{"paper_id":"677a7868-454d-4db9-bd6a-40a54730ca17","body_text":"Introduction  \nDiffusion-weighted imaging (DWI) is a functional imaging technique , applied in Magnetic  \nResonance imaging, whose contrast derives from the random motion of water molecules within \nexplored tissues.  \nSince image contrast is derived from inherent differences in the restriction of the movement of \nwater molecules, no exogenous contrast medium administration is required, so that DWI \nsequences can now be included in routine patient assessment.  \nDWI uses t he measurement of Brownian movements of water molecules by applying symmetric  \npairs of equally weighted diffusion sensitizing gradients about the 180°refocusing pulse of a spin -\necho T2-weighted sequence. Static water molecules develop additional phase inco herencies from \nthe application of the first diffusion gradient, but these incoherencies are eliminated by the \napplication of the second gradient, resulting in no additional net loss of signal (aside from normal \nT2 decay) [1]. However, mobile water is not c ompletely rephased by the second gradient owing to \nmovement to a different microenvironment during the application of the first gradient, so that a \nsubsequent reduction in signal intensity is observed.  DWI sensitivity to water motion is dependent \non three main parameters: the  gradient amplitude, the duration, and the time interval  (b-value) \nbetween paired diffusion gradients [2]. Tissues containing water that is moving the most freely (eg, \nwithin blood vessels, ducts, or the bladder) will demonstrate greate r signal losses after the \napplication of the smallest diffusion gradients (<100 sec/mm2). Signal losses caused by water \nmotion in the extracellular space of tumors occur at higher b values because water motion is \nmodified by interactions with hydrophobic c ell membranes and macromolecules (increased \nextracellular space tortuosity) [3]. In solid tumors of high cellularity, there are additional significant \nreductions in extracellular space, resulting in further restrictions to free water movement. \nWhen DWI is used in gynecologic applications, cervical cancers have been shown to have \nsignificantly lower apparent diffusion coefficient (ADC) values than normal cervical tissue  [4]. \nSimilar findings have been noted in endometrial cancers, with a tendency toward lowe r ADC \nvalues in higher-grade lesions.  \n \n\nADC value \nThe ADC value (measured in mm2/sec) is usually calculated by the slope of the line of the natural \nlogarithm of signal intensity (y axis) versus b values (x axis) [5].  \n \nDWI imaging: applications in female pelvic neoplasms \nCervical cancer \nCervical cancer is the second most common female cancer in the world and it occurs \npredominantly in women between the age of 30 and 44 years [6]. The American Cancer Society \nprovides the following list of risk factors for cervical cancer: Human Papillomavirus (HPV) infection, \nsmoking, HIV infection, chlamydia infection, dietary factors, hormonal contraception, multiple \npregnancies, exposure to the hormonal drug diethylstilbestrol (DES) and a family history of cervical \ncancer [7].  \nCervical cancer: Histopathology  \nThe World Health Organization (WHO) recognizes two main histological types of invasive cervical \ncancer. \n Squamous carcinoma (which constitute about 85% of all cases)  \n Adenocarcinoma (which constitute about 10-12% of all cases)  \nSeveral other types of carcinoma (eg adenosquamous carcinoma, adenoid cystic  carcinoma, \nmetastatic carcinoma) make up the remaining 3-5% of all cases. \nSquamous carcinomas are further typed according to whether they are keratinizing or not \nkeratinizing carcinomas. Keratinizing carcinomas may be well differentiated or moderately \ndifferentiated and are composed of large tumour cells. Non-keratinizing carcinomas (poorly \ndifferentiated carcinomas) may be of large cell or small cell type [8].  \nMost cervical squamous cell carcinomas grow at the squamocolumnar junction (SCJ).  \nIn young women, the SCJ is located outside the external uterine os, and the tumor tends to grow \noutward (exophytic growth pattern). In contrast, in elderly patients, the SCJ is located within the \ncervical canal. In these patients, cervical cancer tends to grow inward along the cervical canal \n(endophytic growth pattern) [9].  \n\nAdenocarcinomas are less commonly found and although each type is histologically distinct, it is \nnot uncommon to find two or more histological forms of adenocarcinoma in a single tumour .The \nfrequent coexistence of glandular and squamous carcinoma suggest that they may have a \ncommon origin in the reserve cells of the cervix as well as a common etiology. The most frequent \ntype of adenocarcinoma to be found in the cervix is the endocervical type of mucinous \nadenocarcinoma. Three grades of endocervical carcinoma are recognized -well differentiated, \nmoderately differentiated and poorly differentiated - depending on the similarity of the tumour cell \nto the glandular epithelial lining the endocervix. In fact, in endocervical adenocarcinoma, \nendocervical type, different subtypes can be found (endometrioid type, clear cell type, papillary \nserous type, intestinal type, mixed type) [10]. \nCervical cancer: MR features  \nAt baselineT2 w.i MR examination, cervical cancers appear as slightly hyperintense masses, while \ntheir predominantly signal intensity on baseline T1 w.i is hypointensity. \nOn vascular dynamic study, cervical cancers can show no enhancement or slighly marginal \nenhancement on arterial phase.  \n \nEndometrial cancer \nEndometrial cancer is the most common malignancy of the genital tract and overall the \nendometrium is the fourth most frequent cancer site. Risk factor for endometrial cancer include \nobesity, diabetes, oestrogen therapy, polycystic ovarian syndrome and westernization of \nlifestyle.[11]. Approximately 75% of cases occur in postmenopausal women, with the median age \nat diagnosis being 70 years.  \nEndometrial cancer: Histopathology  \nEndometrial tumors can be have different histology: endometrial carcinoma (with its \nhistopathologic subtypes: villoglandular  or papillary, secretory, ciliated cell, adenocarcinoma \nwith squamous differentiation), adenocarcinoma (serous, mucinous, clear cell), squamous cell \n\ncarcinoma; undifferentiated carcinoma; mixed carcinoma, metastatic carcinoma and \ncarcinosarcoma.  \nAdenocarcinomas account for 90% of endometrial neoplasms, whereas uterine sarcomas are \nrelatively rare and account for only 2%–6%; the remaining histologic types include \nadenocarcinoma, with squamous cell differentiation and adenosquamous carcinoma [12].  \nEndometrial cancer: MR features \nAt MR examination, endometrial cancer is iso-hypointense in respect to the surrounding normal \nendometrium on baseline T1w.i -weighted images, while it does most commonly show \nheterogeneous, iso up to hyperintensity on baseline T2wi.  \nNeoplasms are usually mildly hyperintense on baseline T2w.i. in respect to myometrium. \nEndometrial cancer can have different pattern of appearances on baseline T2 w.i.: hypointense \npseudonodular lesions, diffuse endometrial thickening, hypointense vegetations, or infiltrative \nendometrial plaques with heterogeneous signal intensity. \nEndometrial carcinomas are divided into two types: one shows as a well-demarcated exophytic \nmass (Type I), while the other shows as an invasive, endophytic growth toward the myometrium \n(Type II). The former subtype is considered to be malignant with favorable prognosis [13].","source_license":"CC0","license_restricted":false}