Biomedical subjects

A Nasir

Publications and source records attributed to A Nasir.

25 records · Page 2Linked to original sources

PubMedDate not supplied

Neoplasms during the progression of pregnancy.

Restricting this review to dealing with pregnancy and its interaction with neoplasms limits us to the child-bearing years. Neoplasms may appear at all stages of species with true tissues and the incidence of malignancy in pregnancy is estimated to be 1:1,000. Almost 50% of these tumors are cervical cancers, followed by breast cancer, with an incidence of approximately 0.03%. The pregnant woman, in the same person, exhibits controlled growth (the pregnancy) and uncontrolled growth (the malignancy). In younger women, the neoplasms represent early stages of biological development and seem to arise practically from all maternal tissues. Geriatric changes in the neoplastic growth processes are missing. This article encompasses a review of the integration of neoplasms, the maternal body, the fetus and the placenta. The morphological and biochemical integration of the different processes is diversified. Mainly, we would like to address the interaction between pregnancy and common human malignancies like breast, cervix, and melanoma, but we will also review rare neoplastic complications. This way it is possible to treat the combined growth processes as they evolve from the initiated sperm, the ovum and continue via the placental development. These processes lead to the fetus and, in the pathological sense, to childhood complications, though most cases develop only portions of the process.

Breast Neoplasms↗

PubMedDate not supplied

Apoptosis and pathogenesis of viral hepatitis C--an update.

Hepatitis C virus is a major causative agent of chronic liver disease. Viral genotype, mutations, virus-host interaction, expression of viral proteins and host immune-reaction are important factors in the pathogenesis of HCV infection. Precise pathogenesis and perpetuation of hepatocellular injury in hepatitis C viral infection remain unclear. Proposed mechanisms include direct viropathic effect, the host immune response mediated through cytotoxic T lymphocytes, both viropathic and cytopathic effects, and macrophages/monocytes. Apoptosis occurs both in acute or chronic hepatitis and has been suggested to be mediated through Fas antigen. In HCV infection, Fas expression is up-regulated in the liver cells in line with the severity of liver inflammation. When HCV-specific T cells migrate into hepatocytes and recognize the viral antigen via the T cell receptor, they become activated and express Fas ligand that transduces the apoptotic death signal to Fas-bearing hepatocytes resulting in their destruction. Thus, the Fas system plays an important role in liver cell injury by HCV infection. Possible inducers of apoptosis in hepatitis C include cytokines, especially tumor necrosis factor-alpha (TNF-alpha), released by inflammatory cells, and acting through TNF and other cytokine receptors.

Apoptosis↗

PubMedDate not supplied

Papillary microcarcinoma of the thyroid: a clinico-pathologic and prognostic review.

Papillary microcarcinoma (PMC) of the thyroid is the most common form of thyroid cancer, which usually remains clinically silent until its incidental histologic diagnosis in autopsy or surgical material. Autopsy incidence varies from 3%-36%. PMC may, however, present with clinical symptoms, the commonest of which is cervical lymphadenopathy with or without palpable thyroid nodules. Other reported presentations include cystic neck mass, pulmonary mass (es), metastases in the skull or vertebral column. The upper limit of size to define PMC is 10 mm in most studies but many studies include lesions up to 15 mm in diameter. Histologic variants include encapsulated and partially encapsulated papillary carcinoma, circumscribed microcarcinoma and occult sclerosing carcinoma. Younger age and size less than 10 mm (< 15 mm in other studies) are considered to be favorable prognostic factors. Size alone, however, cannot be regarded as a determinant of prognosis. Older age, larger tumor size, distant metastases, capsular invasion and multifocality indicate unfavorable prognosis. Loss of heterozygosity (LOH) is an infrequent finding, since small deletions may be missed by southern blot analysis. Activation of oncogenes ret and trk have been reported in papillary carcinoma. Some authors advocate conservative while others favor aggressive therapy including total thyroidectomy with or without Iodine 131ablation. Additional investigative techniques are needed to identify the subset of PMC cases with a potential for aggressive clinical course, thereby targeting more aggressive therapy to an appropriate subset of tumors.

Carcinoma, Papillary↗

PubMedDate not supplied

COX-2, NSAIDs and human neoplasia. Part I: Colorectal neoplasms.

Cyclooxygenase-2 (COX-2), the inducible cyclooxygenase isozyme involved in the conversion of arachidonic acid (AA) to biologically active prostanoids, has become the subject of intense interest during the last few years. The recent surge of interest stems from seminal studies that correlated elevated expression of COX-2 with tumor induction and progression, and epidemiological studies that correlated reduced risk of developing certain types of cancers with chronic use of non-steroidal anti-inflammatory agents (NSAIDs). Although these observations were first reported with colorectal cancer (CRC), similar findings have subsequently been made with other types of cancers. A wide spectrum of studies continue to be undertaken in both laboratory and clinical settings to elucidate the mechanisms underlying these anti-tumor effects of COX-2 for potential translation into cancer chemoprevention and therapy. The aim of this article is to present a review of COX genes, the prostaglandin-cyclooxygenase relationship, the role of COX-2 in carcinogenesis and the rationale for targeting COX-2 with NSAIDs for cancer chemoprevention. Special emphasis is given to the role of COX-2 expression in the genesis and progression of colorectal neoplasia, and its correlation with other pathological characteristics of CRC. Preliminary observations on COX-2 expression in inflammatory bowel disease (IBD)-related colorectal neoplasia are also presented.

Adenoma↗

PubMedDate not supplied

Preneoplastic lesions of the prostate-clinical, pathological and molecular biological aspects.

Needle biopsy is the mainstay of definitive diagnosis of prostate cancer (PCA). While prostate-specific antigen (PSA) screening has facilitated early diagnosis of PCA, it has also resulted in an increase in the proportion of prostate biopsies showing various preneoplastic lesions (PNLs). At times such lesions are the sole finding in the limited amount of tissue available for assessment in an individual biopsy. Hence accurate identification of these lesions is important to avoid errors in the diagnosis of prostatic malignancy and in patient management. Furthermore, some interesting observations have been made regarding the molecular biological aspects of various PNLs during the last decade. In parallel with anatomic and physiological differences in various human races, racial differences have also been observed regarding the incidence of prostatic intra-epithelial neoplasia. This review focuses on prostatic intraepithelial neoplasia (PIN), atypical adenomatous hyperplasia (AAH) and atypical prostatic glands or atypical small acinar proliferation (ASAP) as putative preneoplastic lesions of the prostate. These lesions are reviewed with reference to their overall incidence, histopathological findings, histological differential diagnosis, clinical significance and molecular biological aspects.

Biopsy, Needle↗

PubMedDate not supplied

Value of multilevel sectioning for improved detection of micrometastases in sentinel lymph nodes in invasive squamous cell carcinoma of the vulva.

UNLABELLED: Clinical usefulness of sentinel lymph node (SLN) biopsy has been demonstrated in the management of early vulvar cancer. However, what constitutes a negative SLN has not been well defined. Furthermore, to what extent the SLNs should be sectioned for the greatest likelihood of detection of micrometastases and whether multilevel sectioning will further increase this detection rate in this setting have not been well studied. We analyzed 280 groin lymph nodes (SLNs=45, non-sentinel [NSLNs]=235) in 14 patients with invasive squamous cell carcinoma (ISCC) of the vulva treated with vulvectomy and inguinal SLN and NSLN dissection at the H. Lee Moffitt Cancer Center (HLMCC) between 1996 and 2001. Each SNL was evaluated for micrometastases by H&E and pancytokeratin AE1/3 (CKAE1/3) immunohistochemical staining. All negative SNLs (N=40) were sectioned times 3 (x3) at 50-micron intervals and independently reviewed by two pathologists in order to assess the utility of this inexpensive and logical approach to identifying additional micrometastases. Also, the Wilcoxon Rank Sum Test was used to determine if there was an association between tumor size, depth of invasion and SNL status. The patient age ranged from 35 to 81 years (mean 59 yrs); size of invasive tumor from 1.0 to 7.0 cm (mean 3.4 cm); depth of invasion from 3 to 25 mm (mean 10.8 mm). Of 45 SLNs examined from 14 patients, 11% (5/45) SNLs were positive for micrometastases on initial H&E and/or CKAE1/3 stains. Eighty-nine per cent (40/45) SNLs were negative in the remaining 9 patients. None of the latter 40 SNLs showed micrometastases on additional multilevel sectioning. Instead 3 of 135 NSLNs examined in these 9 patients revealed micrometastases on H&E (skip-micrometastases). Mean tumor size (cm) and depth of invasion (cm) were 4.06 (s.d. 1.89) and 1.20 (s.d. 0.35) for SLN (+) and 3.02 (s.d. 2.12) and 1.01 (s.d. 0.86) for SLN (-) tumor subsets (p values 0.385 and 0.348, respectively). CONCLUSION: Following routine H&E and CK AE1/3 stains, multilevel sectioning does not appear to detect additional micrometastases in sentinel lymph nodes in squamous cell carcinoma of the vulva. Even though mean tumor size and depth of invasion were greater in SNL (+) as compared to SLN (-) tumor subsets in our series, this difference did not reach statistical significance.

Adult↗

PubMedDate not supplied

The etiology of second primary neoplasms.

Neoplasms are derived from normal tissues of the body by cellular transformation. Tumors often represent a less differentiated or an undifferentiated version of the histology of the neoplasms original tissue. Primary tumor(s) may spread by direct extension or by metastasis. For the purpose of this review, second primary tumors will be defined to exclude metastatic lesions or recurrences from an original primary tumor. Second primary tumors arise in several different clinical situations that basically are the result of either inherited or acquired genetic mutations. Second primary tumors may develop soon or very late after treatment of the first primary tumor and may reflect an underlying genetic or immunologic defect in the patient, treatment related genetic damage, or environmental exposure to carcinogens. With the greater success of modern chemotherapy and radiotherapy in achieving long-term remissions in many patients, second primary tumors are a rapidly developing disease-category. This paper will review the clinical circumstances associated with a significantly higher incidence of second primary tumors in patients with an initial primary tumor.

Humans↗