11.09.2015

Breast cancer stage 1 invasive

Women with early-stage breast cancer may have a better chance of survival if they have a lumpectomy plus radiation therapy compared to a mastectomy, according to the largest-ever randomized clinical trial study of women with early-stage breast cancer. Contributor Deborah McBride, RN, PhD, CPON®, is a staff nurse IV at the Kaiser Permanente Oakland Medical Center and an assistant professor at Samuel Merritt University in Oakland, CA. In young women with HGSC or CCC, the possibility of hereditary conditions such as BRCA1 or BRCA2 mutations or Lynch syndrome must be considered. Of the most common histologic subtypes of ovarian cancer, serous carcinoma occurs most often, followed by CCC and EC, which are diagnosed with almost equal frequency. HGSCs are characterized by papillary (Figure 1A), glandular, solid, and transitional (Figure 1B) patterns.
As previously noted, it is now well-established that HGSC and LGSC represent two distinctly different disease entities rather than grades of the same tumor.[3,6-8,41-43] Serous carcinomas were traditionally graded as well-differentiated, moderately differentiated, and poorly differentiated. Although HGSCs are thought to arise from the ovarian surface epithelium or cortical inclusion cysts, no definite precursor lesions have been identified.
Conversely, LGSC is thought to arise from preexisting cystadenoma or serous borderline tumor (SBT) that eventually progresses to invasive carcinoma. Although patients with low-grade neoplasms usually have recurrences that are low-grade tumors, we have encountered cases of LGSC either coexisting with HGSC or recurring as HGSC. In most cases, immunohistochemical stains are not necessary for making a diagnosis of either HGSC or LGSC.
Lastly, from a clinical standpoint, although LGSC presents in younger women and is resistant to chemotherapy, overall survival is better than that of patients who have HGSC.[7,8,41,62] While HGSC responds well to chemotherapy initially, patients frequently experience recurrence and succumb to the disease. Cancer (larger than 2 millimeters) is found in 1 to 3 axillary lymph nodes or in the lymph nodes near the breastbone (found during a sentinel lymph node biopsy); orthe tumor is larger than 2 centimeters but not larger than 5 centimeters. The study results were reported in Cancer.Data from 112,154 patients with stage I or II breast cancer, from the California Cancer Registry from 1990–2004, suggest that the less-invasive breast-conserving therapy (BCT) (a combination of lumpectomy and radiation) was associated with superior disease-specific survival at a median follow-up of 110 months (just over 9 years). The four most common subtypes are serous, endometrioid, clear cell, and mucinous carcinoma. While the majority of ovarian cancers are sporadic, family history is one of the strongest risk factors.
Seidman et al found that among 220 consecutive patients with surface epithelial carcinoma, almost 80% of cases of intra-abdominal carcinomatosis were of serous histology, especially when peritoneal carcinomas, carcinosarcomas, and mixed carcinomas with serous component were included.[30] Thus, it is now well-established that serous carcinomas represent the majority of advanced-stage ovarian cancers. The diagnosis of HGSC is typically straightforward, especially when there is a predominantly papillary pattern with associated psammoma bodies.
While the majority of typical SBTs do not show frankly invasive carcinoma, microinvasion is not uncommon.


Boyd and McCluggage have reported seven cases of LGSC that either coexisted with HGSC or recurred as either HGSC or undifferentiated carcinoma.[5] Close examination of the tumor is recommended, since the areas of HGSC may be focal or admixed with areas resembling SBT.
However, they are useful in the assessment of post-therapy specimens, in which CCC is often considered in the differential diagnosis, or when a diagnosis must be made using small biopsies. Cancer has spread to 1 to 3 axillary lymph nodes or to the lymph nodes near the breastbone (found during a sentinel lymph node biopsy); orlarger than 5 centimeters. Less common are transitional cell tumors, including transitional cell carcinoma and malignant Brenner tumor. The various histologic subtypes are different in terms of risk factors, precursor lesions, clinical course, patterns of spread, molecular genetics, response to conventional chemotherapy, and prognosis.[2-4] Hence, it is imperative to accurately subtype these tumors based primarily on morphology and immunohistochemistry tests, when necessary.
LGSC, on the other hand, is characterized by tumor cells with relative nuclear uniformity, absence of nuclear pleomorphism, and mitotic activity typically < 12 mitoses per 10 high-power fields. Ahmed et al identified TP53 mutations in almost 97% of 145 patients with HGSCs.[59] In mutation-negative cases, p53 dysfunction associated with copy number gain in MDM2 or MDM4 was noted, or the cases were excluded because they represented LGSCs or other malignancies.
Small clusters of cancer cells (larger than 0.2 millimeter but not larger than 2 millimeters) are found in the lymph nodes. While in the past these subtypes were grouped together and designated as epithelial ovarian tumors, these tumor types are now known to be separate entities with distinct clinical and biologic behaviors.
We now know that high-grade serous carcinoma (HGSC), the most common subtype of epithelial ovarian carcinoma, is a different disease from low-grade serous carcinoma (LGSC). The tumors are generally characterized by micropapillae surrounded by clear spaces (Figure 1C); however, glandular, macropapillary, and single cell patterns can also be seen. Typically only a small amount of tumor is present in these biopsies, and numerous immunohistochemical tests are often performed to exclude other entities. From a therapeutic standpoint, current regimens employ standard chemotherapy based on stage and grade rather than histotype. HGSC presents in older women and responds at least initially to chemotherapy but has a worse overall prognosis than LGSC. Less common are tumors such as squamous cell carcinoma, papillary thyroid carcinoma, sebaceous carcinoma, and carcinoid tumors that are typically associated with mature cystic teratomas; these tumor types are beyond the scope of this review. ECs, on the other hand, are associated with squamous differentiation, adenofibromatous background, and endometriosis. Both HGSCs and LGSCs have some overlapping characteristics, as well as some distinct immunophenotypic features. However, this landscape may change in the era of personalized therapy, given that most subtypes (with the exception of high-grade serous carcinoma) are relatively resistant to chemotherapy.


Briefly, the management of ovarian carcinoma has evolved significantly in the past decade—from primary definitive surgery and debulking followed by chemotherapy, to treating patients with neoadjuvant chemotherapy, especially in the setting of miliary disease that cannot be optimally debulked.[36,37] Pathologic review of post-treatment resections poses some problems—including typing of tumors that have undergone therapy-related changes, such as marked atypia and clear cell changes, as well as identifying minimal residual disease in the presence of inflammation and necrosis. Both tumor types are positive for paired box gene 8 (PAX8) and WT1 expression, as well as estrogen receptor (ER) and progesterone receptor (PR) expression. It is now well-accepted that high-grade and low-grade serous carcinomas represent distinct entities rather than a spectrum of the same tumor type.
Lastly, mucinous carcinoma (MUC) of the ovary is a fairly uncommon disease if metastasis has been excluded, and its outcome is highly variable, based on stage at presentation and type of invasion.[9-11] This review focuses on the clinicopathologic and molecular features of epithelial ovarian cancer, with specific attention to genetic predisposition, morphologic challenges, immunohistochemistry, and molecular features.
When the morphologic features are suggestive of serous carcinoma, use of these four markers is sufficient to establish the diagnosis in most cases, and an extensive panel of immunomarkers is usually not necessary.
While they are similar in that patients present with advanced-stage disease, their histologic and molecular features are entirely different. High-grade serous carcinoma is associated with TP53 mutations, whereas low-grade serous carcinomas are associated with BRAF and KRAS mutations. Immunohistochemical stains for p16, p53, and Ki-67 are helpful, since HGSCs show diffuse staining for p16 and p53 and an elevated Ki-67 proliferation index, whereas LGSCs show patchy staining for p16, wild-type staining for p53, and a low Ki-67 proliferation index.[38,57,58] This panel is also helpful in detecting focal HGSC in the background of a tumor that is predominantly an LGSC. Endometrioid and clear cell carcinomas typically present as early-stage disease and are frequently associated with endometriosis. The immunophenotypes of the major epithelial ovarian cancer types are summarized in Table 1. Mucinous carcinomas typically present as large unilateral masses and often show areas of mucinous cystadenoma and mucinous borderline tumor. It must be emphasized that primary mucinous carcinomas are uncommon tumors, and metastasis from other sites such as the appendix, colon, stomach, and pancreaticobiliary tract must always be considered in the differential diagnosis. Lastly, transitional cell tumors of the ovary, specifically malignant Brenner tumors, are quite uncommon. High-grade serous carcinoma often has a transitional cell pattern, and adequate sampling in most cases shows more typical areas of serous carcinoma. Immunohistochemical markers are routinely employed in the diagnosis of epithelial ovarian carcinomas. However, molecular testing of these tumors, unlike in endometrial carcinoma, is not routinely used in clinical practice.



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