent HPV16 causes half of all cervical cancers.

47 ases, 1,395 controls) were at lowest risk of cervical cancer (20-y risk: 8 cancers per 10,000 women)

48 Our model projected that among all cervical cancers, 50% and 75% of women acquired their ca

49 ,951,319 normal smears) and in situ/invasive cervical cancer (75,128 case and 375,640 control women),

50 es more than 12,000 women are diagnosed with cervical cancer, a disease principally caused by human p

51 intraepithelial neoplasia and early invasive cervical cancer adversely affect successful conception a

52 Herein, we evaluated the recurrence of cervical cancer after raloxifene therapy in our preclini

53 f human papillomavirus-associated metastatic cervical cancer after tumor-infiltrating adoptive T cell

54 irst abnormal cytology, in situ and invasive cervical cancer (all P < 0.02).

55 d vaccination could prevent 200,000 cases of cervical cancer and 100,000 deaths in some of the highes

56 distant metastasis was 13.7% (21 of 153) for cervical cancer and 11.8% (24 of 203) for endometrial ca

57 Results There were 153 patients with cervical cancer and 203 patients with endometrial cancer

58 in 179 countries prevented 690,000 cases of cervical cancer and 420,000 deaths during their lifetime

59 f HPV such as HPV16 are the leading cause of cervical cancer and a major cause of genital and orophar

60 HPV assays for use in primary screening for cervical cancer and also provide a framework for the com

61 The high-risk HPV types induce cervical cancer and encode an E7 oncoprotein that plays

62 this protocol were diagnosed with metastatic cervical cancer and had previously received platinum-bas

63 PV before sexual debut in terms of burden of cervical cancer and mortality.

64 as a risk factor for certain cancers such as cervical cancer and oral cancer as well, and the HPV onc

65 est for gliomas and sarcomas and highest for cervical cancer and oropharyngeal head and neck cancer.

66 hat wider implementation will help to reduce cervical cancer and precursors incidence.

67 insights into the treatment of HPV-positive cervical cancer and suggest that hyperthermia therapy co

68 s (HPV) infection is the cause of nearly all cervical cancers and a proportion of other anogenital an

69 nocarcinoma accounts for about 10-30% of all cervical cancers and clinically the lesion can be asympt

70 ction accuracy for the metastasis of primary cervical cancers and for tongue cancer survival.

71 HPV types 16 and 18 are found in over 70% of cervical cancers and produce the oncoprotein, early prot

72 el the dynamics of cell cycle in HeLa (human cervical cancer) and S. cerevisiae cells.

73 omavirus 18 (HPV18) is an etiologic agent of cervical cancer, and as expected, we found robust expres

74 cute myeloid, central nervous system tumour, cervical cancer, and breast cancer experienced 3.8, 2.7,

75 (HR-HPV) cause anogenital cancers, including cervical cancer, and head and neck cancers.

76 1 was overexpressed in oropharyngeal cancer, cervical cancer, and HPV(+) head and neck cancer tumors.

77 ccination coverage, changes in screening for cervical cancer, and risk behaviors for acquiring HPV.

78 gnosis and treatment of early breast cancer, cervical cancer, and selected childhood cancers; and wid

79 tly associated with oropharyngeal cancer and cervical cancer, and TGFbetaR1 was overexpressed in orop

80 ccines protect against 66% of HPV-associated cervical cancers, and a new nonavalent vaccine protects

81 rs such as renal cell carcinoma, ovarian and cervical cancers, and pancreatic neuroendocrine tumours

82 , 55.5; fatigue, 57.3; depression, 51.4) and cervical cancer (anxiety, 53.2; sleep disturbance, 53.4)

83 Development of therapeutic approaches for cervical cancer are hampered by a lack of mechanistic in

84 Breast and cervical cancer are major threats to the health of women

85 Since more than 99% of cervical cancers are caused by human papilloma virus (HP

86 in developed countries, prostate, lung, and cervical cancers are not among the most common cancers i

87 Breast and cervical cancers are the commonest cancers diagnosed in

88 used in screening risk and/or early stage of cervical cancer as well as assessing the efficacies of t

89 he etiologic agent of virtually all cases of cervical cancer, as well as a proportion of other epithe

90 hould start screening average-risk women for cervical cancer at age 21 years once every 3 years with

91 Cases were women (n = 1,341) diagnosed with cervical cancer at age 65-83 y between 1 April 2007 and

92 at age 50-64 y had one-sixth of the risk of cervical cancer at age 65-83 y compared with women who w

93 2019 could reduce age-standardised rates of cervical cancer at ages 25-64 years by 19%, from 15.1 in

94 coverage, European age-standardised rates of cervical cancer at ages 25-79 years will decrease by onl

95 wever, because women can now be screened for cervical cancer at intervals up to every 5 years, the qu

96 nce were performed on 30 women with advanced cervical cancers at three time points (within 2 weeks be

97 (K17) predicts poor outcome in patients with cervical cancer, at early or late stages of disease, sur

98 Bone involvement in patients with cervical cancer, being a rare event, is significant sinc

99 Cervical cancer, being the fourth leading cause of cance

100 64 y was associated with a 75% lower risk of cervical cancer between the ages 65 and 79 y (OR = 0.25,

101 tantly, high IRF1 expression in pretreatment cervical cancer biopsy cells was associated with a signi

102 wanted to examine whether IPSA could improve cervical cancer brachytherapy plans giving D90 < 6 Gy (w

103 elial cells and are causally associated with cervical cancer, but HPV infection is not sufficient for

104 in a pre-clinical orthotopic mouse model of cervical cancer by decreasing oncogenic miRNA-21, suppre

105 We obtained relative risks (RRs) of cervical cancer by screening history (never screened, re

106 Durable, complete regression of metastatic cervical cancer can occur after a single infusion of HPV

107 In this case-control study of 1,486 cervical cancer cases and 1,301 controls, we investigate

108 provide broader coverage and prevent 90% of cervical cancer cases worldwide.

109 to prevent 1 anogential warts (AGW) case or cervical cancer (CC) was similar for routine + catch-up

110 epresents a potential therapeutic option for cervical cancer (CC).

111 The efficacy of cervical cancer cell elimination was drastically increas

112 n, cells of the squamocolumnar junction, and cervical cancer cell line-derived spheroids.

113 prostate cancer cell lines and an aggressive cervical cancer cell line.

114 liferation of a conventional HPV-16 positive cervical cancer cell line.

115 shed oncogenic role of DEK in HPV-associated cervical cancer cell lines and keratinocytes, a function

116 of hyperthermia on HPV-positive cells using cervical cancer cell lines infected with HPV 16 and 18,

117 AT3 was also low or absent in cultured human cervical cancer cell lines, consistent with the in vivo

118 n and, in contrast to all other HPV-positive cervical cancer cell lines, they harbored a gain-of-func

119 ces apoptosis, and arrests the cell cycle in cervical cancer cell lines.

120 rexpressed in HPV-positive keratinocytes and cervical cancer cell lines.

121 xenograft in vivo in nude mice, and suppress cervical cancer cell migration and invasion.

122 of human cervical cancer cells in vitro and cervical cancer cell xenograft in vivo in nude mice, and

123 r expressed receptors, EGFR and p16/Ki-67 in cervical cancer cell, HeLa showed prominent SERS mapping

124 urther mechanistic investigations identified cervical cancer cell-derived IL6 as an important mediato

125 ed by LKB1-deficient A549 (lung) and HeLaS3 (cervical) cancer cell lines.

126 rbitacin D inhibited viability and growth of cervical cancer cells (CaSki and SiHa) in a dose-depende

127 GR), and the microRNA hsa-miR-21 (miR-21) in cervical cancer cells (HeLa).

128 Here we show that HeLa epithelial cervical cancer cells and 143B osteosarcoma cells expres

129 the nanoparticles can cross the membrane of cervical cancer cells and bring the co-entrapped donors

130 nfirmed an over-expression of p16 protein in cervical cancer cells and its association with disease p

131 presented study, single human adenocarcinoma cervical cancer cells are electrochemically investigated

132 Cucurbitacin D treatment of cervical cancer cells arrested the cell cycle in G1/S ph

133 tosis was observed in Cucurbitacin D treated cervical cancer cells as measured by enhanced Annexin V

134 K loss results in cell death in HPV-positive cervical cancer cells at least in part through p53 activ

135 We found that proliferation of cervical cancer cells can be blocked by DOHH inhibition

136 body weight) effectively inhibited growth of cervical cancer cells derived orthotopic xenograft tumor

137 Cervical cancer cells expressing K17 mutations in its NL

138 Proteomic and RNA analyses in HeLa cervical cancer cells identified two groups of proteins

139 nergistically to inhibit the growth of human cervical cancer cells in vitro and cervical cancer cell

140 Furthermore, we show that cervical cancer cells instructed primary cervical fibrob

141 illomavirus type 16 (HPV16) gene expression, cervical cancer cells permissive for HPV16 late gene exp

142 signaling inducing STAT3 activation rendered cervical cancer cells significantly more susceptible to

143 inogenesis and its impact on the response of cervical cancer cells to chemotherapeutic drugs.

144 ted to the tumor phenotype of HPV16-positive cervical cancer cells, as its depletion resulted in decr

145 could reduce metastasis and angiogenesis of cervical cancer cells, thereby constituting an adjuvant

146 s replication fork progression in HeLa human cervical cancer cells.

147 roRNAs (miR-145, miRNA-143, and miRNA34a) in cervical cancer cells.

148 mL(-1) for p16 protein and 28 cells for HeLa cervical cancer cells.

149 slation of the cooperative oncogene CCND1 in cervical cancer cells.

150 ate the effect of extracellular ATP on human cervical cancer cells.

151 RISPR/Cas9), the SIRT1 gene was removed from cervical cancer cells.

152 s, with male circumcision protecting against cervical cancer, cervical dysplasia, herpes simplex viru

153 , and pelvic recurrence for locally advanced cervical cancer clinically limited to the pelvis treated

154 ts Twenty-four patients were enrolled in the cervical cancer cohort.

155 al of HPV vaccination programs is to prevent cervical cancer, condyloma related to HPV types 6 and 11

156 80-2010 (cases) to those of women at risk of cervical cancer (controls).

157 intraepithelial neoplasia (CIN1- CIN3), and cervical cancer (CxCa) from multiple perspectives, revea

158 Application of our algorithms to real cervical cancer data identifies key genomic events in di

159 NA screening-a more sensitive test-to reduce cervical cancer death among older women.

160 To study the multistep process of cervical cancer development, we analyzed 128 frozen cerv

161 ix was used to estimate the lifetime risk of cervical cancer diagnosis and death.

162 ning is predicted to reduce lifetime risk of cervical cancer diagnosis by 18% and of death by 20%, ev

163 o-related cancer and virus-related liver and cervical cancers; diagnosis and treatment of early breas

164 tories of women aged 55-79 years who died of cervical cancer during 1980-2010 (cases) to those of wom

165 present study aimed to investigate the anti-cervical cancer effects of metformin, a first-line thera

166 state, anal, hepatocellular, colorectal, and cervical cancer exhibited alterations in at least 1 PI3K

167 Survivors of cervical cancer experience quality-of-life (QOL) disrupt

168 cohort effects to provide absolute risks of cervical cancer for unscreened women in different birth

169 pelvic examination for conditions other than cervical cancer, gonorrhea, and chlamydia, for which the

170 r any gynecologic cancer or condition except cervical cancer, gonorrhea, and chlamydia, which are cov

171 to HPV-seropositive cases and an independent cervical cancer GWAS.

172 results indicate that estrogen signaling in cervical cancer has dramatic differences from ERalpha+ b

173 tify proteins interacting with TCTP in human cervical cancer HeLa cells.

174 discovery: human embryonic kidney (HEK293), cervical cancer (HeLa), and liver cancer (HepG2).

175 asets that correspond to different stages of cervical cancer: (i) cases currently cytologically norma

176 n = 52), high-grade (HSIL; n = 92), invasive cervical cancer (ICC; n = 5) and healthy controls (n = 2

177 gnosed histologically; and 796 with invasive cervical cancers (ICCs).

178 g average-risk women older than 65 years for cervical cancer if they have had 3 consecutive negative

179 not screen average-risk women of any age for cervical cancer if they have had a hysterectomy with rem

180 o describe the indications for screening for cervical cancer in asymptomatic, average-risk women aged

181 Methods We enrolled sequential patients with cervical cancer in Botswana from 2010 to 2015.

182 s hold an excellent promise for detection of cervical cancer in clinical setting.

183 In the next 25 years, the epidemiology of cervical cancer in England, UK, will change: human papil

184 We estimated age-specific absolute risks of cervical cancer in the absence of screening (derived fro

185 testing has been very effective in reducing cervical cancer in the United States.

186 gue of cucurbitacin (Cucurbitacin D) against cervical cancer in vitro and in vivo.

187 y correlated with nuclear IRF1 expression in cervical cancer in vivo Importantly, high IRF1 expressio

188 omavirus 58 (HPV58) is found in 10 to 18% of cervical cancers in East Asia but is rather uncommon els

189 rted the presence of HPV18, a known cause of cervical cancer, in a small number of additional cancers

190 was associated with a reduction in invasive cervical cancer incidence (crude HR 0.40, 95% CI 0.18-0.

191 ce, progression, or regression; and invasive cervical cancer incidence among women living with HIV.

192 An ecological correlation between invasive cervical cancer incidence and burden of soil-transmitted

193 Cervical cancer incidence and mortality rates are higher

194 fficacy against HPV 16/18, vaccine coverage, cervical cancer incidence and mortality, and HPV type di

195 redict an initial widening of this gap, with cervical cancer incidence in Asian women up to 2.5 times

196 , and falling screening coverage will affect cervical cancer incidence in England up to 2040.

197 be encouraged to eliminate the inequality in cervical cancer incidence in the medium term.

198 we developed a model of HPV transmission and cervical cancer incidence that incorporates state-specif

199 Current standards of care for cervical cancer includes surgery, radiation, and chemoth

200 wever, the significance of LKB1 mutations in cervical cancer initiation and progress has not been exa

201 Cervical cancer is a consequence of persistent infection

202 Metastatic cervical cancer is a prototypical chemotherapy-refractor

203 driver of transformation in this aggressive cervical cancer is not HPV oncogene expression but rathe

204 Cervical cancer is one of the most common cancers among

205 ir "causal" HPV infection that develops into cervical cancer is poorly understood and practically uno

206 Human cervical cancer is the fourth most common carcinoma in w

207 Purpose Cervical cancer is the leading cause of cancer death amo

208 y maintain HPV 31 or 16 episomes, as well as cervical cancer lines that contain integrated genomes su

209 al tumor microenvironment is associated with cervical cancer maintenance and progression.

210 for their anticancer activity against HeLa (cervical cancer), MCF-7 (breast cancer), HL-60 (Human pr

211 value of 47.6%, 93.9%, 55.6%, and 91.9% for cervical cancer metastasis and 66.7%, 93.9%, 59.3%, and

212 value of 54.8%, 97.7%, 79.3%, and 93.1% for cervical cancer metastasis versus 64.6%, 98.6%, 86.1%, a

213 For cervical cancer, national estimates of 5-year survival r

214 ts and contributes to the increased rates of cervical cancer observed in African American women.

215 h could explain the increase in incidence of cervical cancer observed in later life.

216 sis drug bevacizumab for women with advanced cervical cancer on the basis of improved overall surviva

217 cination on infection, anogenital warts, and cervical cancer or precancerous lesions.

218 o/chemotherapy regimens can markedly improve cervical cancer outcome in a subset of patients, while o

219 olling the ability of p27(KIP1) to influence cervical cancer pathogenesis.

220 pplicators were developed for 30 consecutive cervical cancer patients on the basis of computed tomogr

221 We consecutively included stage IA1-IIB1 cervical cancer patients who presented to our tertiary r

222 In cervical cancer patients with high levels of pAKT and MK

223 In cervical cancer patients without enlarged lymph nodes, s

224 In cervical cancer patients, preoperative SLN imaging with

225 Ns) for diagnosing metastases in early-stage cervical cancer patients.

226 teral sentinel lymph node (SLN) detection in cervical cancer patients.

227 biomarkers to improve clinical management of cervical cancer patients.

228 programmed death ligand 1-positive advanced cervical cancer, pembrolizumab demonstrated antitumor ac

229 ed to colposcopy and biopsy for diagnosis of cervical cancer precursors (high-grade squamous intraepi

230 ighly efficacious against the development of cervical cancer precursors attributable to oncogenic gen

231 ficacy trials that have led to licensure for cervical cancer prevention have used the disease endpoin

232 assays based on nfGNPs for HPV detection and cervical cancer prevention.

233 oncogenic HPV types could make prevention of cervical cancer programmatically feasible.

234 st HPV types 16 and 18 (HPV 16/18) could see cervical cancer rates in women aged 25-29 years decrease

235 k was such that in the absence of screening, cervical cancer rates in women aged 65+ would have been

236 n papilloma virus (HPV) vaccination efforts, cervical cancer remains a leading cause of death in wome

237 Cervical cancer remains a major cause of morbidity and m

238 enes, but their precise role in HPV-infected cervical cancer remains unclear.

239 dard chemotherapy for metastatic or relapsed cervical cancer respond poorly to conventional chemother

240 GT genotype was associated with an increased cervical cancer risk (adjusted OR = 1.19, 95% CI = 1.00-

241 e rs4353229 polymorphism was associated with cervical cancer risk (under a recessive model: crude OR

242 tially functional polymorphisms in CASP7 and cervical cancer risk and evaluated their locus-locus int

243 t CASP7 polymorphisms may interact to modify cervical cancer risk by a possible mechanism of regulati

244 ocus-locus interaction effect that modulated cervical cancer risk.

245 programmed cell death and thus contribute to cervical cancer risk.

246 dies, we also found HPV18 transcripts in non-cervical cancer samples, including those from the colon,

247 we found robust expression of HPV18 genes in cervical cancer samples.

248 s time period, and more modest reductions in cervical cancer screening and sexual risk behaviors.

249 idered when clinical practice guidelines for cervical cancer screening are reassessed.

250 cancerous lesions and may be used in primary cervical cancer screening for women >/=30 years of age.

251 an HPV test (the cobas HPV test) for primary cervical cancer screening for women over the age of 25 y

252 Recent changes in the periodicity of cervical cancer screening have led to questions about th

253 lomavirus (HPV) tests are needed for primary cervical cancer screening in lower-resource regions.

254 Studies suggest that cervical cancer screening practice in the United States

255 investments in interventions to improve U.S. cervical cancer screening practice.

256 Current cervical cancer screening practice; improved adherence t

257 Women with abnormal cervical cancer screening results are referred to colpos

258 women referred to colposcopy after abnormal cervical cancer screening results.

259 urring when offering vaccination both at the cervical cancer screening visit and during sexually tran

260 time mass campaign, vaccination at the first cervical cancer screening visit, vaccination at sexual h

261 ffering vaccination to adults, especially at cervical cancer screening visits (for women) and during

262 ared to changes in HPV vaccination coverage, cervical cancer screening, an antecedent event to detect

263 studies to evaluate urine-based sampling for cervical cancer screening, epidemiologic studies, and po

264 and fulfill the criteria for use in primary cervical cancer screening.

265 , similarly to the EIA, useful for HPV-based cervical cancer screening.

266 The majority of metastatic bone lesions in cervical cancer seem to be of osteolytic nature.

267 t chemotherapy plus bevacizumab for advanced cervical cancer significantly improves overall and progr

268 he syntax was based on synonyms of the terms cervical cancer, SPECT/CT, and lymphoscintigraphy.

269 has the potential to reduce the incidence of cervical cancer substantially.

270 swana, HIV infection significantly decreases cervical cancer survival.

271 I] 1.1-2.7) more likely to be diagnosed with cervical cancer than white women (22.8 vs 13.4 cases per

272 For stage IIIB cervical cancer, the addition of cisplatin offers a smal

273 ty of anogenital tract carcinomas, including cervical cancer, the second most common malignancy in wo

274 uman papillomavirus (HPV) is associated with cervical cancer, the third most common cancer in women.

275 predicted to have a relatively high risk of cervical cancer throughout their lives.

276 unclear how Th17 cells are recruited to the cervical cancer tissue.

277 nuclear protein in skin, normal cervix, and cervical cancer tissues, but not in larynx.

278 of human papillomavirus (HPV) infection and cervical cancer to reflect 1) a shift towards health sta

279 nt failure in patients with locally advanced cervical cancer treated with chemo- and radiation therap

280 was conducted in 85 women with stage IB-IVA cervical cancer treated with chemo- and radiation therap

281 ong-term prognosis in patients with advanced cervical cancers treated with CCRT.

282 ong-term prognosis in patients with advanced cervical cancers treated with concurrent chemo-radiother

283 ns, the direct reduction in lifetime risk of cervical cancer varied from 55% (53-56%) among women vac

284 The risk of respiratory tumors or cervical cancer was approximately halved when smoking wa

285 ts with recurrent, persistent, or metastatic cervical cancer was associated with an improvement of 3.

286 man papillomavirus (HPV)-based screening for cervical cancer was compared with cytology-based cervica

287 Incidence of cervical cancer was higher in indigenous women than in n

288 In clinical specimens of cervical cancer, we confirmed that the expressions of K1

289 model that simulates the natural history of cervical cancer, we estimated the cumulative number of c

290 Among 1,696 women who had not developed cervical cancer, we further investigated the link betwee

291 Results A total of 348 women with cervical cancer were enrolled, including 231 (66.4%) wit

292 f bevacizumab into the treatment of advanced cervical cancer were not accompanied by any significant

293 uses (HPV) contributes to the development of cervical cancer, whereas loss of E6AP expression or func

294 se was observed in a patient with metastatic cervical cancer who received 2.7 x 10(9) cells (ongoing

295 a randomized clinical trial in survivors of cervical cancer, who were >/= 9 and less than 30 months

296 eady recommends screening (ie, screening for cervical cancer with a Papanicolaou smear, screening for

297 ans should not screen average-risk women for cervical cancer with cytology more often than once every

298 Screening for cervical cancer with cytology testing has been very effe

299 ancers, we describe the burden of breast and cervical cancer, with an emphasis on global and regional

300 women worldwide are diagnosed with breast or cervical cancer, yet where a woman lives, her socioecono