The histomorphologic spectrum of many epithelial cancers is now recognized to include a subset of cells characterized by groups of nesting high in lacunar spaces that have a "micropapillary" architecture. This pattern was first reported in 1982 by The Henderickson et al. described an aggressive variant of endometrial adenocarcinoma. In this context, an infiltrating pattern, biologically aggressive expansion behavior remarkably reminiscent of ovarian serous papillary carcinoma was evident. Subsequently, a micropapillary variant has been recognized in cancers arising from breast, bladder, thyroid, lung and pancreas, and has therefore come to be seen as a general feature of epithelial cancer. It seems likely that this phenotype arises from a fundamental aspect of epithelial carcinogenesis, and the finding of a "genetic signature" recognizable that cuts across these different sites would not be surprising. Researchers at the MD Anderson Cancer Center were the first to report a subset of bladder cancers showing a micropapillary histomorphology, the publication of the first series of 18 patients in 1994.
As discussed in the context of sarcomatoid and small cell morphology is typical of a micropapillary component seen in a context that includes more typical of CBT. From this first series of patients, micropapillary variant was observed to have a more aggressive clinical course and a particular tendency for prominent lymphovascular invasion. Subsequently published a series of cases in Sweden, Harvard, Australia, Wayne State University, and the City of Mexico, along with many individual case reports. These reports established that micropapillary bladder cancer has a characteristic morphology that can be identified reliably. Moreover, the trend first reported to the clinical subclassification, aggressive behavior, and the relatively poor response to standard systemic chemotherapy has been fully confirmed. Ultrastructural studies in the context of micropapillary breast cancer suggested secretory granules along the basement membrane, ie, loss of normal cell polarity which is the secretory activity in the basal surface, not only on the surface apical.
This concept of "inside out" morphology has been reinforced by the demonstration that the gene product mucinous glycoprotein MUC1 is abnormally located at the basal surface micropapillary cancers, including bladder origin. Although not yet formally established, it seems likely that a mechanical connection is made between this type of abnormal phenotype, early submucosal infiltration and early access to the lymphatic vessels that characterize the clinical course of these cancers. In our experience, the unusual finding of a bladder cancer is the stage pT1N1 almost always associated with micropapillary histology. micropapillary bladder cancer has been reported to occur infrequently. In the series of cases of Sweden, on the basis of a population-based registry, the incidence of bladder cancer was 0.7%. That report-biased Mexico City put the incidence of 38/630 (6%). In a similar registry biased at the MD Anderson Cancer Center, we found 162 cases for an incidence of 4.2%. Of course, these reports come from genetic and environmental contexts very different, and it is very possible that the incidence of different geographic region. The clinical management of micropapillary bladder cancer should take into account the very real possibility that clinically understaged and can grow quickly. Therefore, we call for "early" cystectomy for any tumor that invades the lamina propria, and certainly calls for any patient with disease cT1 or higher after a trial of intravesical therapy will be guided to cystectomy without delay. For patients with locally advanced disease, the prognosis is worse than for patients with TCC conventional systems. In the MD Anderson Cancer Center experience, patients with cT4a cT3b or treated with a combination of systemic chemotherapy and surgery (in any order), had a lower overall cure rate compared with patients with conventional systems TCC. In the metastatic setting, both the response rate and overall survival of patients with micropapillary cancer are below our historical expectations. Despite the aggressive implementation of combination chemotherapy, patients with micropapillary cancer still have a relatively poor outcome. This has been methotrexate / vinblastine / doxorubicin / cisplatin (MVAC), with ifosfamide-based combinations, and gemcitabine / cisplatin. It is important to recognize, however, that
although the overall results are lower than those obtained for patients with conventional TCC, many patients do well, and therefore continue to offer conventional therapy for patients in this subgroup
As discussed in the context of sarcomatoid and small cell morphology is typical of a micropapillary component seen in a context that includes more typical of CBT. From this first series of patients, micropapillary variant was observed to have a more aggressive clinical course and a particular tendency for prominent lymphovascular invasion. Subsequently published a series of cases in Sweden, Harvard, Australia, Wayne State University, and the City of Mexico, along with many individual case reports. These reports established that micropapillary bladder cancer has a characteristic morphology that can be identified reliably. Moreover, the trend first reported to the clinical subclassification, aggressive behavior, and the relatively poor response to standard systemic chemotherapy has been fully confirmed. Ultrastructural studies in the context of micropapillary breast cancer suggested secretory granules along the basement membrane, ie, loss of normal cell polarity which is the secretory activity in the basal surface, not only on the surface apical.
This concept of "inside out" morphology has been reinforced by the demonstration that the gene product mucinous glycoprotein MUC1 is abnormally located at the basal surface micropapillary cancers, including bladder origin. Although not yet formally established, it seems likely that a mechanical connection is made between this type of abnormal phenotype, early submucosal infiltration and early access to the lymphatic vessels that characterize the clinical course of these cancers. In our experience, the unusual finding of a bladder cancer is the stage pT1N1 almost always associated with micropapillary histology. micropapillary bladder cancer has been reported to occur infrequently. In the series of cases of Sweden, on the basis of a population-based registry, the incidence of bladder cancer was 0.7%. That report-biased Mexico City put the incidence of 38/630 (6%). In a similar registry biased at the MD Anderson Cancer Center, we found 162 cases for an incidence of 4.2%. Of course, these reports come from genetic and environmental contexts very different, and it is very possible that the incidence of different geographic region. The clinical management of micropapillary bladder cancer should take into account the very real possibility that clinically understaged and can grow quickly. Therefore, we call for "early" cystectomy for any tumor that invades the lamina propria, and certainly calls for any patient with disease cT1 or higher after a trial of intravesical therapy will be guided to cystectomy without delay. For patients with locally advanced disease, the prognosis is worse than for patients with TCC conventional systems. In the MD Anderson Cancer Center experience, patients with cT4a cT3b or treated with a combination of systemic chemotherapy and surgery (in any order), had a lower overall cure rate compared with patients with conventional systems TCC. In the metastatic setting, both the response rate and overall survival of patients with micropapillary cancer are below our historical expectations. Despite the aggressive implementation of combination chemotherapy, patients with micropapillary cancer still have a relatively poor outcome. This has been methotrexate / vinblastine / doxorubicin / cisplatin (MVAC), with ifosfamide-based combinations, and gemcitabine / cisplatin. It is important to recognize, however, that
although the overall results are lower than those obtained for patients with conventional TCC, many patients do well, and therefore continue to offer conventional therapy for patients in this subgroup