Tumore alla prostata istologico genetically Il tumore della prostata è uno dei più comuni tra gli uomini, e il rischio è direttamente Le biopsie vengono sottoposte ad esame istologico al microscopio. Il tumore della prostata è il secondo tumore più comune negli uomini occidentali, Ci sono diverse forme istologiche del tumore prostatico: l'adenocarcinoma. Grado Istologico. Il punteggio di Gleason (Gleason score) è raccomandato come standard internazionale per la gradazione del carcinoma della prostata: giova. impotenza We recommend downloading the newest version of Flash here, but we support all versions 10 and above. If that doesn't help, please let us know. Unable to load video. Please check your Internet connection and reload this page. If the problem continues, please let us tumore alla prostata istologico genetically and we'll try to help. An unexpected error occurred. Per carcinoma della prostata si intende una categoria diagnostica che annovera le neoplasie maligne che si originano dalle cellule epiteliali della prostata , una ghiandola dell' apparato genitale maschile. Il tumore alla prostata si sviluppa più frequentemente negli ultracinquantenni; è il secondo più comune tipo di tumore negli Stati Uniti , dove è responsabile del maggior numero di morti da tumore, dopo il tumore del polmone. Il tumore prostatico viene più spesso scoperto all' esame obiettivo o per il tramite di esami ematici , come la misurazione del PSA antigene prostatico specifico. Un sospetto tumore alla prostata è tipicamente confermato tramite l'asportazione biopsia di un frammento di tessuto , e il successivo esame istologico. Inizialmente venne classificato come malattia rara, per gli scarsi metodi di indagine e la ridotta speranza di vita media dell'epoca. I primi trattamenti messi in atto furono interventi chirurgici per risolvere l'ostruzione urinaria. La rimozione chirurgica dei testicoli, orchiectomia , come trattamento venne eseguita nel infra Terapia ormonale , ma con successo limitato. Prostatite. Antig prostatico specifico psa totalea 8 48 ng ml 5 tumore prostatico farmaci. per cure linfiammazione della prostata cosa prendere. infiammazione di carne. dolore alle gambe puo dipendere dalla vitamina d. dolore alle ovaie e nausea prima del ciclo. ce inseamna hiperplasia benigna de prostata pdf. Minzione notturna frequente dopo lallenamento. Alimenti per erezione duration. Estratto di pomodoro per prostata. Il mio medico prostata ipertrofica. 7 quali trattamenti sono disponibili per disfunzioni e disturbi sessuali.
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Eckman; J. Trachtenberg; SG. Pauker; AS. Detsky, Screening for prostate cancer. A decision analytic view. Essink-Bot, HJ. Nijs; WJ. Kirkels; PJ. Schröder, Short-term effects of population-based screening for prostate cancer on health-related quality of life.
Tumore alla prostata istologico genetically consultato prostatite 21 dicembre Picchio, C. Messa; C.
Landoni; L. Gianolli; S. Sironi; M. Brioschi; M.
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Matarrese; DV. Matei; F. De Cobelli; A. Del Maschio; F. Rocco, Value of [11C]choline-positron emission tomography prostatite re-staging prostate cancer: a comparison with [18F]fluorodeoxyglucose-positron emission tomography.
Scher, M. Seitz; W. Albinger; R. Tiling; M. Scherr; HC. Becker; M. Souvatzogluou; FJ. Gildehaus; HJ. Wester; S. Tumorzentrum Freiburg Archiviato il 9 ottobre in Internet Archive. Wiley-VCH Verlag, 7. Gupta, M. Varghese; MM. Shareef; MM. Finley, AS. Belldegrun, Salvage cryotherapy for radiation-recurrent prostate cancer: outcomes and complications. Wu, L. Sun; JW. Moul; HY. Wu; DG. McLeod; C. Tumore alla prostata istologico genetically R. Lance; L. Kusuda; T.
Donahue; J. Foley; A. Chung, Watchful waiting and factors predictive of secondary treatment of localized prostate cancer. Zincke, JE. Oesterling; ML. Blute; EJ. Tumore alla prostata istologico genetically RP. Myers; DM. Barrett, Long-term 15 years results after radical prostatectomy for clinically localized stage T2c or lower prostate cancer. Gerber, RA. Thisted; PT. Scardino; HG. Frohmuller; FH. Schroeder; DF. Paulson; AW. Middleton; DB. Rukstalis; JA. Smith; PF. Schellhammer; M. Ohori, Results of radical tumore alla prostata istologico genetically in men with clinically localized prostate cancer.
URL consultato il 25 gennaio Perez, GE. Hanks; SA. Leibel; AL. Zietman; Z. Fuks; WR.
Review of management with external beam radiation therapy. D'Amico, J. Manola; M. Loffredo; AA. Renshaw; A. DellaCroce; PW. Kantoff, 6-month androgen suppression plus tumore alla prostata istologico genetically therapy impotenza radiation therapy alone for patients with clinically localized prostate cancer: a randomized controlled trial.
Lawton, M. Won; MV. Pilepich; SO. Asbell; WU. Shipley; Tumore alla prostata istologico genetically. Hanks; JD. Cox; CA. Perez; WT. Sause; SR. Doggett, Long-term treatment sequelae following external beam irradiation for adenocarcinoma of the prostate: analysis of RTOG studies and Brenner, RE.
Curtis; EJ. Hall; E. An increasing number of studies show the importance of the immune system in the tumor microenvironment and the development of metastasis In this model, due to the usage of an athymic rodent, the ability to assess the effects of the immune system is not possible.
A second limitation is the lack of androgen responsiveness in PC3-M cells. Upon initial diagnosis of PCa, patients frequently will undergo androgen therapy as a first line treatment. However, patients will eventually become androgen-resistant and tumors will begin to grow again.
As PC3-M cells lack the androgen receptor, this model only measures the effects of drug treatment or protein modulation on post-androgen resistant cancer. Though this is tumore alla prostata istologico genetically limitation, androgen-responsive PCa is currently well manageable and has a variety of effective treatment options, and thus androgen-resistant cancer has become more prominently studied.
This model also specifically uses an inbred strain of mice, which minimizes mouse to mouse variability. Tumore alla prostata istologico genetically, this strain may be particularly responsive to particular proteins or small molecules, thus care should be taken when impotenza this data to the clinic.
Though this model provides an effective measurement of drug efficacy in a rapid tumore alla prostata istologico genetically time of weeks, this may not take into consideration long-term drug dosing effects.
After prolonged exposure to many currently available treatments, patients may return with drug-resistant cancers many years Prostatite. The rapid turnaround of this technique does not allow for effective tumore alla prostata istologico genetically of the ability of a tumor to become resistant to a treatment.
However, with modulation of this experiment, treatment-resistant human prostate cancer cells can be implanted, and the effectiveness of a second-generation therapeutic in preventing PCa tumor growth and metastasis can be modeled. Additionally, if a group was attempting to tumore alla prostata istologico genetically the molecular changes in a primary tumor over time, a longer-term model such as the TRAMP model will likely be more effective for those studies. Another limitation of this model is the dissemination of distinct metastasis tumore alla prostata istologico genetically to the lymph nodes and lungs of the animals.
Both of these sites are frequent and clinically relevant sites of metastasis, as demonstrated by human warm autopsy studies However, clinically bone metastasis constitutes a prominent feature of human PCa, and thus models recapitulating this are of interest.
Unfortunately, these are difficult to recapitulate in a mouse model, with very few models showing bone metastasis without tail vein, tumore alla prostata istologico genetically injection, or direct implantation into the bone Thus if targeting to the bone is of key experimental importance, another model may be more effective. However, this model does provide some measure of traffic to the bone in the form of bone marrow circulating tumor cells. Despite these limitations, this technique is a powerful model of human PCa.
The ability to measure effects on both the primary tumor as well as metastatic formation in a short turnaround time provides a wide variety of applications.
In this model, cells must escape the primary organ, enter and survive in the bloodstream, and implant in a secondary site, recapitulating the process in humans. The additional measurement of molecular characteristics of the primary tumor, changes in cell morphology, and presence of circulating tumor cells provides a wide breath of information from one model. This procedure can be used both in the context of drug discovery as well as to study changes in tumor biology.
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Preparation of Cells for Injection This step should Cura la prostatite performed as close as possible to starting surgeries. Tumore alla prostata istologico genetically cells being used for the experiment, remove from plate, and neutralize with media. Le cause di questa neoplasia non sono ancora del tutto chiare: alla base vi è una mutazione nel DNA delle cellule che causa una proliferazione anomala delle stesse, il cui accumulo forma il tumore.
Tenere sotto controllo il peso e limitare il consumo di grassi, soprattutto di quelli tumore alla prostata istologico genetically carni grasse di origine animale e formaggi costituisce la sola forma di prevenzione di questo tumore.
Gli esami di screening fanno spesso parte di una visita medica di routine, soprattutto negli uomini dopo i 40 anni di età. Gli esami comprendono:. Ben-Josef; R. Middleton; H. Porterfield; SA. Sharp; TJ. Smith; ME. Taplin, American Society of Clinical Oncology recommendations for the initial hormonal management of androgen-sensitive metastatic, recurrent, or progressive prostate cancer.
Tammela, Endocrine treatment of prostate cancer. Derleth, EY. Yu, Targeted therapy in the treatment of castration-resistant prostate cancer. URL tumore alla prostata istologico genetically il 6 ottobre archiviato dall' url originale il 12 luglio URL consultato il 6 ottobre Oudard; M. Ozguroglu; S. Hansen; JP. Machiels; I.
Kocak; G. Gravis; I. Bodrogi; MJ. Mackenzie; L. Tumore alla prostata istologico genetically M. Roessner, Prednisone plus cabazitaxel or mitoxantrone for metastatic castration-resistant prostate cancer progressing after docetaxel treatment: a randomised open-label trial. Ning, JL. Gulley; PM. Arlen; S. Woo; SM. Steinberg; JJ. Prostatite HL.
Parnes; JB. Trepel; MJ. Lee; YS. Kim; H.
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Sun, Phase II trial of bevacizumab, thalidomide, docetaxel, and prednisone in patients with metastatic castration-resistant prostate cancer.
Kantoff, CS. Higano; ND. Shore; ER. Berger; EJ. Small; DF. Penson; CH. Redfern; AC. Ferrari; R. Dreicer; RB. Sims; Y.
Xu, Sipuleucel-T immunotherapy for castration-resistant prostate cancer. Food and Drug Administration, 28 aprile Portenoy, Treatment of cancer pain. Yaneva, J. Zlatanova, Histone H1 interacts specifically with certain regions of the mouse alpha-globin gene. Seregni, B. Padovano; A. Coliva; E. Zecca; E. Bombardieri, State of the art of palliative therapy.
Hillegonds, S. Franklin; DK. Shelton; S. Vijayakumar; V. Vijayakumar, The management of painful bone metastases with an emphasis on radionuclide therapy.
Wakai, [Descriptive epidemiology of prostate cancer in Japan and Western countries]. Tumore alla prostata istologico genetically de Beaujeu, Y.
Chavrier, [Deformations of the anterior thoracic wall author's transl ]. Hsing, L. Tsao; SS. Devesa, International trends and patterns of prostate cancer incidence and tumore alla prostata istologico genetically. Osegbe, Prostate cancer in Nigerians: facts and nonfacts. Steiner, CR. Pound, Phase IIA clinical trial to test the efficacy and safety of Toremifene in men with high-grade prostatic intraepithelial neoplasia. Thompson, PJ. Goodman; CM.
Tangen; MS. Lucia; GJ. Miller; LG. Ford; MM. Lieber; RD. Cespedes; JN. Atkins; SM. Lippman; SM. Carlin, The influence of finasteride on the development of prostate cancer. Hamilton, SJ. Altri progetti Wikimedia Commons. Portale Medicina : accedi alle voci di Wikipedia che trattano di tumore alla prostata istologico genetically.
Questa è una voce di qualità. È stata riconosciuta come tale il giorno 4 febbraio — vai alla segnalazione. Naturalmente sono ben accetti altri tumore alla prostata istologico genetically e modifiche che migliorino ulteriormente il lavoro svolto.
Categorie : Carcinomi Neoplasie della prostata. Menu di navigazione Strumenti personali Accesso non effettuato discussioni contributi registrati Prostatite.
Namespace Voce Discussione. Visite Leggi Modifica Modifica Prostatite cronica Cronologia. In altri progetti Wikimedia Commons. Il testo è disponibile secondo la licenza Creative Commons Attribuzione-Condividi allo stesso modo ; possono applicarsi condizioni ulteriori.
Vedi le condizioni d'uso per i dettagli. Le informazioni riportate non sono consigli medici e potrebbero non essere accurate. Finally, orthotopic Myc-CaP tumors are aggressive, fast growing tumors that reach the survival endpoint in approximately 46 days and as early as 35 days due to the primary tumor mass.
Studies requiring slower tumor development or long-term treatments should be optimized empirically for the initial injection cell count and treatment regimen. In contrast to the limitations of s. As the orthotopic tumor model involves the use of in vitro -handled cells, these cells can be modified depending on the needs of the study. Here, we modified these cells to stably express luciferase and mCherry for in vivo tumor monitoring.
With the advantages of the orthotopic tumor model, the ability to study both androgen-dependent prostate cancer and CRPC, and the potential to express imaging modalities or knockdown or overexpress impotenza genes, this protocol serves as a valuable resource for all prostate cancer research.
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Gmail and other free mail providers are ineligible for trials. Please, sign in with Google or fill out the form below to receive a free trial. Cancer Research. Preparation of Surgical Materials and Cancer Cells Before the day of surgery, autoclave the micro-dissecting scissors, Graefe forceps, Graefe tissue forceps, needle holder with suture cutters, and the appropriate number of drapes.
NOTE: Perform all tissue culture under sterile conditions, and verify that all cell lines are mycoplasma-free. The murine prostate cancer tumore alla prostata istologico genetically line utilized in this study, Myc-CaP 32is transduced to stably express both firefly luciferase and mCherry.
The Myc-CaP cell line iss isolated from a c-myc -overexpressing Hi-myc mouse, and these cells contain an amplified androgen receptor ARwhich are androgen-dependent 32 and form CRPC tumors after murine castration Alternative murine prostate cancer cell lines can be used with the mice of appropriate genetic background, as well as human prostate cancer cell lines or primary patient-derived prostate cancer cells with immunodeficient mice.
The tumore alla prostata istologico genetically number of cells per injection should be determined empirically for alternative cell lines. In addition, alternative imaging modalities can be utilized to visualize tumors, including magnetic resonance imaging MRIpositron emission tomography PETor computed tomography CTas well as GFP as an alternative to mCherry.
On the day of surgery, collect the cells by washing them with phosphate buffered saline PBS and detaching with 0. Tumore alla prostata istologico genetically the cells at x g for 5 min. Count the cells and resuspend the cells in PBS at a concentration of 6. La validità degli esami di screening in generale è controversa, tumore alla prostata istologico genetically il tumore della prostata molto eterogeneo.
Alcune forme molto aggressive devono essere identificate precocemente per poter essere guarite, mentre altre forme possono avere una crescita lenta e potrebbero addirittura non essere curate ma solo controllate nel tempo sorveglianza attiva. La diagnosi precoce dei tumori della prostata passa quasi sempre attraverso il dosaggio del PSA.
I campioni di tessuto prostatico prelevati vengono esaminati al microscopio per determinare la presenza di tumore, valutarne estensione numero fi frammenti coinvolti e aggressività Gleason score bioptico.
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If the problem continues, please let us know and we'll try to help. An unexpected error occurred. Issue 79 doi: As cells must escape the primary organ, enter the blood stream, and implant into a secondary site, this model effectively recapitulates the scenario in humans.
Pavese, J. Our laboratory has developed a novel orthotopic implantation model of human prostate cancer PCa.
As PCa death is not due to the primary tumor, but rather the formation of distinct metastasis, the ability tumore alla prostata istologico genetically effectively model this progression pre-clinically is of high value. At experiment termination, several distinct endpoints can be measured, such as size and molecular characterization of the primary tumor, the presence and quantification of circulating tumor cells in the blood and bone marrow, and formation of metastasis to the lung.
In addition to a variety of endpoints, this model provides a picture of a cells ability to invade and escape the primary organ, enter and survive in the circulatory system, and implant and grow in a secondary site. This model has been used effectively to measure metastatic response to both changes in protein expression as well as to response to small molecule therapeutics, in a short turnaround time.
Prostate cancer PCa is the most tumore alla prostata istologico genetically diagnosed cancer in men, and the second leading cause of cancer death in the United States 1. Death from PCa is Prostatite due to formation of the primary tumor, but rather the formation of metastasis.
Therefore, prevention of metastasis in patients is of high importance. Mouse models of PCa offer a diversity of options to uncover critical tumore alla prostata istologico genetically information about this disease. A variety of mouse models of PCa exist, each with inherent tumore alla prostata istologico genetically and limitations.
While the frequency of PCa in humans is high, naturally occurring PCa is extremely uncommon in mice 2despite equal susceptibility of mice overall to cancer 3.
For this reason, induced model systems, such as the TRAMP transgenic adenocarcinoma of the mouse prostate model are commonly used. The TRAMP model can induce transgene expression specifically in the prostate, and undergoes the normal progression of PCa, from hyperplasia to prostatic intraepithelial neoplasia PIN to lymphatic and pulmonary metastasis These models provide the benefits of being able to measure the full impotenza of tumor progression, as well as contain an intact immune system.
However, the molecular events underlying PCa development can differ between mice and humans, and tumore alla prostata istologico genetically between mice and human clinical studies have shown variability.
Additionally, both of these models are time-consuming, as an example Cura la prostatite TRAMP model requires approximately 28 weeks in order to develop metastasis.
In studying metastasis, frequently a tail-vein or tumore alla prostata istologico genetically ventricle injection model is used. This model benefits from rapid turnaround time, and can additionally measure the presence of bone metastasis using specific cell lines and conditions.
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Yang et al. The tumore alla prostata istologico genetically limitations of these models relate to the lack of a primary tumor residing within the prostate gland itself.
Further, for models reliant upon injection of cancer cells into the circulation, this bypasses the whole first half of the metastatic cascade. It thereby precludes examination of initial steps, including invasion through Prostatite primary organ, which are biologically crucial measures of metastatic transformation.
Many regulators of metastatic transformation directly affect early cell invasion. Early steps in the metastatic cascade constitute high priority sites for therapeutic targeting, as once cancer cells disseminate, clonal variation expands greatly, thereby increasing biological diversity and diminishing effective therapeutic targeting. After weeks, tumor size, presence of circulating tumor cells CTCsand metastasis to the lungs and lymph nodes can all tumore alla prostata istologico genetically quantified.
We have effectively used this model to evaluate the efficacy of 4',5,7-trihydroxyisoflavone genistein to inhibit human PCa metastasis Dietary consumption of genistein has been linked to decreases in prostate cancer metastasis and deathbut previously no study had determined whether administering of genistein could alter PCa metastasis in animals or men.
In this study we demonstrated that treatment with genistein greatly reduced the number of lung metastasis. Additionally, we determined genistein altered the activation and expression of several important pro-metastatic proteins in the primary tumor, including focal adhesion kinase FAKp38 mitogen-activated protein kinase p38 MAPKand heat shock protein 27 HSP These results corresponded with observations in the clinic.
Using blood obtained from the mice, we were able to accurately measure the blood concentrations of genistein and observed these to be similar to levels prostatite humans with regular dietary consumption of genistein.
Additionally, a Phase II study performed by our group determined that upon treatment with genistein, men experienced decreases in prostate tissue mRNA expression of genes associated with cellular invasion and metastasis, specifically matrix metalloproteinase type 2 MMP-2 We have also used this model to evaluate the effect of altered gene-product expression in the primary tumor on human PCa metastasis Tumore alla prostata istologico genetically extended these studies to determine the effect of endoglin on human PCa metastasis.
Stable endoglin knockdown, vector control or endoglin over tumore alla prostata istologico genetically cell lines were implanted into mice.
High endoglin implanted mice showed almost complete suppression of lung metastasis, and complete suppression of CTCs. These are just two examples of the wide variety of applications this technique has. From drug discovery, to modeling changes in molecular biology, this model offers a high throughput method of evaluating the effects of various functions on tumor growth and molecular changes, presence of CTCs, and formation of distinct metastasis in tumore alla prostata istologico genetically lung and lymph nodes.
Surgical techniques and animal care conditions were observed by veterinary staff and modified to minimize animal stress or mortality. Individual institutions may have different requirements and it is important to work with IACUC and animal staff when developing and executing this surgical technique. For this experiment, we show a representative group of mice obtained during these surgical procedures. Tumors were allowed to grow for six weeks, and then multiple parameters were evaluated.
In Figures 1A and 1Bwe show the change in body weight and food consumption of mice, respectively. There is a small dip in body weight and food consumption around the date of surgery due to the anesthesia. During the course of the experiment, body weight slowly increases post-surgery, and then begins to decline towards tumore alla prostata istologico genetically end of the experiment as tumor tumore alla prostata istologico genetically reaches a critical level.
This is matched by the food consumption in these mice. In Figures 2A and 2Brepresentative tumor sizes obtained are shown. Individual tumor sizes vary, but on average we tumore alla prostata istologico genetically tumors of approximately 1 gram, with normal variance between 0.
Though the size of the tumors varies, these do not correlate with the number of resultant metastasis, shown both in this paper and our previously published works However, from this model, one can determine the effect tumore alla prostata istologico genetically drug treatment or molecular changes on the tumor weight and size. An important consideration in this model is when the appropriate endpoint for the experiment is.
In Figures 2C and 2Dwe show changes in tumor weight and tumor size in one particular PC3-M cell line stably transfected with GFP and a control vector at 4 weeks and at 6 weeks. In the last two weeks, the average tumor weight increased 2. This shows the addition of extra weeks on the experiment can dramatically influence results. As a multitude of factors can alter the growth of the tumors, including the age and size of mice, number of passages of the cells, etc.
In Figures 3A-3Cthe number of metastases is quantified three different ways. In Figure 3Bthe number of cell loci, or locations where metastatic deposits are present, is shown. Finally, tumore alla prostata istologico genetically Figure 3Cthe number of distinct metastasis, as defined by a clearly bound group Trattiamo la prostatite cells showing 5 or more GFP-positive human PCa cells, is displayed.
Representative pictures of these different conditions are shown in Figures 4A-4D. In Figure 4Aan individual cell at 40x magnitude is highlighted with an arrow.
Note the brown staining and large distinct nuclei. This photo is taken at 40x magnitude and the cell is highlighted with an arrow. In Figure 4Cseveral loci of varying cell number at 10x magnitude are displayed and each locus tumore alla prostata istologico genetically with an arrow.
Lastly, in Figure 4Da metastatic deposit of 10 cells is shown. How these tumore alla prostata istologico genetically influence the data is shown by differences in Mouse 1 and Mouse 3. Mouse 1 has a lower number of total cells in the lung, with an average of However, Mouse 3 has fewer loci, or locations where cells are present than Mouse 1.
Mouse 3 Trattiamo la prostatite relatively few sites of metastasis, but the number of cells per area is very high at 82 cells per loci due to several tumore alla prostata istologico genetically large cell number metastases.
tumore alla prostata istologico genetically
An Orthotopic Murine Model of Human Prostate Cancer Metastasis
In contrast, Mouse 1 has more unique loci, but significantly fewer cells per location at only an average of two cells per location. These different parameters can shed light on the kinetics of cells trafficking to tumore alla prostata istologico genetically lung and their ability to begin to grow and proliferate.
Additionally, in Tumore alla prostata istologico genetically 3Dwe show changes in Prostatite metastatic cells per lung in mice necropsied at four versus six weeks. As described in Figures 2C and 2Dsignificant changes are observed in the tumor weight and size in the final two weeks of an experiment. This is recapitulated in Figure 3D.
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Mice necropsied at four weeks showed no metastatic development, while mice at 6 weeks showed metastatic cells in all mice Cura la prostatite. This further demonstrates the importance of ensuring mice necropsies are performed at a late-stage endpoint to ensure formation of metastasis has occurred.
An added measurement in this model is molecular changes occurring inside the primary tumor. Additionally, protein levels can be quantified using Western blot procedures. Figure 1. Observed body weight and food consumption in animals.
A-B Body weight in grams, or average food consumption per mouse per day tumore alla prostata istologico genetically grams, is recorded throughout the experiment and shown in A and B respectively.
Figure 2. Tumor size and tumor weight in individual Prostatite groups of mice. A-B Tumor weight in grams and tumore alla prostata istologico genetically size in centimeters squared of five representative control mice and the average of the five mice at the end of six weeks are shown in A and B respectively.
C-D A comparison of tumor weight in grams and tumor size in centimeters squared between groups of mice necropsied at four and six weeks. Click here to view larger figure. Figure 3. Metastatic spread in individual and groups of mice. D A comparison of the average number of metastatic cells per lung section per tumore alla prostata istologico genetically between mice necropsied at four and six weeks.
Figure 4. Representative images of lung metastases.