Re: la cura per il cancro ....e se fosse vero?
Inviato da Redazione il 24/3/2006 10:31:54
Buongiorno MIr. Mi scusi per il ritardo, ma in questi giorni mi trovo impegnato su molti fronti contemporaneamente, e fatico a seguire tutto come vorrei.
Dunque, mi aveva chiesto quali "indicazioni" avessi trovato in rete che Simoncini avesse come minimo avuto un'intuizione giusta.
La primissima cosa che ho fatto, non essendo medico, è stata una semplice ricerca su Google dei termini "candida" "fungi" e "cancer" insieme, la quale mi ha restituito qualcosa come 450.000 hits. Ovviamente questo non significa nulla, se non che quasi mezzo milione di siti fanno riferimento ai tre termini all'interno di una stessa pagina. Dopodichè ho aggiunto ai suddetti termini di ricerca la parola Clarke (il cognome di una dottoressa che sostiene che tutti i tumori abbiano un'eziologia di tipo micotico). Sono stati 44.000 gli hits, ovvero un decimo circa delle pagine precedenti contiene anche il nome della dottorerssa al loro interno.
Confortato dal fatto di non trovarmi su un sentiero perduto, ho cominciato ad affinare la ricerca, leggendo e raccogliendo documenti e abstracts un pò dappertutto.
Da quel che ho capito, non solo la connessione è palese, ma vi sono anche diverse fonti mediche, oltre alla Clarke, che si domandano apertamente se la candida non possa essere la CAUSA di certi tumori, se non di tutti, invece della semplice conseguenza.
Le copio-incollo alcune bibliografie e riferimenti, in ordine sparso.
Glielo ripeto, prima che perda tempo a spiegarmelo lei: tutto ciò che le allego non dimostra nulla di specifico, se non che una correlazione di tipo interattivo fra la candida e tumori, esiste di sicuro, e che il dubbio che la prima possa essere addirittura la causa stessa del tumore non alberga certo nel solo Simoncini ("Candida albicans as a promoter of oral mucosal neoplasia", "Possible mycological etiology of oral mucosal cancer", "Does Candida bave a role in oral epithelial neoplasia", ecc.).
Ecco perchè mi sento perfettamente a posto nel dire che Simoncini merita di tutto meno che di essere trattato come un ciarlatano, e ritengo a mia volta ingiusto, oltre che ingiustificato, l'attacco a tutto campo che lei gli porta da tempo.
Massimo Mazzucco
Br J Cancer 1998 Mar;77(6):1015-20
1 di 1
Cross-reactivity between Candida albicans and human ovarian carcinoma as' revealed by monoclonal antibodies PAIOF and C6.
Schneider J, Moragues D, Martinez N, Romero H, Jimenez E, Ponton J
Departmento de Especialidades Medico-Quirurgicas, Facultad de Medicina y Odontologia, Universidad del Pais Vasco, Bilbao, Vizcaya, Spain.
Summary Antibodies against Candida albicans antigenic deterrninants have been reported to cross-react with human tumour cells. We have found that two monoclonal antibodies, C6 and PA 1 OF, developed at our laboratory against C. albicans antigenic deterrninants, cross-react with human ovarian cancer on Western blots and immunohistochenústry. We have subsequently used one of then«~ PA I OOF, to test by means of immunohistochemistry a series of 37 human ovarian carcinomas. Out of 37 tumours, 25 (67.6%) expressed the antigen recognized by PAIOF. The reactivity, however, was concentrated on the subgroup of particularly aggressive, invasive carcinomas in advanced stages of the disease (19 out of 24 positive), whereas the antigen was expressed significantly less (P=0.0007) in the subgroup of much less aggressive stage I tumours of low malignant potential, also called borderline carcinomas (2 out of 13 positive). This cross-reactivity between C. albicans and ovarian carcinoma seems to be attributable to a common antigenic determinant related to tumour aggressiveness.
PNM: 9528850, UI: 98187699-
JNeurosurg 1984 Feb;60(2):428-30
Cerebellar mass caused by Candida species. Case report.
Ilgren EB, Westmorland,D, Adams. CB, Mitcheli RG
1 di 1
The authors report a case of cerebellar pseudotumor caused by a Candida species without evidence of any underlying systenúc disorder or extracranial disease. Total removal followed by treatment with ampliotericin B resulted in a favorable outcome.
PNffD: 6693969, UL 84113895
Chung Hua Kou Chiang Hsueh Tsa Chih 1994 Nov;29(6):3 3 9-41, 3 84
[Effect of candidal infection on the hyperplastic oral epitheliumj.
[Article in Chinese]
Zhang K-H, Wang HJ, Qin JX
School of Stomatology, Beijing Medical University.
1 di 1
DMBA was used to produce oral epithelial changes, from benign hyperplasia to epithellal dysplasia of different severity in golden hamsters. Thereafter, they were inoculated with candida albicans. The result shows that candidal infection can induce epithelial dysplasia in benign hyperplasia; and in epithelial dysplasia, candidal infection wili promote malignant transformation. It implies that candidal infection of the oral leukoplasia should be detected and treated.
PNW: 7743876, UI: 95262502
Chir Ital 1986 Jun;38(3):299-304
[Candida esophagitis simulatìng a neoplasm].
[Article in.Italian]
Rumi A, Testone G, Piccioli R
The authors report a case of Candida esophagitis developed like a malignant neoplasm. They explain the severe lesions according to the last physiopathological findings and emphasize the role of roentgenographic and endoscopic (biopsies and brushing) exanùnations in the differential diagnosis.
PN41D: 3791533, UI: 87078626
Emerg Infeci Dis 1997 Apr-Jun;3(2):113-27
Polycystic kidney disease: an unrecognized emerging ínfectious disease?
Miller-Hjelle NU, Hjelle JT, Jones M, Mayberry WR, Dombrink-Kurtzman AU, Peterson
Nowal'A- DM, Darras FS
Department of Biomedical and Therapeutic Sciences, University of Illinois Cofiege of Medicine at Peoria 61656, USA. Marcia. A.Nfiller@uic.edu
Polycystic kidney disease (PKD) is one of the most conunon genetic diseases in humans. We contend that it may be an emerging infectious disease and/or núcrobial toxicosis in a vulnerable human subpopulation. Use of a differential activation protocol for the Limulus amebocyte lysate (LAL) assay showed bacterial endotoxin and fungal (I-->3)-beta-D-glucans in cyst fluids from human kidneys with PKD. Fatty acid analysis of cyst fluid confirmed the presence of 3-hydroxy fatty acids characteristic of endotoxin. ' Tissue and cyst fluid from three PKD patients were exanùned for fungal components. Serologic tests showed Fusarium, Aspergillus, and Candida antigens. IgE, but not IgG, reactive with Fusarium and Candida were also detected in cyst fluid. Fungal DNA was detected in kidney tissue and cyst fluid from these three PKD patients, but not in healthy human kidney tissue. 3vVe examine the intertwined nature of the actions of endotoxin and fungal components, sphingolipid biology in PKD, the structure of PKD gene products, ínfections, and integrity of gut function to establish a mechanistic hypothesis for microbial provocation of human cystic disease. Proof of this hypothesis will require identification of the microbes and microbial components involved and multifaceted studies of PKD cell biology.
Carcinogenesis 1992 May;13(5):783-6
Candida albicans as a promoter of oral mucosal neoplasia.
O'Grady H, Reade PC
Section of Oral Medicine and Oral Surgery, School of Dental Science, University of Melbourne, Victoria, Australia.
A model of oral mucosal carcinogenesis using the water-soluble carcinogen 4-nitroquinoline-l-oxide (4NQO) was combined with a model of oral mucosal candidosis to exarnine the ability of Candida albicans to promote the development of neoplasia in suitably initiated epithelium. Sprague-Dawley rats were initiated by the application of 4NQO to their palatal and tongue mucosa 3 times weekly for 4 weeks. The animals then received either application of a phorbol ester to act as a promoter, induction of experimental oral Mucosal infection with C. albicans, or no further procedures. Animals were killed at 34 or 52 weeks and the tongues and palates sectioned for light-microscopic examination. Control groups with no treatment, mucosal infection only, phorbol ester application only, 4NQO with the tetracycline or vehicle application only were also used. The development of carcinoma in the experimental groups was similar to that in the positive control groups, indicating that the particular strain of Candida used had a similar ability to promote neoplastic changes as the known promoter phorbol-12,13-didecanoate and caused neoplastic changes to occur by week 34 with no additional lesions occurring by week 52. This indicated that the speculation that strains of C. albicans may participate in causing neoplastic transformation in
humans was well fbunded.
PN11D: 1586990, UI: 92266525
Carcinogenesis 1987 Oct;8(10):1543-8
Possible mycological etiology of oral mucosal cancer: catalytic potential of infecting Candida albicans and other yeasts in productio'n of N-nitr*OsobenzyIrnethylarnine.
Krogh P, Rald B, Holmstrup P
Department of Nficrobiology, Royal Dental College, Copenhagen, Denmark.
Yeasts were isolated from 12 cases of oral precancerous lesions (leukoplakia and erythroleukoplakia) by sampling the lesion as well as normal mucosa of each patient, yielding 21 strains of Candida albicans belonging to 15 biotypes, two strains of C. tropicalis, one strain of C. parapsilosis and two strains of Torulopsis glabrata. Biopsies were obtained from the lesions for histologic examination. The catalytic potential of the yeast strains to form N-nitrosobenzylmethylan-úne (NBMA) from the precursors N-benzylmethylan-úne and nitrite was assessed at pH 6.8. The NBMA produced was identified and quantitated by h.p.l.c. and confirmed by g.c.-m.s. Nitrosation rates were calculated as total nitrosamine subtracted the chemically produced nitrosamine, and related to number of yeast cells. The yeast strains differed in nitrosation potential (P less than 0.001), ranking from 0 to 1.2 micrograms NBMA/10(6) cells. Candida albicans strains~ belonging to the biotypes 051, 147, 151, 153, 157 and 353, which constitute more rarely occurring biotypes, exhibited the highest nitrosation potential. Candida tropicalis, C. parapsilosis and T. glabrata were ranked lower. Strains with high nitrosation potential were generally isolated from lesions with more advanced precancerous changes. The yeast cells were present in the superficial part of the epithelium of the lesions as branching mycelium, and in some cases extending from the mucosal surface to the deeper epithelial cell layers. This might represent a fungal transportation system which could channel precursors in the saliva at the mucosal surface to the deeper part of the epithelium where the produced nitrosannine could be dèposited. Thus, further evidence is provided supporting the hypothesis that certain strains of C. albicans and of other yeasts play a causai role in the development of oral cancer, by means of endogenous nitrosamine production.
PMID: 3652390, UI: 88002673
ROFO Fortschr Geb Rontgenstr Nuklearmed 1986 Jan; 144(1):106-7
[Candida esophagitis with the roentgenologic appearance of a carcinomal.
[Article in German]
Fobbe F, Hamm B, Kroll HU
PNfiD: 3003825, UI: 86122028
MedDoswMìkrobiol 1994-46(1-2).-83-6
[Trial of evaluating co-existent fungal infection during course of neoplastic disease in patients with lung cancerj.
[Article in Polish]
Batura-Gabryel H, Firlik M, Wieczorek U
Kfinika Pneurnonologii, Instytutu Chorob Wewnetrznych AM w Poznaniu.
The study was aimed at deternúnation of possible connection between co-existing fungal infection in patients with lung carcinoma with course of neoplastic disease and ability to achieve remission by application of different methods of treatment. The study involved 25 patients with histologically confirmed lung carcinoma. Their sputum and bronchial rinsings were tested mycologically. The tests were performed at the moment of diagnosis of the diseases, during and after treatment. In all patients occurrence and type of Candída infections was investigated. Dynarnics of fungal infection was measured by a scale from rninimal to very severe. In about 1/3 of patients at the moment of diagnosis of the disease, severe or very severe infection was seen which was dependent of stage of the disease advancement. These preliminary studies scem to indicate that presence of severe or very severe fungal infection is not favourable prognostically and frequently correlates with a progress of neoplastic changes and worse response to treatment.
PMID: 7967936, UI: 95057508
Laryngoscope 1982 Jun;92(6 Pt 1):644-7
Pseudocarcinornatous hyperplasia of the laryiìx due to Candida albicans.
Hicks JN, Peters GE
A fernale patient presented with hoarseness. Findings on physical exarnination showed whitish true vocal cords. Laryngeal biopsies were performed on two two occasions. On the first biopsy a histopathological diagnosis of Candida albicans and acanthosis was controversial because the acanthosis resembled squamous cell carcinoma. On the second biopsy, several months later, the diagnosis of acanthosis was again controversial, but a diagnosis of pseudocarcinomatous hyperplasia was not determined until several months later. Finally, we can point out that pseudocarcinofnatous hyperplasia can be associated with primary candidiasis and state that hoarseness, whitish true vocal cords, and pseudocarcinornatous hyperplasia can masquerade as squamous cell carcinoma of the larynx.
PNfID: 7087625,UI:82218853
ZentralbINéurochir 1998-59(2):129-31
Cerebral candidiasis presenting as a mass lesion.
Hanci M, Kafadar A, Sarioglu A, Islak C, Oz B
Department of Neurosurgery, Cerrahpasa Medical Faculty University of Istanbul, Turkey.
1 di 1
The authors report of a case of pseudotumour caused by Candida species without evidence of any underlying disease. No portal of entry of the infection was fbund. Total removal followed by treatment with flucanazole resulted in- a favorable outcome. We discuss the differential diagnosis of a huge calcified intracranial mass lesíon without any soft tissue component.
PNM: 9674103, UI: 98338908
JMed VetAllycol 1989-127(5):277-94
Does Candida bave a role in oral epithelial neoplasia?
Field EA, Field JK, Ma,rtin MV
Department of Clinical Dental Sciences, University of Liverpool, U.K.
Candida species are responsible for a wide variety of superficial infections of man [59] and the pathogenic role of these yeasts in many conditions has now been defined. There is, however, a great deal of controversy concerning the role of Candida species in the development of epithelial neoplasia. Vagirial and cutaneous candidosis are relatively common but there is little firm clinical or epidenúological evidence to link them to cervical neoplasia or skin carcinoma [59]. The converse is true however for oral candidosis where chronic Candida infection and neoplasia have been strongly linked. The aim of this review is to explore and evaluate the experimental and epidemiological evidence supporting an association between Candida species and oral neoplasia.
PMID: 2689621, Ul: 90095753
Chung Hua Chung Du Tsa Chih 1986 Jan-8(1):42-4
[Morphology of fungi in the slides prepared from esopbageal balloons].
[Article in Chinese]
1,762 cases were selected at randòm from 17,000 persons screened by esophageal balloon in 4 communes of Linxian County. The morphologic appearance of fungi was studied in 4 slides of each case selected. According to the shape of clumps formed by fungi and bacteria in the slides, morphologic 4 types were seen: cotton-like, camel hair-like, hair-like and tree-branch-like. In the prelin-iinary microscopic analysis, the following species of fungi were noted: Candida, Leptothrix, Actinornyces, Alternaria, Fusarium and Penicillium. Some of the fungi in the slides may have been taken from the oral or pharyngeal cavity, which may be due to, at least in part, the poor oral hygiene in the population examined. A positive association was shown between the quantity of fungi in the slides and the esophageal epithelial dysplasia and carcinoma, but íts biological significance should be studied further.
PNfID: 3732022, UL 86273952
Minerva Stomatol 1991 Oct;40(10):675-9
[The elinical aspects of 4 cases of oral Kaposis sarconia].
Piazzi M, Bonazzi V, Degli Esposti R
Istituto Policattedra di Clinica Odontoiatrica, Universita degli Studi di Bologna.
The authors report 4 cases of patients with AIDS and harbouring oral lesions of Kaposi's sarcoma. They describe the macroscopic appearance and clinical signs in relation to epidenúc Kaposi's systemic ones. Because of the anamnestic or coexistence of oral mycosis (Candida), in every case the authors suppose that it may precede Kaposi's manifestations, with a very severe prognosis, correlated to progressive and deadly course of this illness.
PNM: 1803225, UI: 92204101
Immunol Ser 1989;47:293-317
Immunomodulation in response to Candida.
Domer JE, Garner RE.
Tulane University School of Medicine, New Orleans, Louisiana.
Candidiasis may either precede or follow severe modulations in the immune system of the host. The focus of this review has been to survey the data and current interpretations for potential factors responsible for these events of immunomodulation. The mere fact that Candida infections persist is evidence of some underlying abnormality, often associated with, but not exclusively restricted to, the cell-mediated immune system. In some instances, however, the cause and effect relationship is not clear, i.e., did infection with Candida initiate the immunosuppression, or did the underlying condition result in immunosuppression allowing for Candida to initiate disease? It is possible, however, that candidal infections may begin during minor immunosuppressive events, e.g., stress, pregnancy, or selected other primary infections, but then persist beyond these events because of an intrinsic or innate immunomodulatory defect. Under such circumstances, the initial imbalance of immune function should be corrected by normal homeostatic mechanisms, unless persistent colonization with Candida perpetuates the imbalance through the production or release of immunomodulatory factors. One important target for research in this area, then, is the identification and purification of immunomodulatory factors produced or released during disease. To date, only preliminary data are available showing that the immunoregulatory potential of Candida resides in various candidal extracts, especially in the cell wall. Although the relevance of the data gathered in the experimental models might initially appear questionable, the fact that mannan, or molecules containing mannan, are known to circulate during disease (Weiner and Yount, 1976; Kerkering et al., 1979; Lehmann and Reiss, 1980) lends credence to the hypothesis. A second important target for future research is the identification of the cellular target within the immune system that responds to the Candida-derived immunomodulators. The success of these studies may well depend upon the degree of purification of the responsible factors. In fact, much of the variability observed to date in modulatory events may result from the heterogeneity of the modulator, including the possibility that antagonistic or synergistic interactions of the individual components occur. The variability observed in certain clinical settings could result from basic flaws in the normal immunoregulatory pathways in the host also, and if a link could be established between the basic flaws, the candidal extracts, and the target cell of the candidal extracts, it may be possible to manipulate the system through immunotherapy. Finally, the characterization of the candidal substances may provide yet another clinical tool for use as an immunomodulator in such disorders as cancer, inheritable immunodeficiencies, and AIDS.
+++
Do fungi play a role in the aetiology of cancer?
Reviews in Medical Microbiology. 13(1):37-42, January 2002.
Wainwright, Milton
Abstract: The recent recognition that the bacterium Helicobacter pylori potentially plays a role in the aetiology of gastric cancer has highlighted the possibility that other non-virus microorganisms, including yeasts and filamentous fungi, may also cause cancer in humans. For more than a century fungi have been implicated in the aetiology of cancer. Initially, attention was directed to yeasts in the so-called blastomycete-theory of cancer; more recently filamentous fungi have also been implicated in carcinogenesis, based largely on their ability to produce potentially carcinogenic mycotoxins. Here, the widely spread literature on the role of fungi in carcinogenesis is reviewed in the hope that it will stimulate a re-evaluation of the potential carcinogenic role of fungi.
(C) 2002 Lippincott Williams & Wilkins, Inc.
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ALTRA BIBLIOGRAFIA:
"DNA amplification for the in vitro detection of Candida albicans in head and neck squamous cell carcinomas.
" Eur Arch Otorhinolaryngol 1995;252(7):417-21 (ISSN: 0937-4477) Werner JA; Gorogh T; Lippert BM; Rudert H Department of Otorhinolaryngology, Head and Neck Surgery, University of Kiel, Germany.
La conclusione dello studio: "However, samples of DNA obtained from head and neck SCC (Squamous Cells Carcinoma) cells in vitro, Candida glabrata, and Candida parapsilosis after PCR (Polymerase Chain reaction) were found to contain homologous sequences. Application of this technique to head and neck SCC biopsies may help to identify quickly the presence of concurrent candidal species. "
Wickes B.L. (Curr Top Med Mycol 1996 Dec;7(1):71-86), Suzuki T. (J Gen Microbiol 1989 Feb;135 ( Pt 2):425-34),
Lott T.J. (Curr Genet 1993 May-Jun;23(5-6):463-7).
Odds F.C. (J Clin Microbiol 1983 Oct;18(4):849-57) - Ell S.R. (J Laryngol Otol 1996 Mar;110(3):240-2).
Coesistenza della candida e del cancro (alcuni autori):
Hopfer R.L. (J Clin Microbiol 1980 Sep;12(3):329-31): 79%
Kaben U. (Z Gesamte Inn Med 1977 Nov 15;32(22):618-22): 80%
Hughes W.T. (Pediatr Infect Dis 1982 Jan-Feb;1(1):11-8): 91%
Kiehn T.E. (Am J Clin Pathol 1980 Apr;73(4):518-21): 97,1%
Difficoltà di visualizzare i vari tipi di funghi e candide nei materiali organici da esaminare:
Escuro R.S ( Am J Med 1989 Dec;87(6):621-7), Karaev Z.O (Zh Mikrobiol Epidemiol Immunobiol 1992;(5-6):41-3) e Walsh T.J. (N Engl J Med 1991 Apr 11;324(15):1026-31).
Altra BIBLIOGRAFIA:
1. "Killer toxin and enzyme production by Candida albicans isolated from buccal mucosa in patients with cancer"
Rev Soc Bras Med Trop 1998 Nov-Dec;31(6):523-7 (ISSN: 0037-8682) de Oliveira EE; Silva SC; Soares AJ; Attux C; Cruvinel B; Silva M do R Departamento de Microbiologia, Imunologia, Parasitologia e Patologia, Universidade Federal de Goias, Goiania.
2. "Adherence of Candida albicans to epithelial cells from normal and cancerous urinary bladders" Int Urol Nephrol 1994;26(5):519-22 (ISSN: 0301-1623) Skoutelis AT; Lianou PE; Votta E; Bassaris HP; Papavassiliou Department of Medicine, Patras University Medical School, Greece.
3. "Oral colonization, phenotypic and genotypic profiles of Candida species in irradiated, dentate, xerostomic nasopharingeal carcinoma survivors" J Clin Microbiol 2000 Jun;38(6):2219-26 (ISSN: 0095-1137) Leung WK; Dassanayake RS; Yau JY; Jin LJ; Yam WC; Samaranayake LP Faculty of Dentistry, Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. link
4. "DNA amplification for the in vitro detection of Candida albicans in head and neck squamous cell carcinomas"
Eur Arch Otorhinolaryngol 1995;252(7):417-21 (ISSN: 0937-4477) Werner JA; Gorogh T; Lippert BM; Rudert H Department of Otorhinolaryngology, Head and Neck Surgery, University of Kiel, Germany.
5. "Breast cancer-specific expression of the Candida albicans cytosine deaminase gene using a transcriptional targeting approach" Cancer Gene Ther 2000 Jun;7(6):845-852 (ISSN: 0929-1903)
Anderson LM; Krotz S; Weitzman SA; Thimmapaya B Department of Microbiology and Immunology, Northwestern University Medical School, Chicago, Illinois 60611, USA.
6. Pedersen A. (Tandlaegebladet 1989 Sep;93(13):509-13), Krogh P.(Carcinogenesis 1987 Oct;8(10):1543-8), Trotoux J. (Ann Otolaryngol Chir Cervicofac 1982;99(12):553-6) Attestano il nesso causale tra la candida e la formazione del carcinoma epidermoidale della lingua.
7. Zhang K.V (Chung Hua Kou Chiang Hsueh Tsa Chih 1994 Nov;29(6):339-41, 384) O’Grady J.F. (Carcinogenesis 1992 May;13(5):783-6) - Neoplasie del cavo orale.
Hicks J.N (Laryngoscope 1982 Jun;92(6 Pt 1):644-7) - Neoplasia della laringe.
8. Field E.A. (J Med Vet Mycol 1989;27(5):277-94), Wang F.R. (Chung-hua Ping Li Hsueh Tsa Chih 1988Sep;17(3):170-2) e (Chung Hua Chung Liu Tsa Chih 1981 May;3(2) - Cancro del polmone.
9. Joseph P. (Chest 1980 Aug;78(2):340-3) - Mixoma atriale.
10. Rumi A. (Chir Ital 1986 Jun;38(3):299-304), Fobbe F. (ROFO Fortschr Geb Rontgenstr Nuklearmed 1986 Jan;144(1):106-7) Bathia V. (Indian J Gastroenterol 1989 Jul;8(3):171-2) marnejon T. (Am J Gastroenterol 1997 Feb;92(2):354-6) - Cancro dell’esofago.
11. Taguchi T. (J Pediatr Gastroenterol Nutr 1991 Apr;12(3):394-9) - Carcinoma dell’intestino Raina V. (Postgrad Med J 1989 Feb;65(760):83-5) - Morbo di Hodgkin
12. Piazzi M. (Minerva Stomatol 1991 Oct;40(10):675-9) per il M. di Kaposi Mannell A. (S Afr J Surg 1990 Mar, 28(1):26-7) - Tumore del pancreas
Dunque, mi aveva chiesto quali "indicazioni" avessi trovato in rete che Simoncini avesse come minimo avuto un'intuizione giusta.
La primissima cosa che ho fatto, non essendo medico, è stata una semplice ricerca su Google dei termini "candida" "fungi" e "cancer" insieme, la quale mi ha restituito qualcosa come 450.000 hits. Ovviamente questo non significa nulla, se non che quasi mezzo milione di siti fanno riferimento ai tre termini all'interno di una stessa pagina. Dopodichè ho aggiunto ai suddetti termini di ricerca la parola Clarke (il cognome di una dottoressa che sostiene che tutti i tumori abbiano un'eziologia di tipo micotico). Sono stati 44.000 gli hits, ovvero un decimo circa delle pagine precedenti contiene anche il nome della dottorerssa al loro interno.
Confortato dal fatto di non trovarmi su un sentiero perduto, ho cominciato ad affinare la ricerca, leggendo e raccogliendo documenti e abstracts un pò dappertutto.
Da quel che ho capito, non solo la connessione è palese, ma vi sono anche diverse fonti mediche, oltre alla Clarke, che si domandano apertamente se la candida non possa essere la CAUSA di certi tumori, se non di tutti, invece della semplice conseguenza.
Le copio-incollo alcune bibliografie e riferimenti, in ordine sparso.
Glielo ripeto, prima che perda tempo a spiegarmelo lei: tutto ciò che le allego non dimostra nulla di specifico, se non che una correlazione di tipo interattivo fra la candida e tumori, esiste di sicuro, e che il dubbio che la prima possa essere addirittura la causa stessa del tumore non alberga certo nel solo Simoncini ("Candida albicans as a promoter of oral mucosal neoplasia", "Possible mycological etiology of oral mucosal cancer", "Does Candida bave a role in oral epithelial neoplasia", ecc.).
Ecco perchè mi sento perfettamente a posto nel dire che Simoncini merita di tutto meno che di essere trattato come un ciarlatano, e ritengo a mia volta ingiusto, oltre che ingiustificato, l'attacco a tutto campo che lei gli porta da tempo.
Massimo Mazzucco
Br J Cancer 1998 Mar;77(6):1015-20
1 di 1
Cross-reactivity between Candida albicans and human ovarian carcinoma as' revealed by monoclonal antibodies PAIOF and C6.
Schneider J, Moragues D, Martinez N, Romero H, Jimenez E, Ponton J
Departmento de Especialidades Medico-Quirurgicas, Facultad de Medicina y Odontologia, Universidad del Pais Vasco, Bilbao, Vizcaya, Spain.
Summary Antibodies against Candida albicans antigenic deterrninants have been reported to cross-react with human tumour cells. We have found that two monoclonal antibodies, C6 and PA 1 OF, developed at our laboratory against C. albicans antigenic deterrninants, cross-react with human ovarian cancer on Western blots and immunohistochenústry. We have subsequently used one of then«~ PA I OOF, to test by means of immunohistochemistry a series of 37 human ovarian carcinomas. Out of 37 tumours, 25 (67.6%) expressed the antigen recognized by PAIOF. The reactivity, however, was concentrated on the subgroup of particularly aggressive, invasive carcinomas in advanced stages of the disease (19 out of 24 positive), whereas the antigen was expressed significantly less (P=0.0007) in the subgroup of much less aggressive stage I tumours of low malignant potential, also called borderline carcinomas (2 out of 13 positive). This cross-reactivity between C. albicans and ovarian carcinoma seems to be attributable to a common antigenic determinant related to tumour aggressiveness.
PNM: 9528850, UI: 98187699-
JNeurosurg 1984 Feb;60(2):428-30
Cerebellar mass caused by Candida species. Case report.
Ilgren EB, Westmorland,D, Adams. CB, Mitcheli RG
1 di 1
The authors report a case of cerebellar pseudotumor caused by a Candida species without evidence of any underlying systenúc disorder or extracranial disease. Total removal followed by treatment with ampliotericin B resulted in a favorable outcome.
PNffD: 6693969, UL 84113895
Chung Hua Kou Chiang Hsueh Tsa Chih 1994 Nov;29(6):3 3 9-41, 3 84
[Effect of candidal infection on the hyperplastic oral epitheliumj.
[Article in Chinese]
Zhang K-H, Wang HJ, Qin JX
School of Stomatology, Beijing Medical University.
1 di 1
DMBA was used to produce oral epithelial changes, from benign hyperplasia to epithellal dysplasia of different severity in golden hamsters. Thereafter, they were inoculated with candida albicans. The result shows that candidal infection can induce epithelial dysplasia in benign hyperplasia; and in epithelial dysplasia, candidal infection wili promote malignant transformation. It implies that candidal infection of the oral leukoplasia should be detected and treated.
PNW: 7743876, UI: 95262502
Chir Ital 1986 Jun;38(3):299-304
[Candida esophagitis simulatìng a neoplasm].
[Article in.Italian]
Rumi A, Testone G, Piccioli R
The authors report a case of Candida esophagitis developed like a malignant neoplasm. They explain the severe lesions according to the last physiopathological findings and emphasize the role of roentgenographic and endoscopic (biopsies and brushing) exanùnations in the differential diagnosis.
PN41D: 3791533, UI: 87078626
Emerg Infeci Dis 1997 Apr-Jun;3(2):113-27
Polycystic kidney disease: an unrecognized emerging ínfectious disease?
Miller-Hjelle NU, Hjelle JT, Jones M, Mayberry WR, Dombrink-Kurtzman AU, Peterson
Nowal'A- DM, Darras FS
Department of Biomedical and Therapeutic Sciences, University of Illinois Cofiege of Medicine at Peoria 61656, USA. Marcia. A.Nfiller@uic.edu
Polycystic kidney disease (PKD) is one of the most conunon genetic diseases in humans. We contend that it may be an emerging infectious disease and/or núcrobial toxicosis in a vulnerable human subpopulation. Use of a differential activation protocol for the Limulus amebocyte lysate (LAL) assay showed bacterial endotoxin and fungal (I-->3)-beta-D-glucans in cyst fluids from human kidneys with PKD. Fatty acid analysis of cyst fluid confirmed the presence of 3-hydroxy fatty acids characteristic of endotoxin. ' Tissue and cyst fluid from three PKD patients were exanùned for fungal components. Serologic tests showed Fusarium, Aspergillus, and Candida antigens. IgE, but not IgG, reactive with Fusarium and Candida were also detected in cyst fluid. Fungal DNA was detected in kidney tissue and cyst fluid from these three PKD patients, but not in healthy human kidney tissue. 3vVe examine the intertwined nature of the actions of endotoxin and fungal components, sphingolipid biology in PKD, the structure of PKD gene products, ínfections, and integrity of gut function to establish a mechanistic hypothesis for microbial provocation of human cystic disease. Proof of this hypothesis will require identification of the microbes and microbial components involved and multifaceted studies of PKD cell biology.
Carcinogenesis 1992 May;13(5):783-6
Candida albicans as a promoter of oral mucosal neoplasia.
O'Grady H, Reade PC
Section of Oral Medicine and Oral Surgery, School of Dental Science, University of Melbourne, Victoria, Australia.
A model of oral mucosal carcinogenesis using the water-soluble carcinogen 4-nitroquinoline-l-oxide (4NQO) was combined with a model of oral mucosal candidosis to exarnine the ability of Candida albicans to promote the development of neoplasia in suitably initiated epithelium. Sprague-Dawley rats were initiated by the application of 4NQO to their palatal and tongue mucosa 3 times weekly for 4 weeks. The animals then received either application of a phorbol ester to act as a promoter, induction of experimental oral Mucosal infection with C. albicans, or no further procedures. Animals were killed at 34 or 52 weeks and the tongues and palates sectioned for light-microscopic examination. Control groups with no treatment, mucosal infection only, phorbol ester application only, 4NQO with the tetracycline or vehicle application only were also used. The development of carcinoma in the experimental groups was similar to that in the positive control groups, indicating that the particular strain of Candida used had a similar ability to promote neoplastic changes as the known promoter phorbol-12,13-didecanoate and caused neoplastic changes to occur by week 34 with no additional lesions occurring by week 52. This indicated that the speculation that strains of C. albicans may participate in causing neoplastic transformation in
humans was well fbunded.
PN11D: 1586990, UI: 92266525
Carcinogenesis 1987 Oct;8(10):1543-8
Possible mycological etiology of oral mucosal cancer: catalytic potential of infecting Candida albicans and other yeasts in productio'n of N-nitr*OsobenzyIrnethylarnine.
Krogh P, Rald B, Holmstrup P
Department of Nficrobiology, Royal Dental College, Copenhagen, Denmark.
Yeasts were isolated from 12 cases of oral precancerous lesions (leukoplakia and erythroleukoplakia) by sampling the lesion as well as normal mucosa of each patient, yielding 21 strains of Candida albicans belonging to 15 biotypes, two strains of C. tropicalis, one strain of C. parapsilosis and two strains of Torulopsis glabrata. Biopsies were obtained from the lesions for histologic examination. The catalytic potential of the yeast strains to form N-nitrosobenzylmethylan-úne (NBMA) from the precursors N-benzylmethylan-úne and nitrite was assessed at pH 6.8. The NBMA produced was identified and quantitated by h.p.l.c. and confirmed by g.c.-m.s. Nitrosation rates were calculated as total nitrosamine subtracted the chemically produced nitrosamine, and related to number of yeast cells. The yeast strains differed in nitrosation potential (P less than 0.001), ranking from 0 to 1.2 micrograms NBMA/10(6) cells. Candida albicans strains~ belonging to the biotypes 051, 147, 151, 153, 157 and 353, which constitute more rarely occurring biotypes, exhibited the highest nitrosation potential. Candida tropicalis, C. parapsilosis and T. glabrata were ranked lower. Strains with high nitrosation potential were generally isolated from lesions with more advanced precancerous changes. The yeast cells were present in the superficial part of the epithelium of the lesions as branching mycelium, and in some cases extending from the mucosal surface to the deeper epithelial cell layers. This might represent a fungal transportation system which could channel precursors in the saliva at the mucosal surface to the deeper part of the epithelium where the produced nitrosannine could be dèposited. Thus, further evidence is provided supporting the hypothesis that certain strains of C. albicans and of other yeasts play a causai role in the development of oral cancer, by means of endogenous nitrosamine production.
PMID: 3652390, UI: 88002673
ROFO Fortschr Geb Rontgenstr Nuklearmed 1986 Jan; 144(1):106-7
[Candida esophagitis with the roentgenologic appearance of a carcinomal.
[Article in German]
Fobbe F, Hamm B, Kroll HU
PNfiD: 3003825, UI: 86122028
MedDoswMìkrobiol 1994-46(1-2).-83-6
[Trial of evaluating co-existent fungal infection during course of neoplastic disease in patients with lung cancerj.
[Article in Polish]
Batura-Gabryel H, Firlik M, Wieczorek U
Kfinika Pneurnonologii, Instytutu Chorob Wewnetrznych AM w Poznaniu.
The study was aimed at deternúnation of possible connection between co-existing fungal infection in patients with lung carcinoma with course of neoplastic disease and ability to achieve remission by application of different methods of treatment. The study involved 25 patients with histologically confirmed lung carcinoma. Their sputum and bronchial rinsings were tested mycologically. The tests were performed at the moment of diagnosis of the diseases, during and after treatment. In all patients occurrence and type of Candída infections was investigated. Dynarnics of fungal infection was measured by a scale from rninimal to very severe. In about 1/3 of patients at the moment of diagnosis of the disease, severe or very severe infection was seen which was dependent of stage of the disease advancement. These preliminary studies scem to indicate that presence of severe or very severe fungal infection is not favourable prognostically and frequently correlates with a progress of neoplastic changes and worse response to treatment.
PMID: 7967936, UI: 95057508
Laryngoscope 1982 Jun;92(6 Pt 1):644-7
Pseudocarcinornatous hyperplasia of the laryiìx due to Candida albicans.
Hicks JN, Peters GE
A fernale patient presented with hoarseness. Findings on physical exarnination showed whitish true vocal cords. Laryngeal biopsies were performed on two two occasions. On the first biopsy a histopathological diagnosis of Candida albicans and acanthosis was controversial because the acanthosis resembled squamous cell carcinoma. On the second biopsy, several months later, the diagnosis of acanthosis was again controversial, but a diagnosis of pseudocarcinomatous hyperplasia was not determined until several months later. Finally, we can point out that pseudocarcinofnatous hyperplasia can be associated with primary candidiasis and state that hoarseness, whitish true vocal cords, and pseudocarcinornatous hyperplasia can masquerade as squamous cell carcinoma of the larynx.
PNfID: 7087625,UI:82218853
ZentralbINéurochir 1998-59(2):129-31
Cerebral candidiasis presenting as a mass lesion.
Hanci M, Kafadar A, Sarioglu A, Islak C, Oz B
Department of Neurosurgery, Cerrahpasa Medical Faculty University of Istanbul, Turkey.
1 di 1
The authors report of a case of pseudotumour caused by Candida species without evidence of any underlying disease. No portal of entry of the infection was fbund. Total removal followed by treatment with flucanazole resulted in- a favorable outcome. We discuss the differential diagnosis of a huge calcified intracranial mass lesíon without any soft tissue component.
PNM: 9674103, UI: 98338908
JMed VetAllycol 1989-127(5):277-94
Does Candida bave a role in oral epithelial neoplasia?
Field EA, Field JK, Ma,rtin MV
Department of Clinical Dental Sciences, University of Liverpool, U.K.
Candida species are responsible for a wide variety of superficial infections of man [59] and the pathogenic role of these yeasts in many conditions has now been defined. There is, however, a great deal of controversy concerning the role of Candida species in the development of epithelial neoplasia. Vagirial and cutaneous candidosis are relatively common but there is little firm clinical or epidenúological evidence to link them to cervical neoplasia or skin carcinoma [59]. The converse is true however for oral candidosis where chronic Candida infection and neoplasia have been strongly linked. The aim of this review is to explore and evaluate the experimental and epidemiological evidence supporting an association between Candida species and oral neoplasia.
PMID: 2689621, Ul: 90095753
Chung Hua Chung Du Tsa Chih 1986 Jan-8(1):42-4
[Morphology of fungi in the slides prepared from esopbageal balloons].
[Article in Chinese]
1,762 cases were selected at randòm from 17,000 persons screened by esophageal balloon in 4 communes of Linxian County. The morphologic appearance of fungi was studied in 4 slides of each case selected. According to the shape of clumps formed by fungi and bacteria in the slides, morphologic 4 types were seen: cotton-like, camel hair-like, hair-like and tree-branch-like. In the prelin-iinary microscopic analysis, the following species of fungi were noted: Candida, Leptothrix, Actinornyces, Alternaria, Fusarium and Penicillium. Some of the fungi in the slides may have been taken from the oral or pharyngeal cavity, which may be due to, at least in part, the poor oral hygiene in the population examined. A positive association was shown between the quantity of fungi in the slides and the esophageal epithelial dysplasia and carcinoma, but íts biological significance should be studied further.
PNfID: 3732022, UL 86273952
Minerva Stomatol 1991 Oct;40(10):675-9
[The elinical aspects of 4 cases of oral Kaposis sarconia].
Piazzi M, Bonazzi V, Degli Esposti R
Istituto Policattedra di Clinica Odontoiatrica, Universita degli Studi di Bologna.
The authors report 4 cases of patients with AIDS and harbouring oral lesions of Kaposi's sarcoma. They describe the macroscopic appearance and clinical signs in relation to epidenúc Kaposi's systemic ones. Because of the anamnestic or coexistence of oral mycosis (Candida), in every case the authors suppose that it may precede Kaposi's manifestations, with a very severe prognosis, correlated to progressive and deadly course of this illness.
PNM: 1803225, UI: 92204101
Immunol Ser 1989;47:293-317
Immunomodulation in response to Candida.
Domer JE, Garner RE.
Tulane University School of Medicine, New Orleans, Louisiana.
Candidiasis may either precede or follow severe modulations in the immune system of the host. The focus of this review has been to survey the data and current interpretations for potential factors responsible for these events of immunomodulation. The mere fact that Candida infections persist is evidence of some underlying abnormality, often associated with, but not exclusively restricted to, the cell-mediated immune system. In some instances, however, the cause and effect relationship is not clear, i.e., did infection with Candida initiate the immunosuppression, or did the underlying condition result in immunosuppression allowing for Candida to initiate disease? It is possible, however, that candidal infections may begin during minor immunosuppressive events, e.g., stress, pregnancy, or selected other primary infections, but then persist beyond these events because of an intrinsic or innate immunomodulatory defect. Under such circumstances, the initial imbalance of immune function should be corrected by normal homeostatic mechanisms, unless persistent colonization with Candida perpetuates the imbalance through the production or release of immunomodulatory factors. One important target for research in this area, then, is the identification and purification of immunomodulatory factors produced or released during disease. To date, only preliminary data are available showing that the immunoregulatory potential of Candida resides in various candidal extracts, especially in the cell wall. Although the relevance of the data gathered in the experimental models might initially appear questionable, the fact that mannan, or molecules containing mannan, are known to circulate during disease (Weiner and Yount, 1976; Kerkering et al., 1979; Lehmann and Reiss, 1980) lends credence to the hypothesis. A second important target for future research is the identification of the cellular target within the immune system that responds to the Candida-derived immunomodulators. The success of these studies may well depend upon the degree of purification of the responsible factors. In fact, much of the variability observed to date in modulatory events may result from the heterogeneity of the modulator, including the possibility that antagonistic or synergistic interactions of the individual components occur. The variability observed in certain clinical settings could result from basic flaws in the normal immunoregulatory pathways in the host also, and if a link could be established between the basic flaws, the candidal extracts, and the target cell of the candidal extracts, it may be possible to manipulate the system through immunotherapy. Finally, the characterization of the candidal substances may provide yet another clinical tool for use as an immunomodulator in such disorders as cancer, inheritable immunodeficiencies, and AIDS.
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Do fungi play a role in the aetiology of cancer?
Reviews in Medical Microbiology. 13(1):37-42, January 2002.
Wainwright, Milton
Abstract: The recent recognition that the bacterium Helicobacter pylori potentially plays a role in the aetiology of gastric cancer has highlighted the possibility that other non-virus microorganisms, including yeasts and filamentous fungi, may also cause cancer in humans. For more than a century fungi have been implicated in the aetiology of cancer. Initially, attention was directed to yeasts in the so-called blastomycete-theory of cancer; more recently filamentous fungi have also been implicated in carcinogenesis, based largely on their ability to produce potentially carcinogenic mycotoxins. Here, the widely spread literature on the role of fungi in carcinogenesis is reviewed in the hope that it will stimulate a re-evaluation of the potential carcinogenic role of fungi.
(C) 2002 Lippincott Williams & Wilkins, Inc.
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ALTRA BIBLIOGRAFIA:
"DNA amplification for the in vitro detection of Candida albicans in head and neck squamous cell carcinomas.
" Eur Arch Otorhinolaryngol 1995;252(7):417-21 (ISSN: 0937-4477) Werner JA; Gorogh T; Lippert BM; Rudert H Department of Otorhinolaryngology, Head and Neck Surgery, University of Kiel, Germany.
La conclusione dello studio: "However, samples of DNA obtained from head and neck SCC (Squamous Cells Carcinoma) cells in vitro, Candida glabrata, and Candida parapsilosis after PCR (Polymerase Chain reaction) were found to contain homologous sequences. Application of this technique to head and neck SCC biopsies may help to identify quickly the presence of concurrent candidal species. "
Wickes B.L. (Curr Top Med Mycol 1996 Dec;7(1):71-86), Suzuki T. (J Gen Microbiol 1989 Feb;135 ( Pt 2):425-34),
Lott T.J. (Curr Genet 1993 May-Jun;23(5-6):463-7).
Odds F.C. (J Clin Microbiol 1983 Oct;18(4):849-57) - Ell S.R. (J Laryngol Otol 1996 Mar;110(3):240-2).
Coesistenza della candida e del cancro (alcuni autori):
Hopfer R.L. (J Clin Microbiol 1980 Sep;12(3):329-31): 79%
Kaben U. (Z Gesamte Inn Med 1977 Nov 15;32(22):618-22): 80%
Hughes W.T. (Pediatr Infect Dis 1982 Jan-Feb;1(1):11-8): 91%
Kiehn T.E. (Am J Clin Pathol 1980 Apr;73(4):518-21): 97,1%
Difficoltà di visualizzare i vari tipi di funghi e candide nei materiali organici da esaminare:
Escuro R.S ( Am J Med 1989 Dec;87(6):621-7), Karaev Z.O (Zh Mikrobiol Epidemiol Immunobiol 1992;(5-6):41-3) e Walsh T.J. (N Engl J Med 1991 Apr 11;324(15):1026-31).
Altra BIBLIOGRAFIA:
1. "Killer toxin and enzyme production by Candida albicans isolated from buccal mucosa in patients with cancer"
Rev Soc Bras Med Trop 1998 Nov-Dec;31(6):523-7 (ISSN: 0037-8682) de Oliveira EE; Silva SC; Soares AJ; Attux C; Cruvinel B; Silva M do R Departamento de Microbiologia, Imunologia, Parasitologia e Patologia, Universidade Federal de Goias, Goiania.
2. "Adherence of Candida albicans to epithelial cells from normal and cancerous urinary bladders" Int Urol Nephrol 1994;26(5):519-22 (ISSN: 0301-1623) Skoutelis AT; Lianou PE; Votta E; Bassaris HP; Papavassiliou Department of Medicine, Patras University Medical School, Greece.
3. "Oral colonization, phenotypic and genotypic profiles of Candida species in irradiated, dentate, xerostomic nasopharingeal carcinoma survivors" J Clin Microbiol 2000 Jun;38(6):2219-26 (ISSN: 0095-1137) Leung WK; Dassanayake RS; Yau JY; Jin LJ; Yam WC; Samaranayake LP Faculty of Dentistry, Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China. link
4. "DNA amplification for the in vitro detection of Candida albicans in head and neck squamous cell carcinomas"
Eur Arch Otorhinolaryngol 1995;252(7):417-21 (ISSN: 0937-4477) Werner JA; Gorogh T; Lippert BM; Rudert H Department of Otorhinolaryngology, Head and Neck Surgery, University of Kiel, Germany.
5. "Breast cancer-specific expression of the Candida albicans cytosine deaminase gene using a transcriptional targeting approach" Cancer Gene Ther 2000 Jun;7(6):845-852 (ISSN: 0929-1903)
Anderson LM; Krotz S; Weitzman SA; Thimmapaya B Department of Microbiology and Immunology, Northwestern University Medical School, Chicago, Illinois 60611, USA.
6. Pedersen A. (Tandlaegebladet 1989 Sep;93(13):509-13), Krogh P.(Carcinogenesis 1987 Oct;8(10):1543-8), Trotoux J. (Ann Otolaryngol Chir Cervicofac 1982;99(12):553-6) Attestano il nesso causale tra la candida e la formazione del carcinoma epidermoidale della lingua.
7. Zhang K.V (Chung Hua Kou Chiang Hsueh Tsa Chih 1994 Nov;29(6):339-41, 384) O’Grady J.F. (Carcinogenesis 1992 May;13(5):783-6) - Neoplasie del cavo orale.
Hicks J.N (Laryngoscope 1982 Jun;92(6 Pt 1):644-7) - Neoplasia della laringe.
8. Field E.A. (J Med Vet Mycol 1989;27(5):277-94), Wang F.R. (Chung-hua Ping Li Hsueh Tsa Chih 1988Sep;17(3):170-2) e (Chung Hua Chung Liu Tsa Chih 1981 May;3(2) - Cancro del polmone.
9. Joseph P. (Chest 1980 Aug;78(2):340-3) - Mixoma atriale.
10. Rumi A. (Chir Ital 1986 Jun;38(3):299-304), Fobbe F. (ROFO Fortschr Geb Rontgenstr Nuklearmed 1986 Jan;144(1):106-7) Bathia V. (Indian J Gastroenterol 1989 Jul;8(3):171-2) marnejon T. (Am J Gastroenterol 1997 Feb;92(2):354-6) - Cancro dell’esofago.
11. Taguchi T. (J Pediatr Gastroenterol Nutr 1991 Apr;12(3):394-9) - Carcinoma dell’intestino Raina V. (Postgrad Med J 1989 Feb;65(760):83-5) - Morbo di Hodgkin
12. Piazzi M. (Minerva Stomatol 1991 Oct;40(10):675-9) per il M. di Kaposi Mannell A. (S Afr J Surg 1990 Mar, 28(1):26-7) - Tumore del pancreas
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