Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Kum Cooper is active.

Publication


Featured researches published by Kum Cooper.


Cancer | 1997

Follicular dendritic cell sarcoma

John K. C. Chan; Christopher D. M. Fletcher; Simon Nayler; Kum Cooper

The goal of this study was to characterize the clinicopathologic features of follicular dendritic cell sarcoma, a very uncommon neoplasm.


Laryngoscope | 1997

Adenoid cystic carcinoma of the salivary glands: a review of 10 years.

Ranjan Sur; Bernard Donde; Victor Levin; Juan Pacella; Jeff Kotzen; Kum Cooper; Martin Hale

A retrospective analysis was performed of 50 patients with adenoid cystic carcinoma who were seen in the Department of Radiation Oncology, University of Witwatersrand, Johannesburg, South Africa, in the past 10 years. There were 25 men and 25 women with a mean age of 52 years (age range, 21 to 88 years). Five patients had metastatic disease, and 17 had neural invasion. Thirty‐four patients had surgery (11, complete; 23, microscopic residual). Sixteen patients had radiotherapy as initial management. The disease‐free survival was 26%, overall survival was 29%, and local control was 30% at 10 years. Most recurrences occurred in the first 3 years. Nine patients had metastasis following treatment. The mean survival after metastasis was 15 months. Seven prognostic variables were analyzed using the log‐rank test. There was no impact of age, site, type of salivary gland (major vs. minor), tumor stage, node positivity, or neural invasion on disease‐free survival, overall survival, or local control. Extent of surgical resection (complete vs. microscopic residual) had a significant impact on disease‐free survival and local control (P < 0.05) but no impact on overall survival (P > 0.05) because of the slow‐growing nature of these tumors. Similarly, patients who had microscopic residual after surgery and were treated with radiotherapy did better than those who had biopsy and radiotherapy, although this was not significant statistically (P > 0.05). Thus, whenever possible, every attempt must be made to remove all microscopic tumor by surgery. Addition of postoperative radiotherapy with high‐energy photons did not improve the locoregional control or survival in our series. There is a place for neutrons in the treatment of adenoid cystic carcinomas in advanced cases of inoperable or recurrent tumors, as a review of literature shows.


Pathology | 1998

THE ROLE OF THE HUMAN PAPILLOMA VIRUS IN ESOPHAGEAL CANCER

Monalisa Sur; Kum Cooper

Summary Esophageal squamous cell carcinoma (ESCC) demonstrates wide regional variation in incidence and causal associations. Human papillomavirus (HPV) has been implicated in ESCC, particularly the sub‐types 16 and 18. Transforming proteins E6 and E7 from these high risk sub‐types, interact with p53 protein and Rb protein respectively, leading to loss of function of these tumor suppressor gene products. These interactions further lead to inactivation of the growth suppressive effects of the p53 and Rb proteins, resulting in abnormal proliferative states. p53 protein expression has been found in both HPV‐positive and ‐negative tumors, indicating that HPV and p53 protein expression are not mutually exclusive and can occur together in the same tumor. It has been observed that HPV plays a more significant role in esophageal carcinogenesis in geographic areas with a high prevalence of the disease. A variation in the association between HPV and ESCC worldwide may be due to environmental and geographic factors, or to genetic susceptibility to esophageal HPV infections. Variations in the sensitivity of techniques used in the detection of the virus and in the methodology for processing the tumor tissues, may also be responsible for global differences. Esophageal carcinogenesis is a complex multistep process with a multifactorial etiology. Infection with oncogenic HPV types may be an integral part in a multistep process that leads to ESCC.Abbreviations: ESCC, esophageal squamous cell carcinoma; HPV, human papillomavirus; ISH, in situ hybridisation; SCC, squamous cell carcinoma.


Histopathology | 1998

Spindle epithelial tumour with thymus‐like element (SETTLE): the predominantly monophasic variant

Runjan Chetty; S Goetsch; Simon Nayler; Kum Cooper

To describe two cases of spindle epithelial tumour with thymus‐like element (SETTLE) which are composed predominantly of spindle cells. In addition, to highlight some unusual histological features in SETTLE and discuss its separation from histological mimics.


Cancer | 1996

Morphologic alterations in esophageal squamous cell carcinoma after preoperative high dose rate intraluminal brachytherapy.

Monalisa Sur; Ranjan Sur; Kum Cooper; Vic Levin; Damon Bizos; Norman Dubazana

Total esophagectomy specimens from 4 patients given preoperative high dose rate intraluminal brachytherapy (HDRILBT) of 20 Gray (Gy) in 2 fractions of 10 Gy each week were reviewed for radiation changes.


Histopathology | 1996

Malignant transformation in a schwannoma

Simon Nayler; Gladwyn Leiman; T. Omar; Kum Cooper

The two most common benign neoplasms of peripheral nerve sheath are neurofibromas and schwannomas (neurilemmomas). Malignant change is well known to occur in neurofibromas, in the setting of type 1 neurofibromatosis. In this context, up to 5% of neurofibromas undergo malignant transformation, this being a complex multistep process involving the NF-1 gene, and the p53 gene. Malignant transformation of schwannomas, in contrast, is an exceedingly rare occurrence, with no hereditary predisposition. It has been stated that malignant change is so rare, that for practical purposes it may be disregarded. In a recent review of 32 previously reported cases, 25 were found to be unacceptable examples; hence there are, to our knowledge, only nine acceptable examples of malignant transformation in benign schwannomas. We present a case of sarcomatous change within a benign schwannoma probably representing the earliest example yet reported.


Pathology | 2001

Investigation of human papillomavirus in transitional cell carcinomas of the urinary bladder in South Africa

Monalisa Sur; Kum Cooper; Ulrike Allard

Aim: To investigate the prevalence of human papillomavirus in transitional cell carcinoma of the urinary bladder in South Africa. Methods: Ninety‐one archival samples of bladder transitional cell carcinoma were subjected to polymerase chain reaction (PCR) and non‐isotopic in situ hybridisation (NISH) for the detection of human papillomavirus 6, 11, 16, 18, 31, and 33 genotypes. Results: HPV was detected in only one case with PCR. HPV was not detected in any of the cases subjected to the NISH system. Conclusion: This study shows that although HPV has been shown to be associated with uterine cervical and esophageal squamous cell carcinomas in South Africa, this virus is not present in the transitional cell carcinoma of the urinary bladder in this geographical location. It is suggested that other factors, including nitrosamine exposure, p53 mutation, and additional unknown chromosomal events, may play a role in the carcinogenesis of this neoplasm in the bladder.


Histopathology | 1998

Biotin inclusions: a potential pitfall in immunohistochemistry

Simon Nayler; S Goetsch; Kum Cooper

Sir : In the November 1997 issue of Histopathology, Bussolati et al. describe the restoration of endogenous biotin reactivity following antigen retrieval (using pressure cooking and to a lesser extent microwave retrieval). The authors suggest that blocking of endogenous biotin by sequential avidin–biotin treatment prevents the erroneous detection of biotin. Intra-nuclear biotin inclusions have been previously misinterpreted to be those of Herpes simplex virus (HSV), using the streptavidin–biotin complex (StrepABC). We have also described biotin intranuclear inclusions in gestational endometria closely resembling HSV inclusions. This error can be easily avoided by paying careful attention to the negative control. We have noted the negative control to be invariably positive, due to the presence of endogenous biotin, with the StrepABC immunodetection system. This false positive immunoreaction should be the clue to the alert pathologist that there is endogenous biotin reactivity. Despite attempts to block endogenous biotin with free avidin and biotin as recommended, we have demonstrated residual positivity in the negative control, using the StrepABC system. We have also compared the alkaline-phosphatase– anti-alkaline phosphatase (APAAP) and the peroxidase– anti-peroxidase (PAP) detection systems and found that whilst the negative control was negative with the former, there was aberrant immunoreactivity with the PAP system. Curiously this was eliminated with microwave pretreatment prior to immunohistochemistry. These curious results serve to underscore the complexities of antigen retrieval. We use retrieval methods such as pressure cooking, microwave technology and even ultrasound, barely understanding the mechanisms of antigen retrieval. It is inevitable that aberrant and puzzling results are obtained. It is imperative that diagnostic pathologists interpret immunohistochemical findings in the light of positive and negative controls, and also with full knowledge of the pitfalls and limitations of the varying detection systems used in their laboratories. We advocate that the optimal detection system for immunohistochemistry in the tissues containing endogenous biotin, as so comprehensively demonstrated by Bussolati et al. is either the APAAP or PAP immunodetection system (the latter with microwave pretreatment), rather than the StrepABC method. Embarrassing and potentially dangerous errors can thus be avoided. S J Nayler S Goetsch K Cooper


Diagnostic Cytopathology | 1998

Natural killer cell lymphoma in cytology : Breaking all the rules : A case report

Colleen A. Wright; Kum Cooper; Gladwyn Leiman; Marilyn Davidge-Pitts

A testicular mass aspirate was received from a 22‐yr‐old patient with known non‐Hodgkins lymphoma. The cells were large and pleomorphic, occurring in syncytial fragments and demonstrating abundant cytoplasm. No lymphoglandular bodies were seen. As characteristic lymphoma criteria were not present, a cytodiagnosis of germ‐cell tumor was suggested, and testicular biopsy advised. The final histopathology report, however, was of a CD 56‐positive (large‐cell) T‐natural killer cell lymphoma, of which this appears to be the first example described and illustrated cytologically. Diagn. Cytopathol. 1998;19:9–11.


Archive | 2000

Schistosoma hematobium and Bladder Cancer

Monalisa Sur; Kum Cooper

It has been estimated that more than 250 million people in the tropical and subtropical regions of the world suffer from schistosomiasis, also known as bilharziasis. The parasitic disease may cause morbidity that is protean in character, and it has a mortality rate that is difficult, if not impossible, to calculate, especially in Third World countries. Of the major species of human schistosomes, Schistosoma japonicum, is restricted to the Far East while S. hematobium is almost confined to the African continent and parts of Asia Minor and the Arabian peninsula. S. mansoni is found in Africa and tropical parts of the Western hemisphere.

Collaboration


Dive into the Kum Cooper's collaboration.

Top Co-Authors

Avatar

Simon Nayler

University of the Witwatersrand

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Colleen A. Wright

University of the Witwatersrand

View shared research outputs
Top Co-Authors

Avatar

Gladwyn Leiman

University of the Witwatersrand

View shared research outputs
Top Co-Authors

Avatar

S Goetsch

University of the Witwatersrand

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

John K. C. Chan

Palo Alto Medical Foundation

View shared research outputs
Top Co-Authors

Avatar

Basil van Iddekinge

University of the Witwatersrand

View shared research outputs
Top Co-Authors

Avatar

Bernard Donde

University of the Witwatersrand

View shared research outputs
Researchain Logo
Decentralizing Knowledge