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PubMedDate not supplied

[Lymph node metastasis of adenoid cystic carcinoma].

BACKGROUND: The adenocystic carcinoma (ACC) of the head and of the neck is rather uncommon. It is characterized by a very slow biological behaviour, which leads to locoregional recurrences and distant metastasis. Most reports concentrate on the unpredictable long-term behaviour of this tumor, whereas lymph nodes metastasis are not usually discussed in detail. The aim of this study was to evaluate the difficulties connected with the lymph node metastasis in ACC. METHODS: A group of 33 patients from 1980 to 1998, was observed. These patients have been subjected to surgical treatment in the Maxillo-Facial Surgery Department of the Policlinico-Umberto I of Rome. RESULTS: Among 33 patients with ACC, 10 patients (30%) revealed, initially or during observation, cervical lymph node metastasis, which is a most common event in male subjects (70%). The lymph node involvement is much more common in carcinomas localized in the parotid and in the sublingual glands with a solid rather than a tubular histologic pattern. Direct correlation between age and metastasis lymph node involvement have not been documented. CONCLUSIONS: Surgery for node disease has a very little impact on the locoregional and on the distant metastasis evolution of the tumor. Thus, our protocol of treatment of lymph nodes metastatic lesions follows the trend of most of the international authors, considering that the neck dissection should be performed only with a lymph adenopathy clinically evident or strongly suspected.

Aged↗
PubMed2006

Potential use of humanized antibodies in the treatment of breast cancer.

With the growing knowledge of key cellular pathways in tumor induction and evolution, targeted therapies make up an increasing proportion of new drugs entering clinical testing. In the treatment of breast cancer, humanized antibodies have become a major option. The humanized monoclonal antibody trastuzumab (Herceptin); Genentech, Inc., CA, USA) for HER2-overexpressing, metastatic breast cancer, represents a successful agent associated with impressive survival benefits when combined with chemotherapy. Based on impressive results, trastuzumab will become a standard in the adjuvant treatment of HER2-overexpressing breast cancer. The role of trastuzumab in the neoadjuvant setting is promising, but must be further evaluated in large prospective, randomized trials. However, there is still a large proportion of patients overexpressing HER2 that do not respond to trastuzumab. Regarding this patient cohort, the optimal combination of trastuzumab with other agents needs further evaluation. In breast cancer lacking HER2 amplification, the role of the new antibody pertuzumab remains to be defined. The role of antibodies interfering with angiogenesis, tumor stroma or glycoproteins is of a preliminary nature and warrants further investigation. Here, an overview of humanized antibodies in human breast cancer is provided, with emphasis on the recent advances and future prospects in treating malignant breast cancer.

Antibodies, Monoclonal↗
PubMed1999

Should prolactin be reconsidered as a therapeutic target in human breast cancer?

Although prolactin (PRL) has been long suspected to be involved in the progression of human breast cancer, the failure of clinical improvement by treatment with dopamine agonists, which lower circulating levels of PRL, rapidly reduced the interest of oncologists concerning a potential role of this pituitary hormone in the development of breast cancer. Within the last few years, however, several studies reported first, that PRL is also synthesized in the mammary gland, and second that it exerts its proliferative action in an autocrine/paracrine manner. These observations have led to a reconsideration of the role of PRL as an active participant in breast cancer and are an impetus to search for alternative strategies aimed at inhibiting the proliferative effects of PRL on tumor mammary cells. In this report, we discuss the three possible levels that can be targeted for this purpose: the mammary synthesis of PRL, the interaction of the hormone with its receptor at the surface of mammary cells, and the intracellular signaling cascades triggered by the activated receptor. For each of these steps, we discuss the molecular event(s) that can be targeted, our understanding of the mechanisms involving these putative targets as well as the tools currently available for their inhibition. Besides its proliferative effect, PRL is also involved in the control of angiogenesis through one of its cleaved fragments, named PRL 16K, which has been shown to inhibit the angiogenic process. In view of this biological activity, we discuss first the cleavage of PRL with respect to the human mammary gland and, second, the hypothesis speculating that a balance between the proliferative effect of intact PRL and the anti-angiogenic activity of its 16K-like fragments might be physiologically relevant in the evolution of mammary tumors. If true, our hypothesis would suggest that the enzymatic cleavage of PRL could represent a new molecular target in the search for alternative strategies in the treatment of breast cancer.

Breast Neoplasms↗
PubMed2001

Large demyelinating brain lesion mimicking a herniating tumor.

We describe the case of a large brain lesion whose computed tomography appearance and clinical evolution mimicked a herniating tumor. The patient progressed to coma within 6 days of hospitalization despite high-dose steroid treatment. Emergency excision of the lesion was carried out. Histological analysis showed massive demyelination, axon preservation and no tumor cells. No lesion recurrence was seen during a 55-month follow-up. Recognition of such lesions through magnetic resonance imaging or spectroscopy may spare unnecessary surgery or biopsy. However, our case shows that such lesions may still require resection in the face of a rapid clinical progression and poor response to medical treatment.

Adult↗
PubMed2003

Microvessel density (MVD) as a prognosticator in endometrial carcinoma.

PURPOSE: To assess microvessel density (MVD) as a marker for angiogenesis in endometrial carcinoma (EC) and normal endometrium at the proliferative and secretory phase, and to determine its prognostic value on survival among cases with EC. METHODS: Forty-three endometrial carcinoma cases were surgically staged and recruited for this case-control study. Tissue specimens from hysterectomies due to benign conditions (uterine descensus, myoma uteri, chronic pelvic pain, adenomyosis), that belonged to proliferative (n = 10) and secretory (n = 10) endometrium (n = 10), were studied as the control group (n = 20). MVD was assessed in hot areas where a high density of microvessels were detected within tumoral tissue and normal endometrium at proliferative and secretory phases. Among EC, various prognosticators such as tumor stage, histological and nuclear grade, tumor size, lympho-vascular space involvement (LVSI), cervical involvement, myometrial invasion, adnexal and lymph node involvement, peritoneal cytology and MVD were analysed in regard to survival. RESULTS: The mean age of cases with EC was 58.3 +/- 1.4. MVD was apparently high in EC cases (p < 0.05). Among control cases, endometrium from proliferative and secretory phases of the menstrual cycle was not statistically different (48.5 +/- 3.6 vs 47.4 +/- 3.8, respectively). MVD was correlated with high surgical stage (p < 0.001), cervical involvement (p = 0.01), adnexal involvement (p = 0.04), lympho-vascular space involvement (p = 0.02), pelvic and para-aortic lymph node metastasis (p < 0.001) and positive peritoneal cytology (p < 0.001). On univariate analysis, with a MVD cut-off value of 81/0.739 mm2, surgical stage (p < 0.001), LVSI (p < 0.001), retroperitoneal lymph node involvement (p < 0.001), adnexal metastasis (p < 0.001), peritoneal cytology (p = 0.005) and MVD count (p < 0.001) appeared to be independent factors for survival. On multivariate analysis, only pelvic lymph node involvement (p = 0.03) and MVD (p = 0.02) were found to be independent prognosticators on survival. CONCLUSIONS: Angiogenesis is apparent in both initial and further evolution of a tumoral process. MVD appears to have a substantial prognostic value on survival in EC cases.

Adult↗
PubMed1998

[Malignant kidney tumors in adults in Senegal: diagnostic and therapeutic problems].

The aim of this study was to analyze problems posed by adult renal malignant tumors both in the diagnostical and therapeutical viewpoints. We have performed a retrospective study including 48 cases of confirmed renal cancer. Have been included adult patients who presented a cancer of the kidney operated or not. Studied parameters were age, sex, clinical signs, complementary explorations i.e. biology, renal ultrasonography, IVU, Computerized tomography, the operative indication and the prognosis. We have used Robson's staging to classify our patients. The average age was 51 years with extremes of 18 and 83 years. However 60% of them were less than 50 years. Adenocarcinoma was the main histological form encountered. It has been found in 93% of cases. The flank mass has been the mode of discovery in 70.8% of cases. The classic symptomatic triad associating hematuria, pain and the renal mass has been found in 20.8% of cases. Ultrasonography and Intravenous urography (IVU) have allowed to pose the diagnosis in 93.75% of cases. Patients were often referred very late with an average delay of consultation of 14 month. So, 25% of them presented with metastasis at the moment of the diagnosis. Radical nephrectomy was performed in 60% of cases. 40% of patients have not been operated due to the advanced evolution of the tumor. The global mortality to 1 year was estimated at 38%. We conclude that renal malignant tumors in the adulthood, in our practice, presents some particularities. Indeed, patients are referred late when clinical symptoms are sufficiently evocative to suspect the diagnosis. At these advanced stages, there is no curative therapeutic. So, a precocious diagnosis is necessary in order to propose to patients radical nephrectomy which remains the only efficient therapeutical procedure of the localized renal cancer in the adulthood.

Adolescent↗
PubMed2026

Multi-Omics Biomarker Signatures for Precision Diagnosis and Prognosis in Primary Liver Cancer: A Literature Review.

Primary liver cancer (PLC) is a biologically heterogeneous group of malignancies dominated by hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (iCCA), and a smaller subset of combined hepatocellular-cholangiocarcinoma (cHCC-CCA), and its clinical burden remains high because current diagnostic and prognostic tools do not adequately capture molecular diversity. Conventional imaging, serum markers, and histopathological assessment remain insufficient for precise early diagnosis, subtype-resolved classification, and outcome stratification, while tissue and liquid biopsy approaches have expanded the range of analytes available for clinical assessment. Recent studies have identified candidate biomarker signatures across genomic, epigenomic, transcriptomic, proteomic, metabolomic, and circulating layers, suggesting that integrated multi-omics profiling may better represent tumor lineage, clonal evolution, immune context, and therapeutic vulnerability than isolated molecular readouts. However, these layers are not equally mature for clinical use: genomic testing is closest to routine therapeutic application in iCCA, plasma methylation assays are advancing for HCC surveillance augmentation, and many proteomic or metabolomic panels remain validation-stage tools. Their clinical value remains constrained by sampling bias, biospecimen-dependent signal loss, assay standardization, cost, and the need for prospective validation across clinically diverse populations. This narrative review critically synthesizes current evidence on multi-omics biomarker signatures for precision diagnosis and prognosis in primary liver cancer and argues that clinically useful signatures should be question-specific, stage-aware, and specimen-aware rather than universal multi-analyte panels.

Humans↗
PubMed2006

[The fluorescence: a "bright" concept for the study of the metastatic process].

The forming of secondary tumors, called metastases, constitutes the first cause of death of the patients reached by a cancer and represents one of the major obstacles in the fight against this disease. The characterization of mechanisms governing the passage of the cancerous phenotype into metastasis thus turns out to be a crucial stage for the discovery of new treatments. The understanding, and finally the inhibition of a so complex and multifactorial process, require the implementation of various strategies of study (e.g. inhibition of the neo-angiogenesis, impact of the expression or of the inhibition of a gene, test of a new molecule, etc.). However, whatever is the envisaged type of work, the use of in vivo models remains always essential. Unfortunately, although the classic approaches to show and count the metastases (histology, immunohistochemistry, etc.) allowed the better understanding of the metastatic process, these techniques dramatically underestimate the real number of metastases in a given tissue, because they do not allow the detection of the micrometastases. The aim of this article is to present a new approach in the models of studies of the metastases, using cancerous cells stably expressing the green fluorescent protein (GFP). The fluorescence emitted by the GFP, induced by UV radiation, allows to show up to the unicellular level the cancerous cells present to the healthy tissue of the host and so to estimate in a relative precise way their number. In addition, the power of detection of these models can be combined to video devices, allowing to follow the evolution of the tumor growth and the metastatic spread during time, and it on the same animal. These new models radically change the classic approaches of study of metastatic spread and open the way new types of works till now impracticable. In addition, besides the aptness of these models, we will also discuss their weaknesses, and will present some recent examples of applications.

Animals↗
PubMed1989

[Extensive resection of primary malignant tumors of the sacrum].

The most common primary tumors of the sacrum are chondrosarcoma, and giant cell tumors. These tumors can display a great development at the time of first examination on account of their slow growth, delayed expression of pelvic organs compression and metastases. The spontaneous long lasting evolution of sacral primary tumors is disastrous with neurological involvement, painful visceral complications and a high incidence of lethal evolution. Local control and cure of these tumors is possible only if radical resection is done regardless to neurological sequelae. The author proposes a surgical procedure for a carcinologic resection using two different anterior and posterior approaches in one stage with two teams. Six patients were treated in this way and the follow-up ranges from 5 to 11 years. One patient died two years post-operatively (malignant teratoma); the others survive: 2 chordomas (11 and 5 years post-op.), 2 chondrosarcomas (8 and 6 years pos-op.) and 1 giant cell tumor (6 years post-op.). These results with prolonged survival without recurrence justify our proposal of an aggressive surgical approach to treat these malignant tumors.

Adult↗
PubMed1996

Cytogenetic analysis of aggressive meningiomas: possible diagnostic and prognostic implications.

BACKGROUND: Published karyotypes from aggressive (atypical and malignant) meningiomas are few, but suggest clonal evolution from benign tumors with monosomy 22 to aggressive forms with additional abnormalities. The goal of this study was to identify the most frequent karyotypic abnormalities associated with aggressive histopathology and biologic behavior. METHODS: Eight intracranial meningiomas exhibiting histologically atypical features at the time of intraoperative diagnosis were chosen for cytogenetic analysis. The study set was comprised entirely of histologically atypical meningiomas. Four were considered malignant; three on the basis of brain invasion and one due to extracranial metastases. None was histologically anaplastic. RESULTS: Chromosomal abnormalities were demonstrated in 6 cases (75%), 5 of which were complex (63%). Loss of chromosome 22 was identified in two cases, both of which were associated with additional aberrations. Abnormalities most frequently involved chromosomes 1 (63%), 3 (50%), and 6 (63%). Four cases (50%) had dicentric or ring chromosomes. An additional 47 previously reported karyotypes from atypical and malignant meningiomas were reviewed. Comparison with published karyotypes of 200 histologically benign meningiomas served to underscore the increased frequency of complex karyotypes, chromosome 1, 3, and 6 abnormalities, and telomeric associations in the aggressive tumors. Apparently normal karyotypes as well as monosomy 22 alone were more frequently associated with benign, nonatypical histopathology. CONCLUSIONS: These findings suggest a possible role for cytogenetic analysis in determining the prognosis and perhaps in refining the diagnosis of atypical or aggressive meningiomas. Further studies are necessary to determine the significance of complex karyotypes, chromosome 1, 3, and 6 abnormalities, and telomeric associations, particularly whether they portend a more aggressive clinical course in meningiomas lacking features of histologic atypia.

Adult↗
PubMed1997

Clinically aggressive metastasizing pleomorphic adenoma: report of two cases.

BACKGROUND: It has been suggested that metastasizing pleomorphic adenomas may represent unrecognized malignancy. METHODS: The cytologic and clinical characteristics of two metastasizing pleomorphic adenomas diagnosed by fine-needle sampling are reported. RESULTS: Both showed malignant evolution: the primary tumors arose from the palate and the parotid salivary glands, respectively. Metastases occurred simultaneously with local recurrence in the first patient and after a second local recurrence in the second patient. Both patients were treated by surgery and radiotherapy but died of disseminated disease 8 and 4 years after initial diagnosis. No histologic evidence of malignancy was observed on cytology smears or histology sections in either case. CONCLUSION: Clinically, our cases support the hypothesis that metastasizing pleomorphic adenomas represent unrecognized malignancy, because the biologic course of two tumors led to unequivocally lethal outcome.

Adenoma, Pleomorphic↗
PubMed1983

Gastrosplenic fistula following successful chemotherapy for disseminated histiocytic lymphoma.

A case is presented of a patient with diffuse histiocytic lymphoma with splenic involvement who developed a communication between the greater gastric curvature and the splenic parenchyma after successful antineoplastic chemotherapy. This fistula was diagnosed by CT scan and confirmed by upper gastrointestinal barium series and fiberoptic endoscopy. This complication was managed successfully by an enbloc resection of the greater curvature of the stomach, splenectomy, and distal pancreatectomy. Histologic assessment of the stomach and spleen failed to reveal residual tumor. The clinical evolution of this rare complication is discussed and the literature on this subject is reviewed.

Antineoplastic Agents↗
PubMed1989

Prolonged survival in a patient with disseminated malignant teratoma in the presence of a persistently elevated serum alpha-fetoprotein level.

The authors report a patient with disseminated malignant teratoma who has survived for 3.5 years after discontinuation of treatment despite a persistent and nonprogressive elevation of his serum alpha-fetoprotein level. Potential sources of the marker in his case are discussed and the possibility of a chemotherapeutically induced evolution of his tumor considered.

Adult↗
PubMed2005

Use of chromosome painting for detecting stable chromosome aberrations induced by melphalan in mice.

Chromosomal aberrations are a measure of genomic instability, which is known to play a key role in the initiation and promotion of carcinogenesis. Stable reciprocal translocations are of particular importance since they are often involved in neoplastic transformation and tumor cell clonal evolution. In this study, chromosome painting analysis was used to test for stable aberrations induced in the bone marrow of C57BL/6J and FVB mice exposed for 4 weeks to 2 or 4 mg/kg of melphalan (MLP), a chemotherapeutic agent with carcinogenic potential. To compare the chemical-induced damage in different tissues, chromosome aberrations were also analyzed by chromosome painting in the spleen of C57BL/6J mice. At the 2 mg/kg dose, MLP induced comparable levels of chromosome-type aberrations in bone marrow cells of both mouse strains and in splenocytes of C57BL/6J mice. At 4 mg/kg, no further increase in aberrations was detected in bone marrow, while a dose-effect relationship was found in spleen cells. This different response may result from a negative selection against highly damaged bone marrow cells during mitotic proliferation. The results indicate that chromosome painting is a useful tool for detecting stable chromosome aberrations in somatic cells exposed to MLP and possibly to other genotoxic chemical carcinogens.

Animals↗
PubMed1994

Relationship between loss of estrogen and progesterone receptor expression and of 6q and 11q chromosome arms in breast cancer.

The expression of estrogen (ER) and progesterone (PR) receptors was quantified in a series of 95 cytogenetically characterized breast cancers. The relationship between deficiencies of 6q and 11q arms (where genes for ER and PR are mapped, respectively) and ER and PR expression was analyzed. The range of variations in expression was very large by comparison to that of the number of chromosome arms. Furthermore, low expression without chromosome loss and high expression with chromosome loss were occasionally observed. Thus, major variations in ER and PR expression were independent of the number of copies of the corresponding gene. However, both the decrease in ER expression and 6q arm losses were correlated with cytogenetic evolution of the tumors, this correlation being less significant for PR and the 11q arm. In addition, 6q- but not 11q- tumors have, on the average, a low ER/PR ratio, whereas 11q- but not 6q- tumors have a low PR/ER ratio. When all 6q- or 11q- tumors were compared to those with no 6q or 11q losses, the average ER or PR value of the former was about half of the later. These data suggest that, in addition to a regulatory change of non-genetic origin, gene dosage effect plays a secondary, but significant, additional role.

Breast Neoplasms↗
PubMed1995

Role of the pathologist in biomarker studies.

Cancer chemoprevention is defined as intervention by chemical agents prior to invasion to inhibit or slow the carcinogenic process. Using surrogate endpoint biomarkers in chemoprevention studies may reduce the size, length and cost of clinical prospective randomized trials in high-risk populations. Intermediate biomarkers are measurable alterations in the tissues at risk and include differentiation, genetic composition, biochemical expression, and proliferation. Assessment is possible because invasive epithelial neoplasms are known to begin as intraepithelial proliferations with a spectrum of cellular abnormalities extending to carcinoma in situ. Genetic heterogeneity begins in the intraepithelial phase; a stochastic accumulation of genetic errors characterizes the progression of clonal evolution within the tumor through the process of invasion and metastasis. Pathologic features associated with this process include tumor classification as well as whether it is intraepithelial or invasive. If the process is intraepithelial, the grade and extent of the intraepithelial lesion are reported. If the neoplasm is invasive, tumor size, extent, degree of differentiation (histologic and nuclear grade), mitotic rate, vascular invasion, and lymph node involvement are evaluated. In assessing biomarkers relevant chemoprevention, and without complete regression of the neoplasm with the chemopreventive agent or agents, measurable parameters along with histopathologic features are applicable. Three methods readily applicable for this purpose that can be applied to paraffin-embedded, formalin-fixed tissue include quantitative pathology, immunohistochemistry, and molecular biologic applications. These methods require some consistency in handling and processing the tissues under study; results may deteriorate due to a number of processing variables, including time to fixation, time in fixative, and fixative type. Quantitative pathology, including static image analysis and flow cytometry, can determine total DNA content. Using static image analysis, very small tumors can be studied. In addition, adjacent intraepithelial and invasive components of a tumor may be studied from a single slide. Steroid receptors, oncogenes, and other proteins detectable through immunohistochemical or molecular biologic methods can be quantitated by this technique as well. Cell cycle synthetic function is assayable by both methods. Flow cytometry can calculate the total percentage of cells in S-phase, or the tumor cell S-phase fraction based on the percentage of cells detected between the G0, G1 peak and the G2 + M peak. A similar approach is generally not applicable with current image analysis equipment; however, cell cycle related proteins such as MIB-1 (Ki-67 associated) can be quantified. Immunohistochemical methods can employ a wide variety of monoclonal antibodies to detect oncogene related proteins, including HER-2/neu (c-erbB-2) and p53. Molecular biologic methods, including in situ hybridization, polymerase chain reaction, and in situ PCR, can have many applications when applied to paraffin-embedded tissues, including detection of viral DNA, identification and measurement of apoptosis, and defining gene deletions.

Biomarkers, Tumor↗
PubMed1994

Expression of the imprinted gene H19 in the human fetus.

The H19 gene is a parenterally imprinted maternally expressed gene which has a pivotal role in embryogenesis and fetal development. It is tightly linked to the IGF-II gene on chromosome 11p15.5 which is reciprocally imprinted. We studied the expression of the human H19 by in situ hybridization in an embryo 35 days post coitus (dpc) and in a fetus from the second trimester of pregnancy. The expression pattern of H19 in the human fetal tissues was similar to its expression in the mouse, and paralleled, with some exceptions, the expression of IGF-II in human fetuses. Abundant expression was found in organs comprising the fetoplacental unit: the placenta, the fetal adrenal, and liver. The expression in the fetal adrenal cortex was most prominent in the definitive cortex and somewhat weaker in the fetal zone. Considerable expression of H19 was found in the fetal liver as early as 35 dpc and in the second trimester. Hematopoietic cells in fetal liver did not express the gene. Moderate expression of H19 was detected in the epithelium of the small intestines, in endometrial stroma and Fallopian tube. In the kidney conspicuous labeling of the metanephric blastema was noted, which was markedly reduced with differentiation to tubules. This pattern of expression is identical to that of IGF-II in the fetal kidney and is relevant to the evolution of Wilms' tumor. No expression of H19 was found in the neural tube of the first trimester embryo or in the developing fetal brain in the second trimester, nor were transcripts detected in the choroid plexus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed2002

Loss of heterozygosity in the clonal evolution of flat colorectal neoplasms.

In contrast to invasive colorectal carcinomas that develop in typical exophytic adenoma-carcinoma sequences, some invasive cancers may evolve from flat mucosal dysplastic lesions. Despite their relatively small size, these flat colorectal lesions are often associated with high-grade dysplasia and may show an aggressive clinical course. To delineate the genetic pathways in the clonal evolution of these tumors, multiple foci were microdissected from 13 cases and the allelic deletions of 15 chromosomal arms were analysed. Loss of heterozygosity (LOH) was detected most frequently on 17p (77%), followed by 18q (69%), and 5q (54%). In five cases with concomitant low-grade adenomas, only one case showed LOH in low-grade adenoma foci. In high-grade dysplasia with/without submucosal invasion, early and homogeneous LOH of one to several chromosomal arms was detected. Overall, homogeneous and thus early LOH were most frequently detected on 17p (seven of 10 cases with 17p LOH), followed by 3p (two of three cases with 3p LOH), and 5q (four of seven cases with 5q LOH). In addition to homogeneous LOH, the LOH patterns observed in different portions of dysplasias and invasive cancers in individual cases identified several different genetic patterns of tumour progression, either with linear or branching (divergent) trees. Positive immunostaining for p53 was detected in 10 of the 13 cases; of these, five cases were concomitant with 17p LOH in all of the microdissected foci, four cases were concomitant with 17p LOH in a majority of foci and, one case showed retention of 17p. Except for the flat configuration and early 17p LOH, genetic heterogeneity in the flat high-grade dysplastic foci was found to be similar to genetic chaos in the late dysplastic and preinvasive stages of exophytic adenoma. These findings suggest a potentially aggressive course for these neoplasms.

Adenoma↗