{"paper_id":"2a4ed993-dd78-47d6-98c3-871d2f5e7b74","body_text":"Offizielles Organ:  AGRBM,  BRZ,  DVR,  DGA,  DGGEF ,  DGRM,  D·I·R,  EFA,  OEGRM,  SRBM/DGE\nKrause & Pachernegg  GmbH, Verlag für Medizin und Wirtschaft, A-3003 Gablitz\nJournal für\nReproduktionsmedizin \nund Endokrinologie\n– Journal of Reproductive Medicine and Endocrinology –\nAndrologie • Embryologie & Biologie • Endokrinologie • Ethik & Recht • Genetik \nGynäkologie • Kontrazeption • Psychosomatik • Reproduktionsmedizin • Urologie\nIndexed in EMBASE/Excerpta Medica/Scopus\nwww.kup.at/repromedizin\nOnline-Datenbank mit Autoren- und Stichwortsuche\nPathogenesis of Early-Onset Endometriosis\nBenagiano G, Gargett C, Brosens I\nJ. Reproduktionsmed. Endokrinol 2015; 12 (4), 227-231\n\n\n20.-21. März 2026\nUniversitätsmedizin Mainz\nENDOKRINOLOGIE & FERTILITÄT\nFÜR KLINIK & PRAXIS\nWeitere Informationen\n& Anmeldung unter\nEinladung zu unserer wissenschaftlichen Veranstaltung Endo-Ferti-Forum\nBrücke(n) zwischen Unikliniken und Praxen an Rhein und Main(z)\n– die aus dem bisherigen Format „Ferti Forum“ ab 2026 hervorgeht –\nFreuen Sie sich auf spannende Vorträge und den lebendigen Austausch mit Kolleg:innen und Expert:innen aus Klinik und\nPraxis. Freitagabend laden wir Sie herzlich zu einem entspannten Empfang ein –\neine perfekte Gelegenheit, Kontakte zu knüpfen und den T ag genussvoll ausklingen zu lassen.\nWissenschaftliche Leitung: Univ.-Professorin Annette Hasenburg, Dr. Susanne Theis, Universitätsmedizin Mainz,\nSanitätsrat Dr. Werner Harlfinger, BVF Rheinland-Pfalz Dr. Rüdiger Gaase, BVF Hessen Dr. Klaus J. Doubek\nSchirmherrschaften: Prof. Nicole Sänger, Uniklinik Bonn, Prof. Jan-Steffen Krüssel, Uniklinik Düsseldorf,\nDr. Annette Bachmann, Uniklinik Frankfurt am Main, Prof. Christine Skala, Uniklinik Köln\n\n227J Reproduktionsmed Endokrinol_Online 2015; 12 (4)\nPathogenesis of Early-Onset Endometriosis\nG. Benagiano1, C. Gargett2, J. J. Brosens3, I. Brosens4\nThree main theories have been put forward to explain the pathogenesis of endometriosis, that of a retrograde menstrual transpla ntation, that of an induc-\ntion of endometrial cells, and that of an in situ development. These hypotheses belong to two main groups: those proposing that implants originate from the \nendometrium and those advocating an origin from extra-uterine tissues. More recently, the discovery that stem/progenitor cells from bone marrow can dif-\nferentiate into endometrial cells suggests a novel pathway through which these cells may colonize peritoneal and extra-peritoneal organs and differentiate \ninto ectopic endometrium. \nOn the other hand, for early-onset endometriosis a different pathogenetic mechanism may be in place. The possibility exists that in neonates endometrial \ncells and stroma are retrogradely disseminated in the pelvis, thanks to the presence of uterine bleeding, either visible or occult. Since menstrual desquama-\ntion causing neonatal bleeding may contain endometrial stem cells, they may in turn be responsible, through a variety of mechanisms, for early onset endo-\nmetriosis. J Reproduktionsmed Endokrinol_Online 2015; 12 (4): 227–31.\nKey words: endometriosis, endometrium, adenomyosis, neonatal uterine bleeding\n  Introduction\nThe first descriptions of what were ini-\ntially designated as “mucosal invasions \nof peritoneal organs”, namely the condi-\ntions we call today adenomyosis and en-\ndometriosis, date back more than a hun-\ndred years and by the end of the 19\nth cen-\ntury they were given a common name, \nthat of “adenomyoma” [1].\nIn spite of intensive research, even today \nthese two diseases deserve the appella-\ntive of “elusive”, utilised by Emge [2] \nand Bird et al [3] to describe adenomyo-\nsis and endometriosis respectively, back \nin the nineteen sixties and seventies. Elu-\nsive, because the exact pathogenetic \nmechanisms are still incompletely un-\nderstood and the diagnosis often made \nafter considerable time.\nIn the early days of the 20th century, re-\nsearchers concentrated on the histogene-\nsis of adenomyomas. Intriguingly, C. \nRokitansky, the first to describe a case \nof what we would identify today as an \n“adenomyomatous polyp”, immediately \nrecognised the endometrial nature of the \nepithelial cells found in the lesion. He \nmentioned that in a number of autopsies \nof women he found “fibrous polyps of \nthe uterus” and that “among them there \nare some, in which glandular tubes are \nfound” [4]; having found them protrud-\ning from the endometrium, he correctly \nidentified the “glandular tubules” as of \nendometrial nature. Unfortunately, his \nscientific publication carries the title \n“On the neoplasm of uterus glands and \nuterine and ovarian sarcomas”, and this \nseems to have distracted his contempo-\nraries from the significance of his work. \nIndeed, ignoring Rokitansky’s conclu-\nsions, during the second part of the 19\nth \ncentury many pathologists argued that \n“adenomyomas” were the result of dis-\nplacement of Wolffian or mesonephric \nvestiges; the most famous among them \nwas F. D. von Recklinghausen [5]. They \nrejected the possibility that the glands \nthey discovered as invading peritoneal \norgans were “endometrial” and opted for \nan embryologic origin.\nThe first clear description of the morpho-\nlogical and clinical picture of adenomyo-\nma was made by T. Cullen. In his book \n“Adenomyoma of the Uterus” [6] he de-\nscribes an observation made in 1882 and \nclearly mentions that “the uterine muco-\nsa was at many points flowing into the \ndiffuse myomatous tissue”. Cullen’s the-\nory was dismissed for years and it was \nonly during the second decade of the 20\nth \ncentury that it finally gained acceptance \n[7] and, by 1920, most researches agreed \nthat the epithelial cells and stroma in an \nadenomyoma were of endometrial na-\nture.\nOnce, the histogenesis was determined, \nit remained to clarify the pathogenesis of \nadenomyomas. This however, would \nonly be possible once a relationship was \nfound with another condition initially \ncalled “chocolate cysts of the ovary”, or \n“ovarian haematomas”, the ovarian en-\ndometrioma.\nThe presence of endometrial glands and \nstroma in an ovary was first mentioned \nby W. W. Russel [8] in 1899 in a pre-\nmenopausal woman who underwent sur-\ngery for a cystic adenocarcinoma of the \nleft ovary. Opening the abdominal cavity, \nRussel found the right ovary enveloped \nin adhesion of the posterior face of the \nbroad ligament and at microscopic ex-\namination a number of areas were ob-\nserved that “were an exact prototype of \nthe uterine glands and interglandular \nconnective tissue”. In line with the theo-\nries of the time, Russel believed that the \n“tumor” was due to the presence of \n“ aberrant portions of the Müllerian \nduct” in the ovary. A number of addi-\ntional descriptions of “haematoma of the \novary” and of “chocolate cysts of the \novary” were also published at the begin-\nning of the 20\nth century [1]. Then, in \n1921, J. Sampson published the first of \nhis articles on the condition he later \nnamed “endometriosis”, describing 23 \ncases of “ovarian haematomas of endo-\nmetrial type” [9]. Initially, he preferred \nto call the cyst’s epithelium “Müllerian”, \nbecause he felt that in some cases the \nepi thelium lining these ovarian ‘haema-\ntomas’ or ‘cysts’ may have been derived \nfrom the tubal epithelium. Sampson \nFor personal use only. Not to be reproduced without permission of Krause & Pachernegg GmbH.\nReceived and accepted: January 27th, 2015.\nFrom the 1Department of Gynecology-Obstetrics and Urology, Sapienza University, Rome, Italy; 2The Ritchie Centre, Hudson Institute of Medical Research and Department of \n Obstetrics and Gynecology, Monash University, Australia; 3Division of Reproductive Health, Warwick Medical School, Clinical Sciences Research Laboratories, University Hospital, \nCoventry, UK, and the 4Catholic University Leuven, Leuven Institute for Fertility and Embryology, Leuven, Belgium\nCorrespondence: Professor Giuseppe Benagiano, MD, Department of Gynecology-Obstetrics and Urology, Sapienza University, Piazzale Aldo Moro 5, I-00185 Rome, Italy; \ne-mail: Giuseppe.Benagiano@uniroma1.it\n\nPathogenesis of Early-Onset Endometriosis\n228 J Reproduktionsmed Endokrinol_Online 2015; 12 (4)\nquickly developed a theory whereby the \novary would act as an incubator in the \ndevelopment of pelvic implantation of \nadenomas of the endometrial type [10]. \nFinally, in 1927, Sampson detailed his \ntheory that the rupture of the endometrial \ncyst was the cause of peritoneal endome-\ntriosis [11], whereas several authors pro-\nposed the opposite mechanism, namely \nthat endometriotic lesions on the perito-\nneum moving to the cortex invaded the \novary, or that endometrial cells arrived \ninside the ovary via lymphatic vessels \n[12]. It was only in 1957 that P. E. \nHughesdon demonstrated histologically \nin ovaries with chocolate cysts in situ \nthat in 90% of the cases the wall of the \ncyst originated from invaginated ovarian \ncortex, but was frequently modified by \ncortical fibrosis and smooth muscle \nmetaplasia of the inner cortex obscuring \nthe presence of follicles in the deeper \nlayers [13]. In the meantime, O. Frankl \nhad developed his theory that adenomyo-\nmas growing within the uterine wall \nwere a distinct entity which he named \n“adenomyosis” [14].\nAt this stage, endometriosis and adeno-\nmyosis became known as different noso-\nlogical entities with allegedly a different \npathogenesis and, for decades to come, \nthe two were considered independent \ndiseases.\n  Adult Endometriosis\nOver the years, Sampson’s theory of a \nretrograde menstrual origin of endo-\nmetrio sis [11] gained acceptance and is \ntoday the most widely accepted hypoth-\nesis for its existence. Nonetheless, the \npresence of various forms of endometri-\nosis (peritoneal superficial, deep, ovarian \nand extra-peritoneal) have led some to \nbelieve that they constitute separate \nnoso logical entities [15] and therefore \nthat their pathogenesis may present dif-\nferent connotations.\nIn 1980, Simpson et al [16] and Malinak \net al [17] were the first to explore genetic \nand familial aspects of endometriosis \nand found that female siblings of sub-\njects with histologically proven endome-\ntriosis are almost 7-times more likely to \ndevelop the disease than women without \na family history of endometriosis. To ex-\nplain their findings they opted for a poly-\ngenic/multifactorial aetiology and con-\ncluded that an apparently healthy woman \nwith an affected first-degree relative \nwould have a 7% chance of developing \nendometriosis. Aberrant gene expression \nin endometriosis is not confined to the \nectopic lesions but is also apparent in the \neutopic endometrium [18–20]. In this re-\nspect, it is more and more evident that \nthe characteristics of the endometrium \nplay a key role in the complex sequence \nof events leading to the adherence of \nnests of endometrial cells and stroma to \nthe peritoneum, its acquisition of a blood \nsupply and ultimately its survival.\nRecently, Burney and Giudice [21] ex-\npressed the opinion that theories regard-\ning the pathogenesis of endometriosis \ncan be reduced to two main groups: those \nproposing that implants originate from \nthe endometrium and those advocating \nan origin from extra-uterine tissues. This \nis indeed the prevailing view of this enig-\nmatic disease today.\nSome 10 years ago, Nap et al [22] re-\nviewing the subject concluded that 3 the-\nories on the pathogenesis of endometrio-\nsis seem the most acceptable: the retro-\ngrade transplantation, the induction and \nthe in situ development theories.\nThe Retrograde Menstruation \nTheory\nAs mentioned, today the most widely ac-\ncepted hypothesis for the genesis of en-\ndometriosis is that presented by Sampson \nin 1927, i. e. peritoneal endometriosis is \ncaused by retrograde dissemination and \nimplantation of endometrial tissue frag-\nments into the peritoneal cavity at the \ntime of menstruation [11]. Years later \nSampson [23] presented a complete ver-\nsion of his theory, specifying that in \nwomen with patent tubes, fragments of \nendometrial tissue are retrogradely trans-\nported into the peritoneal cavity where, \nunder facilitating conditions, they are \nable to adhere to peritoneal mesothelial \ncells and establish a blood supply that \nenables them to survive and proliferate. \nA number of observations support the re-\nflux theory, from the distribution of the \nlesions in the abdominal cavity, to the in \nvitro proven viability of shed menstrual \nendometrium, to animal experiments in \nwhich a forced increase in retrograde \nshedding increases the chance of devel-\noping endometriosis [22].\nIt has been pointed out that menstrual re-\nflux, while a pre-condition for its occur-\nrence, is not per se  sufficient to cause \n endometriosis: indeed, retrograde men-\nstruation seems to occur in the vast ma-\njority of women [24], whereas only a mi-\nnority of them develop the disease. One \nof the proposed explanations for this dis-\ncrepancy is that natural immunity is al-\ntered in women with endometriosis; this \ndecrease in a vital defence mechanism \ncan cause an impairment of the physio-\nlogic clearing ability of the peritoneum \nto remove endometrial fragments shed in \nretrograde menstruation [25, 26].\nMore recently, it has been found that nat-\nurally-occurring endometrial stem cells \n(ESCs) play a role in the cyclic regenera-\ntion of the endometrium [27]. These \nESCs can also have an important role in \nthe pathogenesis of endometriosis, since \nthey have been found in menstrual blood \n[28].\nIn summary, whereas “there is virtually \nno other scientific evidence supporting \nalternate mechanisms of development of \nendometriosis” [29], there are still many \nquestions that require an answer before \nSampson’s theory can be fully accepted.\nThe Induction (or Coelomic \nMetaplasia) Theory\nThe oldest theory, dating back more than \na century, to explain “epithelial invasions \nof peritoneal organs” involved a mecha-\nnism called “coelomic metaplasia”, \nnamely the transformation of peritoneal \nmesothelial tissue into epithelial glands \nand stroma. However, the endometrial \nnature of these epithelial nests was not \ninitially recognised [30] and, as a conse-\nquence of the work of Cullen [31], the \nmetaplasia theory was all but abandoned \nuntil the nineteen fifties when it was res-\nurrected by Levander and Normann [32] \nand, a decade later by Merrill [33]. Ac-\ncording to this hypothesis, endometriosis \nmay develop through a series of meta-\nplasic changes induced by the release of \ncellular factors from degenerating men-\nstrual endometrium. \nIn 1999, Ohtake et al [34] developed an \nin vitro experimental model for ovarian \nendometriosis employing a three-dimen-\nsional culture of human ovarian surface \nepithelial cells in collagen gel. Using this \nsystem, they obtained evidence that \nwhen both ovarian surface epithelium \nand ovarian stromal cells are co-cultured \nwith oestradiol, endometrial-like nests \n\nPathogenesis of Early-Onset Endometriosis\n229J Reproduktionsmed Endokrinol_Online 2015; 12 (4)\ncan develop through a process of meta-\nplasia. In these co-culture experiments \novarian surface epithelial and endometri-\nal stromal cells formed an epithelial \nstructure with lumen, surrounded by \nstromal cells. Immunoreactivity for cyto-\nkeratin and epithelial membrane antigen \nwas detected in the glandular cells and \ncilia were identified on the cell surface \nby electron microscopy. Importantly, \nnone of these structures were detected in \nthe absence of oestradiol.\nWhile in vitro models support the induc-\ntion theory, direct evidence of the forma-\ntion of endometrial cells and stroma as a \nconsequence of a metaplastic process is \nas yet lacking [22].\nThe In-situ Development Theory\nThis hypothesis involves the growth of \nendometrial cells and stroma from multi-\npotent cells and embryonic remnants and \nwas first presented by Ferguson et al who \nproposed that the peritoneal lining con-\ntains undifferentiated cells that can dif-\nferentiate into endometrial cells under \ncertain circumstances [35].\nIt has been invoked to explain cases of \nperitoneal endometriosis occurring be-\nfore menarche, in women who have nev-\ner menstruated, and in postmenopausal \nwomen. It has also been invoked to ex-\nplain extra-peritoneal cases, such as the \nlesions found in right-sided thoracic or-\ngans and in castrated men treated with \noestrogens [36]. The theoretical basis of \nthis hypothesis has been put forward by \nFujii [37] who believes that a shared em-\nbryologic origin exists for coelomic epi-\nthelium-related tissues and Müllerian-\nderived epithelia of the adult. Thus, tis-\nsues derived from the coelomic epithelial \nand mesenchymal cells have the poten-\ntial to differentiate into Müllerian-type \nepithelium and stroma and this mecha-\nnism can be involved in the pathogenesis \nof endometriosis.\nNew Theories\nThe discovery that stem/progenitor cells \nfrom bone marrow can differentiate into \nendometrial cells suggests a novel path-\nway for the development of ectopic en-\ndometriotic implants. In a remarkable \nexperiment, Taylor [38] obtained proof \nthat endometrial cells can be derived \nfrom bone marrow cells, studying female \nallogenic bone marrow transplant recipi-\nents receiving a graft under conditions \nallowing identification of the donated \ncells. This investigation demonstrated \nthe presence of donor-derived endome-\ntrial cells in endometrial biopsies of the \nrecipients, suggesting that bone marrow-\nderived cells can differentiate into hu-\nman uterine endometrium. \n  Early-Onset Endometriosis\nInitially, endometriosis was considered a \ndisease of adult women; however, taking \na life cycle’s approach [39], it became \nclear that its presence had been described \nin foetuses in the posterior pelvic cavity \n[40], in girls before menarche [41], and \nduring adolescence on the pelvic organs, \nincluding the ovaries [42, 43].\nIt seems logical that this intraperitoneal \nvariant in young adolescents possessing \nin a majority of instances characteristic \nsubtle superficial lesions with strong \nneo-angiogenesis, but also manifesting it \nwith ovarian endometriomas, may have a \npathogenesis that differs from cyclic \nretro grade menstruation. For this reason, \nwe became interested in the pathogene-\nsis of this early form and decided to in-\nvestigate whether they may draw their \norigin from a totally neglected, but well \nproven endometrial bleeding, that occur-\nring at birth in some neonates.\nTo our surprise, over the last 30 years, \nwe found only one report dealing with \nNeonatal Uterine Bleeding (NUB) pub-\nlished in a Yugoslavian Journal and not \nmentioned in any of the most widely \nconsulted data bases [44]. By contrast, \nearlier publications exist on foetal and \nneonatal endometrium. Specifically, in \nthe nineteen seventies French and Ger-\nman investigators described NUB in \ngreat detail [45–49]. \nFeatures of neonatal endometrium were \ncarefully detailed some sixty years ago \nby two Harvard pathologists [50] who \ndescribed the different features of neona-\ntal endometrium at birth as an indifferent \nor proliferative phase in some 2/3 of the \ncases. They recorded secretory activity \nand decidual changes in 27% and 5% of \ncases, respectively. Changes of the type \nobserved at menstruation in adults were \nobserved in 5 out of a total of 169 new-\nborn infants, all of whom had died within \n3 days after birth. Observed features in \nthe five babies included the presence of \nclotted blood in the endometrial cavity; \nin the coagulum, sloughed endometrial \nstructures were occasionally identifiable. \nThe development of the endometrium \nduring foetal life was carefully investi-\ngated more than 40 years ago by Huber \net al [51] who documented that no glan-\ndular development occurs before the 20\nth \nweek, whereas signs of secretory activity \ncan be observed in some foetuses begin-\nning around the 34\nth week. After birth the \nendometrium starts a process of regres-\nsion and at one week becomes quiescent.\nThere is now unequivocal evidence that \nthe neonatal endometrium can mount a \ndecidual response in 5% of the neonates, \na prerequisite for menstrual shedding. It \nis also established that overt vaginal \nbleeding occurs in 3–5% of the neonates \nand that in an unspecified larger number \nof new-born bleeding is occult. Regurgi-\ntation of sloughed endometrial frag-\nments into the peritoneal cavity is likely \npromoted in the neonate by the thick en-\ndocervical mucus in the relatively long \ncervical canal [52].\nAt this stage we outlined a theory to ex-\nplain early-onset endometriosis based on \nthe possibility that in some foetuses and \nneonates endometrial cells and stroma \nmay be retrogradely disseminated in the \npelvis around the time of birth, thanks to \nthe presence of uterine bleeding, either \nvisible or occult [53]. This preliminary \ncommunication was followed by a full \nreport detailing the new theory [54] and \nby a further article in which we discussed \nthe possibility that menstrual debris pres-\nent in NUB may contain endometrial \nstem cells. These neonatal ESCs may in \nturn be responsible, through a variety of \nmechanisms, for early onset endometrio-\nsis [55].\nToday there is evidence that ESCs have \nthe ability of establishing endometriotic \nimplants [56] and several experiments \nsupport the hypothesis of their involve-\nment in the development of the disease \n[57]. Following this line of thinking, we \nhypothesised that ESCs are shed into the \npelvic cavity in concomitance with \nNUB. We further postulated that during \nthe neonatal and pre-pubertal period \nESCs can survive in the pelvic cavity \neven in the absence of circulating oestro-\ngens, thanks to the support of niche cells, \nalso shed during neonatal uterine bleed-\ning. Then, at the time of thelarche, under \n\nPathogenesis of Early-Onset Endometriosis\n230 J Reproduktionsmed Endokrinol_Online 2015; 12 (4)\nthe influence of rising oestrogen levels, \nESCs can proliferate and – in specific \ncases – establish nests of ectopic endo-\nmetrial cells and stroma [55].\nIn support of our theory, two populations \nof ESCs have been recently identified: \nepithelial and mesenchymal progenitor \ncells (eEPCs and eMSCs). Both show a \nhigh proliferative potential, are capable \nof undergoing self-renewal in vitro and \nare capable of differentiating into mature \nprogeny and of reconstituting tissue in \nvivo [58–60]. There is evidence that \n eMSCs from endometriotic lesions show \ngreater invasiveness and migration abili-\nty, as well as the capability to stimulate \nneo-angiogenesis compared to those in \neutopic tissue [61]. These properties in \nturn may promote ESCs survival and the \nability to quickly implant in the peritone-\nal/ pelvic cavity [62], where they can lay \ndormant for years [63]. \nAttractive as it may sound, before the \nnew theory can be accepted it will re-\nquire clinical and experimental confir-\nmation. To this aim, we have suggested \nseveral lines of investigations [64].\n  Conclusions\nIf proven true, the new hypothesis will \nhave practical consequences also outside \nits possible role in early-onset endome-\ntriosis. NUB occurs rarely in pre-term \nbabies, increases in those at term and is \nfrequent in post-mature infants. If a tem-\nporal relationship could be established \nbetween endometrial maturation and \nNUB, its occurrence might be taken as a \nreflection of the maturity of progester-\none response in the endometrium. Pre-\neclampsia, particularly if severe, low for \ngestational age birth weight, and feto-\nmaternal blood incompatibility seem to \nrepresent factors increasing the frequen-\ncy of NUB [47]. For this reason, a series \nof new feto-maternal markers can be en-\nvisaged to evaluate the risk of endome-\ntriosis in adolescents and young women \n[65].\nFinally, it has been shown that the occur-\nrence of major obstetric syndromes can \nbe caused by impaired placental bed spi-\nral artery remodelling [66]; these are \nprevalent in teenage pregnancies and in-\nclude pre-eclampsia, foetal growth re-\nstriction and spontaneous preterm labour \n[67]. It can be argued that, if the partial \nprogesterone resistance observed in new-\nborn foetuses and babies can persist into \nadolescent years, this phenomenon may \nimpair physiological deep placentation \nin case of pregnancy [66]. Thus, under-\nstanding the mechanisms of functional \nmaturation of the uterus during the early \nreproductive years may yield novel in-\nsights into the major obstetric syndromes \n[68].\n  Conflict of Interest\nAll authors declare no conflict of interest.\nReferences:\n1. Benagiano G, Brosens I, Lippi D. The history of endometriosis. \nGynecol Obstet Invest 2014; 78: 1–9.\n2. Emge L. The elusive adenomyosis of the uterus. Am J Obstet \nGynecol 1962; 83: 1541–63.\n3. Bird CC, McElin TW, Manalo-Estrella P. The elusive adenomy-\nosis of the uterus. Am J Obstet Gynecol 1972; 112: 583–93.\n3. Rokitansky C. Über Uterusdrüsen-Neubildung in Uterus- und \nOvarial-Sarcomen. [On the neoplasm of uterus glands on uterine \nand ovarian sarcomas]. Zeitschr Gesellschaft der Aerzte in Wien \n1860; 16: 577–81.\n4. von Recklinghausen F. 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