Methods: Cost and workload data were obtained from hospital records for 2015. Time allocation of staff between laboratory testing and other activities was determined using assumptions from published workload studies.
Results: The laboratory received 20,093 cases for testing in 2015, and total expenditures were US $1.20 million, ie, $61.97 per case. The anatomic pathology laboratory accounted for 5.2% of the laboratory budget at the hospital, compared to 64.3% for the clinical laboratory and 30.5% for the microbiology laboratory. We provide comparisons to a similar laboratory in the United States.
Conclusions: Anatomic pathology is more costly than other hospital laboratories due to the labor-intensive work, but is essential, particularly for cancer diagnoses and treatment.
METHODS: In this descriptive, retrospective study, we selected all prostate biopsies received by the diagnostic pathology department of a tertiary hospital in Malaysia in the year 2020, from adult patients for analysis. Data on demographics, specimen preparation processes, and final histopathological diagnosis was extracted from the Laboratory Information System (LIS). The cost incurred for each biopsy diagnosed as cancer was calculated with the cost prices referenced from laboratory documentation. Statistical analysis was performed using SPSS, version 28.
RESULTS: The total cost for detection of cancer using TR biopsy ranged from RM11.22 - RM271.02 with mean of RM47.53. The standard deviation, s is RM43.45. For TP biopsies, the total cost ranged from RM112.20 - RM349.56 with mean of RM160.85, standard deviation of RM80.37. TR biopsies had a detection rate of 43.2%, while TP biopsies had a 24.2% cancer detection rate. There is a 3.38-fold increase in costs between TR and TP biopsy.
CONCLUSION: The results show a 3.38-fold increase in costs and a reduction in cancer detection rate when comparing TR and TP biopsy. The reason for the reduced detection rate is unascertained in this study.
MATERIALS AND METHODS: Formalin-fixed paraffin- embedded tumour tissue of 144 no special type (NST) invasive breast carcinomas histologically diagnosed between January 2009 and December 2012 in Hospital Sultanah Bahiyah, Alor Setar, Kedah were immunostained with COX-2 antibody. COX-2 overexpression was analysed against demographic data, hormone receptor status, HER2- neu overexpression, histological grade, tumour size and lymph node status.
RESULTS: COX-2 was overexpressed in 108/144 (75%) tumours and was significantly more prevalent (87%) in hormone receptor-positive tumours. There was no correlation between COX-2 overexpression and HER2/neu status. Triple negative cancers had the lowest prevalence (46%) (p<0.05). A rising trend of COX-2 overexpression with increasing age was observed. There was a significant inverse relationship with tumour grade (p<0.05), prevalences being 94%, 83% and 66% in grades 1, 2 and 3 tumours, respectively. A higher prevalence of COX-2 overexpression in smaller size tumours was observed but this did not reach statistical significance. There was no relationship between COX-2 expression and lymph node status.
CONCLUSIONS: This study did not support the generally held notion that COX-2 overexpression is linked to poor prognosis, rather supporting a role in tumorigenesis. Larger scale studies with outcome data and basic studies on cancer pathogenetic pathways will be required to cast further light on whether COX-2 inhibitors would have clinical utility in cancer prevention or blockage of cancer progression. In either setting, the pathological assessment for COX-2 overexpression in breast cancers would have an important role in the selection of cancer patients for personalized therapy with COX-2 inhibitors.
Methods: Eighty (40 right-sided and 40 left-sided) formalin-fixed, paraffin-embedded primary CRC were immunohistochemically studied for CD133, a putative CRC stem cell marker, and MMR proteins MLH1, MSH2, MSH6 and PMS2. CD133 expression was semi-quantitated for proportion of tumor immunopositivity on a scale of 0-5 and staining intensity on a scale of 0-3 with a final score (units) being the product of proportion and intensity of tumor staining. The tumor was considered immunopositive only when the tumor demonstrated moderate to strong intensity of CD133 staining (a decision made after analysis of CD133 expression in normal colon). Deficient MMR (dMMR) was interpreted as unequivocal loss of tumor nuclear staining for any MMR protein despite immunoreactivity in the internal positive controls.
Results: CD133 was expressed in 36 (90.0%) left-sided and 28 (70.0%) right-sided tumors (p 0.05).
Conclusion: Proficient MMR correlated with high levels of CD133-marked putative cancer stem cells in both right- and left-sided tumors, whereas significantly lower levels of CD133-marked putative cancer stem cells were associated with deficient MMR status in colorectal carcinomas found on the right.