Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-three patients with invasive adenocarcinoma of the gallbladder were postoperatively studied in order to determine their general immunological status as well as the local immunohistological reaction to the tumor. At the end of the follow-up, they formed two groups: 19 living patients (group GL) and 24 dead patients (group GD). As a control group (GC), 21 patients with cholecystectomy or cholelithiasis and without carcinoma were simultaneously evaluated. In GL, most of the tumors were limited to the gallbladder wall, and in GD, most of the tumors were already disseminated at the time of diagnosis. GD presented a lower percentage of peripheral blood B lymphocytes, as compared to GL and GC cases. Skin tests of delayed hypersensitivity were significantly more reactive in GL cases than in GD cases, and less reactive in GD than in GC cases. The immunohistological evaluation of the gallbladder yielded a lower B lymphocyte infiltration in GD tumors than in the control cases. GL cases showed a higher intratumoral lymphocytic and mononuclear cell infiltration than GD cases. Although the clinical stage was higher in GD than in GL cases, there were also significant differences in the local immune response and the general immunological status. Patients with invasive gallbladder adenocarcinoma showing longer postoperative survival revealed normal or increased local and general immunological reactions, whereas patients with disseminated tumors showed an important humoral and cellular secondary immunodeficiency.
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PMID:Immunological evaluation of patients with invasive carcinoma of the gallbladder. 850 41

From January 1988 to December 1993, we identified six men with minimally invasive (stage I) squamous cell carcinoma of the anus and 10 men with anal carcinoma in situ (CIS). Of the six patients with invasive carcinoma, four were infected with human immunodeficiency virus (HIV), including one with AIDS. Of the 10 patients with CIS, eight were infected with HIV, including four with AIDS. Anal pain and bleeding were the most common symptoms of minimally invasive anal cancer and anal CIS. Anal irritation, burning, or pruritus occurred more frequently in patients with CIS, whereas anal ulcers, masses, or abscesses were more frequent in patients with minimally invasive cancer. Several patients with CIS had a discrete area of leukoplakia in the anal canal or a pigmented plaque of the anus and anal canal. These lesions were not observed in patients with minimally invasive anal cancer. The symptoms and signs of early-stage anal cancer in men at risk for developing HIV infection or men infected with HIV often resemble those of other common anorectal diseases in homosexual men. Anal cancer in HIV-infected men is not limited to those individuals with AIDS.
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PMID:Clinical presentation of minimally invasive and in situ squamous cell carcinoma of the anus in homosexual men. 852 51

A total of 158 women who either HIV-infected or under iatrogenic immunosuppression were examined regularly during a 4-year period to evaluate if certain vulvar neoplasms and cervical neoplasia have similar associated risk factors. Patients with CIN were matched prospectively with immunocompetent controls with CIN. Forty-eight cervical lesions were detected among patients, including 2 invasive carcinoma and 15 CIN-3 lesions, compared to 11 vulvar lesions, including 2 invasive carcinoma and 7 VIN-3 lesions. Women who have more than five life-time partners were more likely to have HPV-DNA positive cervical swabs and vulvar scrapes as well as cervical and/or vulvar neoplasia. Compared to 2.7% of controls 15.2% of patients with CIN had coexisting high-grade lesions of the vulva. With 1 exception all patients with vulvar neoplasia either suffered from symptomatic immunodeficiency or received immunosuppressive drugs for more than 10 years. Except for 1 VIN-3 lesions, all vulvar neoplasms were associated with HPV-DNA types 16, 31, and/or 33. Six of nine patients as well as the 2 controls with coexisting vulvar and cervical neoplasia had the same HPV-type associated with both lesions. All vulvar lesions were classified as either "warty" or "basaloid". In conclusion cervical and bowenoid/basaloid vulvar neoplasia seem to have a similar HPV-related genesis. Malfunction of the cellular immune response appears to be a cofactor in the genesis of HPV-associated neoplasia at both sites.
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PMID:Human papillomavirus is associated with the frequent detection of warty and basaloid high-grade neoplasia of the vulva and cervical neoplasia among immunocompromised women. 855 24

A case of a woman having a large invasive vulvar carcinoma is reported. Because of the early age of onset and recurrent pneumonia, immunodeficiency was suspected. There appeared to be a repetitive low CD4+ T-lymphocyte count, without evidence of HIV infection or other diseases or therapies known to be clearly associated with T-cell depletion. This is suspected for the rare disorder known as idiopathic CD4+ T-lymphocytopenia which is often associated with opportunistic infections. A case of suspected idiopathic CD4+ T-lymphocytopenia in a patient having an invasive vulvar carcinoma is described.
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PMID:Suspected idiopathic CD4+ T-lymphocytopenia in a young patient with vulvar carcinoma stage IV. 864 26

In a previous study, we described a cell line (BRG-P) derived from a woman with Burkitt's lymphoma (BL) and acquired immunodeficiency syndrome that shared the same characteristic cytogenetic abnormalities as the patient's malignant cells. This cell line contained subclones that displayed an isotype switch from IgM to IgA1 and an accumulation of point mutations in the Vh region genes. Because these two features suggested an antigen-driven process, we began a search for the antigen responsible for the stimulation of the malignant B cells. Specifically, we hypothesized that because the patient's tumor had presented as a lymphomatous infiltration of the breast, the malignant B cells were recruited to this site because of the reactivity of their surface lg with breast tissue. A hybridoma (BRG-H) was obtained by fusing BRG-M cells (an IgM producing subclone of the BRG-P cell) with an appropriate cellular partner. The monoclonal antibody (BRG MoAb) produced by this hybridoma reacted strongly with two of five breast cancer cell lines and stained normal and malignant ductal epithelial cells on breast tissue sections. The antigen recognized by the BRG MoAb consisted of a single, minimally glycosylated polypeptide chain of 45 kD (p45). The BRG MoAb failed to react with a panel of human cell lines from different tissues, except for one cell line from a uterine cervical carcinoma. No reactivity was detected for a panel of exogenous antigens from various pathogens, including human immunodeficiency virus and self-antigens frequently recognized by polyspecific antibodies. Experiments were performed to investigate the functional consequences of the interaction of surface IgM with its specific ligand. Coculture of BRG-M cells with p45+, but not with p45-, breast cells caused apoptosis of BRG-M cells. The specificity of the interaction was shown by the observation that apoptosis was prevented by pretreatment of BRG-M cells with a monovalent F(ab') fragment of rabbit IgG antibody to human mu chains. Moreover, only BRG-M cells, but not other BL cells, underwent apoptosis after exposure to p45+ breast cells. The interaction between the CD40 molecule expressed by BRG-M cells and its specific ligand (CD40L) prevented p45-induced cell apoptosis. Because this interaction mimics that occurring in vivo between T and B cells during immune responses, our data suggest that various events contributed to the emergence of the BL, in this particular patient, including antigenic stimulation possibly assisted by T-cell help.
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PMID:Apoptosis of Burkitt's lymphoma cells induced by specific interaction of surface IgM with a self-antigen: implications for lymphomagenesis in acquired immunodeficiency syndrome. 869 8

LMP-1, an Epstein-Barr viral (EBV) latency protein, is considered a viral oncogene because of its ability to transform rodent fibroblasts in vivo and render them tumorigenic in nude mice. In human B cells, EBV LMP-1 induces DNA synthesis and abrogates apoptosis. LMP-1 is expressed in EBV-transformed lymphoblastoid cell lines, nasopharyngeal carcinoma (NPC), a subset of Hodgkin's disease (HD), and in EBV-associated lymphoproliferative disorders (EBV-LPDs). Recently, focused deletions near the 3' end of the LMP-1 gene (del-LMP-1, amino acids 346-355), in a region functionally related to the half-life to the LMP-1 protein, have been reported frequently in human immunodeficiency virus (HIV)-associated HD (100%) and EBV+ Malaysian and Danish peripheral T-cell lymphomas (100%, 61% respectively), but less frequently in cases of HD not associated with HIV (28%, 33%) and infectious mononucleosis (33%). To further investigate the potential relationship of del-LMP-1 to EBV-LPDs associated with immunosuppression or immunodeficiency, we studied 39 EBV-associated lymphoproliferations (10 benign, 29 malignant) from four distinct clinical settings: posttransplant (4 malignant, 1 reactive); HIV+ (18 malignant, 2 reactive); nonimmunodeficiency malignant lymphoma (ML) (7 cases); and sporadic EBV infection with lymphoid hyperplasia (7 cases). The presence of EBV within lymphoid cells was confirmed by EBV EBER1 RNA in situ hybridization or by polymerase chain reaction (PCR) analysis. EBV strain type and LMP-1 deletion status were determined by PCR. EBV strain types segregated into two distinct distributions: HIV+ (9 A; 11 B) and non-HIV (19 A, 0 B), consistent with previous reports. Overall, del-LMP-1 were found in 1 of 5 (20%) Burkitt lymphomas (BL); 17 of 24 (71%) aggressive non-Hodgkin's lymphoma (agg-NHL), and 2 of 10 (20%) reactive lymphoid proliferations. Of the agg-NHLs, del-LMP-1 were present in 4 of 4 PT-ML (100%); 10 of 15 HIV+ ML (67%); and 3 of 5 nonimmunodeficiency malignant lymphoma (ML, 60%). A total of 2 of 7 (28%) sporadic EBV-associated lymphoid hyperplasias contained a del-LMP-1. All del-LMP-1 were identical by DNA sequence analysis. No correlation was identified between the presence of del-LMP-1 and the EBV strain type observed. The high incidence of del-LMP-1 observed in agg-NHLs (71%), in contrast to the relatively low incidence observed in reactive lymphoid proliferations (28%), suggests that the deleted form may be preferentially selected in lymphomatous processes. All posttransplant agg-NHLs contained a del-LMP-1, and a similar frequency of del-LMP-1 was observed in both HIV-associated ML (66%) and nonimmunodeficiency ML (60%), suggesting that impairment of immune function alone is not a requirement for the expansion of malignant cells infected by EBV stains containing the deleted LMP-1 gene.
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PMID:Epstein-Barr virus latent membrane protein-1 oncogene deletions: correlations with malignancy in Epstein-Barr virus--associated lymphoproliferative disorders and malignant lymphomas. 870 80

A 48 yr old HIV seropositive female presented with a right breast mass and bilateral axillary lymphadenopathy. Fine needle biopsy (FNB) revealed an adenocarcinoma with abundant mucin production and features suggestive of a cribriform and micropapillary ductal carcinoma in situ (DCIS). Histopathological examination of the tumor confirmed an invasive mixed colloid carcinoma with extensive DCIS. There have been 4 previous reports in the literature of breast carcinoma associated with HIV seropositivity. This case initially diagnosed by FNB is the first case reported in Australia. In spite of the somewhat more favourable histological type of breast carcinoma, this tumor shows numerous unfavourable prognostic factors and has had an aggressive clinical course with relapse of disease in the contralateral breast and distant metastases within 4 wks of surgery, probably related to the patient's immunodeficiency.
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PMID:FNB diagnosis of breast carcinoma associated with HIV infection: a case report and review of HIV associated malignancy. 871 81

We prospectively evaluated the frequency of lymphadenopathy in the right upper abdominal quadrant as detected by sonography in 650 consecutive unselected patients, after excluding patients with a known lymphoma or abdominal carcinoma and patients with acquired immunodeficiency disease. Evidence of enlarged lymph nodes (few in number, with an elongated shape and isoechoic to the liver, 8 to 22 mm in size), found primarily in the gastrohepatic ligament and porta hepatis, was seen on sonographic scans in 106 patients (16.3%). Associated conditions in 69 of 106 patients (65%) were hepatobiliary or pancreatic diseases and, less frequently, other benign entities (12 patients; 11.3%); in 25 cases (23.5%) no significant abdominal or systemic disease was present. Comparison with CT or surgical findings, or both, was available in 36 cases. We conclude that lymphadenopathy in the right upper abdominal quadrant may be found in relation to different non-neoplastic conditions as well as in the absence of any significant intra-abdominal disease. The frequency of this finding on sonographic scans must be recognized to prevent misdiagnosis of lymphoma or metastatic disease as well as to avoid overstaging of local (hepatobiliary, pancreatic, gastric) neoplasms.
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PMID:Abdominal lymphadenopathy in benign diseases: sonographic detection and clinical significance. 873 41

Verrucous lesions in patients with human immunodeficiency virus (HIV) disease may be caused by viruses other than the human papillomavirus. We describe a 32-year-old HIV-positive black man who presented with a verrucous lesion of the intergluteal cleft that clinically resembled condyloma acuminata or verrucous carcinoma. Histopathological examination revealed the changes of herpes virus infection, and culture of the tissue confirmed the presence of herpes simplex virus. Human papillomavirus was not detected by in situ hybridization or the polymerase chain reaction. Significant regression of the lesion was seen after 6 weeks of treatment with oral acyclovir.
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PMID:Herpes simplex virus infection masquerading as condyloma acuminata in a patient with HIV disease. 873 96

Substantial evidence indicates that several common viruses are clearly or probable causal factors in the etiology of specific malignancies. These viruses either normally establish latency or can become persistent infections. Oncogenesis is probably linked to an enhanced level of viral activation in the infected host, reflecting heavy viral dose or compromised immune control. The major virus-malignancy systems include hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatocellular carcinoma; human lymphotropic virus-type 1 (HTLV-1) and adult T-cell leukemia/lymphoma (ATL); Epstein-Barr virus (EBV) and endemic Burkitt's lymphoma, nasopharyngeal carcinoma, and Hodgkin's disease; and human papilloma virus (HPV) and cervical cancer. Of these, a vaccine is available only for HBV. These malignancies tend to occur in early to mid-life and account for a substantial amount of morbidity and person-years lost. They are also likely to occur as "opportunistic malignancies" among individuals infected with human immunodeficiency virus type-1, particularly among those who experience prolonged survival.
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PMID:Overview: viral agents and cancer. 874 95


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